Pub Date : 2024-06-06DOI: 10.4103/wjtcm.wjtcm_71_24
Yong Shi, Feng Yue
Metaphors are ubiquitous in Traditional Chinese Medicine (TCM) thinking. This study focuses on the cognitive mechanism for combining TCM theories with conceptual metaphorical theories and analyzes how TCM explains its theories through metaphor. Metaphorical thinking of TCM (MTT) is explicitly defined as a proper integration of many key concepts in traditional Chinese philosophy and medicine, such as “correspondence between man and the universe,” “Yin-Yang and five-phase doctrines,” “Xiang-based analogy and categorization,” “syndrome differentiation and treatment,” “theory of visceral manifestation,” and “six climate exopathogens and seven emotions.” Three essential features of MTT are proposed: double mapping structures, including simple and categorization styles; double thinking centers, including entity-based and process-based thinking patterns; and double operational functions, including descriptive and inferential functions. Analysis of the complicated features of MTT is helpful not only for enriching the study of metaphors but also for revealing the original appearance of TCM, the real meaning of TCM theories, and providing a new way to develop TCM.
{"title":"Metaphorical Thinking of Traditional Chinese Medicine and Its Features","authors":"Yong Shi, Feng Yue","doi":"10.4103/wjtcm.wjtcm_71_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_71_24","url":null,"abstract":"\u0000 \u0000 \u0000 Metaphors are ubiquitous in Traditional Chinese Medicine (TCM) thinking.\u0000 \u0000 \u0000 \u0000 This study focuses on the cognitive mechanism for combining TCM theories with conceptual metaphorical theories and analyzes how TCM explains its theories through metaphor.\u0000 \u0000 \u0000 \u0000 Metaphorical thinking of TCM (MTT) is explicitly defined as a proper integration of many key concepts in traditional Chinese philosophy and medicine, such as “correspondence between man and the universe,” “Yin-Yang and five-phase doctrines,” “Xiang-based analogy and categorization,” “syndrome differentiation and treatment,” “theory of visceral manifestation,” and “six climate exopathogens and seven emotions.”\u0000 \u0000 \u0000 \u0000 Three essential features of MTT are proposed: double mapping structures, including simple and categorization styles; double thinking centers, including entity-based and process-based thinking patterns; and double operational functions, including descriptive and inferential functions.\u0000 \u0000 \u0000 \u0000 Analysis of the complicated features of MTT is helpful not only for enriching the study of metaphors but also for revealing the original appearance of TCM, the real meaning of TCM theories, and providing a new way to develop TCM.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141377570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stress is the main factor that leads to hair loss, and no effective therapeutics have been developed for stress alopecia. Polygonum multiflorum Thunb. (PM) is a famous traditional Chinese medicine for tonifying the kidney and nourishing the liver, which is used to treat hair loss. This study aimed to demonstrate that PM is a promising agent for the treatment of chronic stress-induced hair loss. C57BL/6J male mice were subjected to chronic restraint stress to inhibit hair follicle growth. Subsequently, the effect of PM was examined by oral administration of the PM water extract or cortisone, followed by histological analysis, immunofluorescence of follicle samples, serum metabolomics, and adrenal proteomics. Hair regeneration in a mouse model was severely inhibited by chronic restraint stress. After PM treatment, hair regeneration in model mice was promoted, including an increased length of hair shafts in skin sections, an increased number of 5-Ethynyl-2’- deoxyuridine-positive cells, and a decreased number of apoptotic cells around the hair follicles. The various test indicators of these PM-treated mice almost recovered to levels comparable to those of the control mice. Through metabolomics and proteomics analyses, we identified 181 endogenous differential metabolites and 75 differential proteins, which may be the potential targets for PM. Pathway enrichment analysis showed that steroid biosynthesis (the main pathway through which stress leads to an imbalance in glucocorticoid secretion by the adrenal gland) may play an important role in the therapeutic effects of PM. In addition, omics analysis revealed that glycolysis/gluconeogenesis, pyruvate metabolism, lipid metabolism, and other glucocorticoid-related metabolic pathways differed significantly after PM treatment. PM is an important natural drug that regulates hair regeneration in mice under stress, and its underlying mechanism is closely related to the regulation of adrenal glucocorticoids and their metabolism.
{"title":"Investigation on the Therapeutic Effect of Polygonum multiflorum Thunb. in Chronic Stress-induced Hair Loss in Mice Coupled with Metabolomics and Proteomics","authors":"Yong-Kang Zhao, Rui-Xian Guo, Rui-Sheng Li, Wei Shi, Hai-Ying Gong, Run-Ran Ma, Han Gao, Zhen Li, Ke-Jian Hu, Zhao-fang Bai, Xiao-He Xiao, Qing-Ce Zang, Wei-Jun Kong, Peng Li, Ming Niu, Jia‐bo Wang, Yuan Gao","doi":"10.4103/wjtcm.wjtcm_78_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_78_24","url":null,"abstract":"\u0000 \u0000 \u0000 Stress is the main factor that leads to hair loss, and no effective therapeutics have been developed for stress alopecia. Polygonum multiflorum Thunb. (PM) is a famous traditional Chinese medicine for tonifying the kidney and nourishing the liver, which is used to treat hair loss. This study aimed to demonstrate that PM is a promising agent for the treatment of chronic stress-induced hair loss.\u0000 \u0000 \u0000 \u0000 C57BL/6J male mice were subjected to chronic restraint stress to inhibit hair follicle growth. Subsequently, the effect of PM was examined by oral administration of the PM water extract or cortisone, followed by histological analysis, immunofluorescence of follicle samples, serum metabolomics, and adrenal proteomics.\u0000 \u0000 \u0000 \u0000 Hair regeneration in a mouse model was severely inhibited by chronic restraint stress. After PM treatment, hair regeneration in model mice was promoted, including an increased length of hair shafts in skin sections, an increased number of 5-Ethynyl-2’- deoxyuridine-positive cells, and a decreased number of apoptotic cells around the hair follicles. The various test indicators of these PM-treated mice almost recovered to levels comparable to those of the control mice. Through metabolomics and proteomics analyses, we identified 181 endogenous differential metabolites and 75 differential proteins, which may be the potential targets for PM. Pathway enrichment analysis showed that steroid biosynthesis (the main pathway through which stress leads to an imbalance in glucocorticoid secretion by the adrenal gland) may play an important role in the therapeutic effects of PM. In addition, omics analysis revealed that glycolysis/gluconeogenesis, pyruvate metabolism, lipid metabolism, and other glucocorticoid-related metabolic pathways differed significantly after PM treatment.\u0000 \u0000 \u0000 \u0000 PM is an important natural drug that regulates hair regeneration in mice under stress, and its underlying mechanism is closely related to the regulation of adrenal glucocorticoids and their metabolism.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141099358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sepsis-induced acute lung injury (ALI) is a clinically critical condition with a high mortality rate. Shenfu injection (SFI) is a Chinese herbal medicine extracted from red ginseng and Aconite, Radix Aconiti, with various pharmacological activities. This study aimed to investigate the potential mechanism of action of SFI in preventing sepsis-induced ALI. We established a mouse model of sepsis-induced ALI by cecal ligation and puncture (CLP). The mice were randomly divided into three groups (n = 8): Sham, CLP, and SFI (10 mL/kg). Bronchoalveolar lavage fluid (BALF) and lung tissue were collected for pathological analysis, enzyme-linked immunosorbent assay, immunohistochemistry (IHC), and protein detection. Our results showed that SFI significantly ameliorated pathological damage caused by CLP-induced ALI. SFI treatment significantly decreased the lung wet-to-dry weight ratio. In addition, SFI treatment significantly reduced the protein levels and cell numbers in the BALF. SFI could significantly reduce the levels of tumor necrosis factor-α, interleukin-6 (IL-6), and IL-1β in plasma and BALF. SFI significantly reduced the protein expression of Bax and cleaved caspase-3 and increased the protein levels of Bcl-2. Western blotting and IHC results showed that SFI reduced the phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3). In a septic ALI mouse model, SFI inhibited apoptosis and inflammation through the JAK2/STAT3 pathway, providing a candidate drug for the treatment of septic ALI.
{"title":"Protective Effect of Shenfu Injection against Sepsis-induced Acute Lung Injury by Suppressing Inflammation and Apoptosis Through the Regulation of the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Pathway","authors":"Li-Juan Cao, Hai-Tang Xie, Zhong-Xia Chu, Yue Ma, Ming-Ming Wang, Zhuang Shi","doi":"10.4103/wjtcm.wjtcm_76_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_76_24","url":null,"abstract":"\u0000 \u0000 \u0000 Sepsis-induced acute lung injury (ALI) is a clinically critical condition with a high mortality rate. Shenfu injection (SFI) is a Chinese herbal medicine extracted from red ginseng and Aconite, Radix Aconiti, with various pharmacological activities. This study aimed to investigate the potential mechanism of action of SFI in preventing sepsis-induced ALI.\u0000 \u0000 \u0000 \u0000 We established a mouse model of sepsis-induced ALI by cecal ligation and puncture (CLP). The mice were randomly divided into three groups (n = 8): Sham, CLP, and SFI (10 mL/kg). Bronchoalveolar lavage fluid (BALF) and lung tissue were collected for pathological analysis, enzyme-linked immunosorbent assay, immunohistochemistry (IHC), and protein detection.\u0000 \u0000 \u0000 \u0000 Our results showed that SFI significantly ameliorated pathological damage caused by CLP-induced ALI. SFI treatment significantly decreased the lung wet-to-dry weight ratio. In addition, SFI treatment significantly reduced the protein levels and cell numbers in the BALF. SFI could significantly reduce the levels of tumor necrosis factor-α, interleukin-6 (IL-6), and IL-1β in plasma and BALF. SFI significantly reduced the protein expression of Bax and cleaved caspase-3 and increased the protein levels of Bcl-2. Western blotting and IHC results showed that SFI reduced the phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3).\u0000 \u0000 \u0000 \u0000 In a septic ALI mouse model, SFI inhibited apoptosis and inflammation through the JAK2/STAT3 pathway, providing a candidate drug for the treatment of septic ALI.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141105084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-23DOI: 10.4103/wjtcm.wjtcm_72_24
Feng Zhang, N. Weng, Jian-Xiu Zhai, Guangyang Jiao, Ye-Jian Wang, Tao Pang, Jing-Lei Liang, Yan-Hong Chen, Dou-Dou Huang, Zhi-Peng Wang, Han Jun, Yiyi Ma, Xia Tao, Jun Yin, Wan-Sheng Chen
The study aimed to establish an effective strategy for systematically characterizing and verifying compounds in Huangkui capsules (HKCs). An ultrahigh-performance liquid chromatography quadrupole time-of-flight mass spectrometry (MS) method was effectively established and utilized for the chemical compound characterization in HKC, with the support of MS-DIAL, MS-FINDER, and Global Natural Product Social Molecular Network. Multiple rat samples were analyzed after the oral administration. Metabolites were identified based on specific cleavage behaviors, and metabolic pathways were predicted. Semi-quantitative analysis of the metabolome profiles was conducted using post-data processing. High concentrations in vivo were investigated for their role in tacrolimus-induced death of HK-2 cells. In total, 129 compounds were identified in HKC, of which 74 were reported for the first time. In this study, we successfully identified and uncovered 19 prototypes and 123 metabolites from the biosamples. The concentrations of glucuronidation and methylation metabolites of quercetin were the highest in the kidney and intestinal tissues. In contrast, significant glucuronidation of quercetin metabolites was observed with high blood concentrations. Notably, quercetin glucuronidation and methylation metabolites protected HK-cell against tacrolimus-induced injury in a dose-dependent manner. This study successfully established a reliable and efficient strategy for comprehensive characterization of traditional Chinese medicine compounds. This strategy harnessed the power of various intelligent postprocessing technologies to provide a more thorough understanding of active components and their metabolic transformations in the body. These results suggest that quercetin metabolites should be evaluated for their protective capacity against kidney disease.
{"title":"Rapid Classification and Identification of Chemical Compounds and Semi-Quantitative Metabolism of Huangkui Capsules and the Protective Effects of Its Quercetin Derivatives against Tacrolimus-induced HK-cell Reduction","authors":"Feng Zhang, N. Weng, Jian-Xiu Zhai, Guangyang Jiao, Ye-Jian Wang, Tao Pang, Jing-Lei Liang, Yan-Hong Chen, Dou-Dou Huang, Zhi-Peng Wang, Han Jun, Yiyi Ma, Xia Tao, Jun Yin, Wan-Sheng Chen","doi":"10.4103/wjtcm.wjtcm_72_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_72_24","url":null,"abstract":"\u0000 \u0000 \u0000 The study aimed to establish an effective strategy for systematically characterizing and verifying compounds in Huangkui capsules (HKCs).\u0000 \u0000 \u0000 \u0000 An ultrahigh-performance liquid chromatography quadrupole time-of-flight mass spectrometry (MS) method was effectively established and utilized for the chemical compound characterization in HKC, with the support of MS-DIAL, MS-FINDER, and Global Natural Product Social Molecular Network. Multiple rat samples were analyzed after the oral administration. Metabolites were identified based on specific cleavage behaviors, and metabolic pathways were predicted. Semi-quantitative analysis of the metabolome profiles was conducted using post-data processing. High concentrations in vivo were investigated for their role in tacrolimus-induced death of HK-2 cells.\u0000 \u0000 \u0000 \u0000 In total, 129 compounds were identified in HKC, of which 74 were reported for the first time. In this study, we successfully identified and uncovered 19 prototypes and 123 metabolites from the biosamples. The concentrations of glucuronidation and methylation metabolites of quercetin were the highest in the kidney and intestinal tissues. In contrast, significant glucuronidation of quercetin metabolites was observed with high blood concentrations. Notably, quercetin glucuronidation and methylation metabolites protected HK-cell against tacrolimus-induced injury in a dose-dependent manner.\u0000 \u0000 \u0000 \u0000 This study successfully established a reliable and efficient strategy for comprehensive characterization of traditional Chinese medicine compounds. This strategy harnessed the power of various intelligent postprocessing technologies to provide a more thorough understanding of active components and their metabolic transformations in the body. These results suggest that quercetin metabolites should be evaluated for their protective capacity against kidney disease.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141104261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-23DOI: 10.4103/wjtcm.wjtcm_74_24
Qin-Dan Cui, Li-Dan Shen, Yuan Bai, Muhammad Azhar, Jun Deng, Xian-Ju Huang, Hai-Ying Tong
The objective of the study was to explore the potential signaling mechanism of Aconitum tanguticum (Maxim.) Stapf (ATS) and its impact on intestinal fibrosis in vitro. Network pharmacology was used to screen the active components of ATS and predict their potential targets in intestinal fibrosis. The protein–protein interaction network graph was constructed using drug–disease intersection targets retrieved from the Search Tool for Retrieval of Interacting Genes/Proteins database. The network diagram was analyzed using Cytoscape 3.6.1’stopology function. The gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted using the database for annotation, visualization, and integrated discovery platform. Intestinal fibroblast model in vitro was constructed using transforming growth factor-β1 (TGF-β1)-induced CCD-18Co cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to verify the network pharmacology-predicted antifibrotic signaling pathway of ATS and the traditional antifibrotic signaling pathway. Network pharmacology revealed that there were 19 active components in ATS, suggesting that ATS could be involved in the regulation of mitogen-activated protein kinase 1 (MAPK1), PIK3CA, MAPK3, and other important targets that are present in cancer pathways, including proteoglycans, influenza A, and phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) signaling pathways. The results of quantitative reverse transcription-polymerase chain reaction (qRT-PCR) demonstrated that 0.1–1 μg/mL ATS may suppress tissue inhibitor of metalloproteinase 1, collagen I, and alpha-smooth muscle actin expression levels. The expression of the TGF-β/suppressor of the mother against decapentaplegic (Smad) and PI3K/Akt signaling pathways was controlled by ATS. In addition, ATS inhibited the PI3K/Akt pathway by reducing the expression of MAPK1, HSP90AA1, and PIK3CA. It has been confirmed that ATS is a multipathway and multitarget treatment for intestinal fibrosis. This study suggested that ATS might alleviate intestinal fibrosis by blocking both the TGF-β/Smad and the PI3K/Akt pathway.
{"title":"Inhibiting Effect and Mechanism of Aconitum tanguticum (Maxim.) Stapf on Intestinal Fibrosis of CCD-18Co Cells","authors":"Qin-Dan Cui, Li-Dan Shen, Yuan Bai, Muhammad Azhar, Jun Deng, Xian-Ju Huang, Hai-Ying Tong","doi":"10.4103/wjtcm.wjtcm_74_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_74_24","url":null,"abstract":"\u0000 \u0000 \u0000 The objective of the study was to explore the potential signaling mechanism of Aconitum tanguticum (Maxim.) Stapf (ATS) and its impact on intestinal fibrosis in vitro.\u0000 \u0000 \u0000 \u0000 Network pharmacology was used to screen the active components of ATS and predict their potential targets in intestinal fibrosis. The protein–protein interaction network graph was constructed using drug–disease intersection targets retrieved from the Search Tool for Retrieval of Interacting Genes/Proteins database. The network diagram was analyzed using Cytoscape 3.6.1’stopology function. The gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were conducted using the database for annotation, visualization, and integrated discovery platform. Intestinal fibroblast model in vitro was constructed using transforming growth factor-β1 (TGF-β1)-induced CCD-18Co cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to verify the network pharmacology-predicted antifibrotic signaling pathway of ATS and the traditional antifibrotic signaling pathway.\u0000 \u0000 \u0000 \u0000 Network pharmacology revealed that there were 19 active components in ATS, suggesting that ATS could be involved in the regulation of mitogen-activated protein kinase 1 (MAPK1), PIK3CA, MAPK3, and other important targets that are present in cancer pathways, including proteoglycans, influenza A, and phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) signaling pathways. The results of quantitative reverse transcription-polymerase chain reaction (qRT-PCR) demonstrated that 0.1–1 μg/mL ATS may suppress tissue inhibitor of metalloproteinase 1, collagen I, and alpha-smooth muscle actin expression levels. The expression of the TGF-β/suppressor of the mother against decapentaplegic (Smad) and PI3K/Akt signaling pathways was controlled by ATS. In addition, ATS inhibited the PI3K/Akt pathway by reducing the expression of MAPK1, HSP90AA1, and PIK3CA.\u0000 \u0000 \u0000 \u0000 It has been confirmed that ATS is a multipathway and multitarget treatment for intestinal fibrosis. This study suggested that ATS might alleviate intestinal fibrosis by blocking both the TGF-β/Smad and the PI3K/Akt pathway.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141103758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-23DOI: 10.4103/wjtcm.wjtcm_69_24
Yong-Jia Song, Jia-Min Bao, Zeng-Qiao Zhang, Y. Hai, Hao-Nan Wen, Tian-Jun Zhai, Wei Feng, Min Song
Osteoarthritis (OA) is a progressive joint disease characterized by degeneration and destruction of articular cartilage. Arctiin (ARC) has been shown in many studies to have potential anti-inflammatory, anti-apoptotic, and antioxidant effects in various diseases. However, the mechanism by which ARC exerts its protective effects in OA is not fully understood. Here, we explore the mechanism by which ARC plays its protective role in OA. Mouse chondrocytes were isolated and characterized through toluidine blue staining and collagen II immunofluorescence labeling. A mouse-based experimental model was developed to induce chondrocyte inflammation through Interleukin-1β (IL-1β). Subsequently, ARC was administered in various doses to mitigate this inflammation. Techniques such as biochemical assays, Enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunofluorescence labeling were employed to detect changes in nitric oxide (NO), lactate dehydrogenase (LDH), inflammatory markers, and components of the cartilage matrix in chondrocytes. RNA-sequencing (RNA-seq) was utilized to explore variations in gene expression among chondrocytes across different groups. The genes and signaling pathways that were identified underwent analysis through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment studies. Validation of gene and protein expression was carried out using qRT-PCR, Western blotting, and cellular flow cytometry, based on the results from sequencing. Furthermore, Safranin-O fast green staining and immunohistochemistry staining were performed on slices of the mice knee joint to evaluate the OA Research Society International score, alterations in the cartilage matrix, and levels of apoptosis-related proteins at sites of knee cartilage damage in an arthritis model induced by monosodium iodoacetate (MIA) and physical activity. It was found that ARC effectively inhibits the production of IL-1β-induced chondrocytes’ inducible NO synthase, cyclooxygenase-2, NO, LDH, IL-6, and tumor necrosis factor-α. ARC exhibited a dose-dependent effect on chondrocytes by reducing IL-1β-induced matrix metalloproteinase-3 (MMP-3) and a disintegrin and metalloproteinase with thrombospondin motifs-5 levels while increasing Aggrecan levels. RNA-seq and bioinformatics analysis revealed that ARC’s therapeutic effects involve apoptotic signaling pathways through the downregulation of Bcl-2-associated X protein (Bax) and caspase-3 expression and the upregulation of B-cell lymphoma-2 (Bcl-2) expression in IL-1β-induced chondrocytes. ARC significantly raised the levels of aggrecan and Bcl-2 and decreased the levels of MMP-3, Bax, and caspase-3 in an arthritis model induced by MIA and movement. Through RNA-seq, in vitro cell assays, and in vivo experiments, this research established the link between apoptosis and inflammation in the progression of OA and confirmed the protective ef
骨关节炎（OA）是一种以关节软骨退化和破坏为特征的渐进性关节疾病。许多研究表明，牛蒡子素（ARC）在多种疾病中具有潜在的抗炎、抗凋亡和抗氧化作用。然而，ARC 在 OA 中发挥保护作用的机制尚未完全明了。在此，我们探讨了 ARC 在 OA 中发挥保护作用的机制。 通过甲苯胺蓝染色和胶原蛋白 II 免疫荧光标记，我们分离并鉴定了小鼠软骨细胞。建立了一个基于小鼠的实验模型，通过白细胞介素-1β（IL-1β）诱导软骨细胞炎症。随后，施用不同剂量的 ARC 以缓解这种炎症。实验采用了生化分析、酶联免疫吸附试验、定量实时聚合酶链反应（qRT-PCR）、Western 印迹和免疫荧光标记等技术来检测软骨细胞中一氧化氮（NO）、乳酸脱氢酶（LDH）、炎症标志物和软骨基质成分的变化。利用 RNA 序列分析（RNA-seq）探索不同组别软骨细胞基因表达的变化。通过基因本体论和《京都基因和基因组百科全书》的富集研究，对鉴定出的基因和信号通路进行了分析。根据测序结果，使用 qRT-PCR、Western 印迹和细胞流式细胞术对基因和蛋白质的表达进行了验证。此外，还对小鼠膝关节切片进行了Safranin-O快绿染色和免疫组织化学染色，以评估在碘乙酸钠（MIA）和体力活动诱导的关节炎模型中，膝关节软骨损伤部位的OA研究协会国际评分、软骨基质的改变以及凋亡相关蛋白的水平。 研究发现，ARC 能有效抑制 IL-1β 诱导的软骨细胞诱导性 NO 合酶、环氧化酶-2、NO、LDH、IL-6 和肿瘤坏死因子-α 的产生。ARC 对软骨细胞有剂量依赖性作用，它能降低 IL-1β 诱导的基质金属蛋白酶-3（MMP-3）和具有血栓软骨素基序的崩解素和金属蛋白酶-5 的水平，同时增加 Aggrecan 的水平。RNA-seq和生物信息学分析表明，在IL-1β诱导的软骨细胞中，ARC通过下调Bcl-2相关X蛋白（Bax）和caspase-3的表达以及上调B细胞淋巴瘤-2（Bcl-2）的表达，发挥了涉及凋亡信号通路的治疗作用。在 MIA 和运动诱导的关节炎模型中，ARC 能明显提高 aggrecan 和 Bcl-2 的水平，降低 MMP-3、Bax 和 caspase-3 的水平。 通过 RNA-seq、体外细胞检测和体内实验，这项研究确定了凋亡和炎症在 OA 进展过程中的联系，并证实了 ARC 对软骨细胞及其关键靶点的保护作用。这凸显了 ARC 的治疗潜力及其在开发 OA 治疗方法中的作用。
{"title":"Arctiin Protects Chondrocytes From Interleukin-1β-Induced Inflammation and Apoptosis by RNA Sequence In vivo and In vitro","authors":"Yong-Jia Song, Jia-Min Bao, Zeng-Qiao Zhang, Y. Hai, Hao-Nan Wen, Tian-Jun Zhai, Wei Feng, Min Song","doi":"10.4103/wjtcm.wjtcm_69_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_69_24","url":null,"abstract":"\u0000 \u0000 \u0000 Osteoarthritis (OA) is a progressive joint disease characterized by degeneration and destruction of articular cartilage. Arctiin (ARC) has been shown in many studies to have potential anti-inflammatory, anti-apoptotic, and antioxidant effects in various diseases. However, the mechanism by which ARC exerts its protective effects in OA is not fully understood. Here, we explore the mechanism by which ARC plays its protective role in OA.\u0000 \u0000 \u0000 \u0000 Mouse chondrocytes were isolated and characterized through toluidine blue staining and collagen II immunofluorescence labeling. A mouse-based experimental model was developed to induce chondrocyte inflammation through Interleukin-1β (IL-1β). Subsequently, ARC was administered in various doses to mitigate this inflammation. Techniques such as biochemical assays, Enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunofluorescence labeling were employed to detect changes in nitric oxide (NO), lactate dehydrogenase (LDH), inflammatory markers, and components of the cartilage matrix in chondrocytes. RNA-sequencing (RNA-seq) was utilized to explore variations in gene expression among chondrocytes across different groups. The genes and signaling pathways that were identified underwent analysis through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment studies. Validation of gene and protein expression was carried out using qRT-PCR, Western blotting, and cellular flow cytometry, based on the results from sequencing. Furthermore, Safranin-O fast green staining and immunohistochemistry staining were performed on slices of the mice knee joint to evaluate the OA Research Society International score, alterations in the cartilage matrix, and levels of apoptosis-related proteins at sites of knee cartilage damage in an arthritis model induced by monosodium iodoacetate (MIA) and physical activity.\u0000 \u0000 \u0000 \u0000 It was found that ARC effectively inhibits the production of IL-1β-induced chondrocytes’ inducible NO synthase, cyclooxygenase-2, NO, LDH, IL-6, and tumor necrosis factor-α. ARC exhibited a dose-dependent effect on chondrocytes by reducing IL-1β-induced matrix metalloproteinase-3 (MMP-3) and a disintegrin and metalloproteinase with thrombospondin motifs-5 levels while increasing Aggrecan levels. RNA-seq and bioinformatics analysis revealed that ARC’s therapeutic effects involve apoptotic signaling pathways through the downregulation of Bcl-2-associated X protein (Bax) and caspase-3 expression and the upregulation of B-cell lymphoma-2 (Bcl-2) expression in IL-1β-induced chondrocytes. ARC significantly raised the levels of aggrecan and Bcl-2 and decreased the levels of MMP-3, Bax, and caspase-3 in an arthritis model induced by MIA and movement.\u0000 \u0000 \u0000 \u0000 Through RNA-seq, in vitro cell assays, and in vivo experiments, this research established the link between apoptosis and inflammation in the progression of OA and confirmed the protective ef","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141107565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell co-culture technology has been widely used to analyze the effects of drugs on cell proliferation and the expression of some proteins in cells, especially in the field of traditional Chinese medicine (TCM); however, the interactions between cells and the transmission of TCM effects between cells have not been adequately studied. Using data on gene transcription regulation, biological response, signal channel, and cell-specific expression protein, we built a network for cell types based on entity grammar. Through the correspondence and location information of signal molecules and receptors, type-specific networks of single cells were connected and a multicellular network of smooth muscle cells, neurons, and vascular endothelial cells was constructed. The mechanism of action of nimodipine was analyzed based on the multicellular communication network and its simulation capability was evaluated. The outputs generated by the model developed in this study showed that nimodipine inhibited smooth muscle contraction, due to the overload of Ca2+ and the toxicity of excitatory amino acids, and protected neurons and vascular endothelial cells by supporting cell proliferation and inhibiting cell apoptosis. These results were consistent with the known mechanism of nimodipine action, thus confirming that the multicellular network can be used to study the transmission of drug effects among cells. This study lays a foundation for the analysis of the transmission of drug effects in multi-cells, tissues, organs, and other spatial scales through multicellular co-culture experiments, based on a multicellular communication network. In addition, it provides a biological network model for the analysis of TCM action mechanisms.
{"title":"Construction of a Multicellular Communication Network Model for Cell Co-Culture Technology and Evaluation of Its Simulation Capability","authors":"Yuan-Yuan Geng, Chao Wei, Guo-Fei Chen, Bai-Xia Zhang","doi":"10.4103/wjtcm.wjtcm_73_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_73_24","url":null,"abstract":"\u0000 \u0000 \u0000 Cell co-culture technology has been widely used to analyze the effects of drugs on cell proliferation and the expression of some proteins in cells, especially in the field of traditional Chinese medicine (TCM); however, the interactions between cells and the transmission of TCM effects between cells have not been adequately studied.\u0000 \u0000 \u0000 \u0000 Using data on gene transcription regulation, biological response, signal channel, and cell-specific expression protein, we built a network for cell types based on entity grammar. Through the correspondence and location information of signal molecules and receptors, type-specific networks of single cells were connected and a multicellular network of smooth muscle cells, neurons, and vascular endothelial cells was constructed. The mechanism of action of nimodipine was analyzed based on the multicellular communication network and its simulation capability was evaluated.\u0000 \u0000 \u0000 \u0000 The outputs generated by the model developed in this study showed that nimodipine inhibited smooth muscle contraction, due to the overload of Ca2+ and the toxicity of excitatory amino acids, and protected neurons and vascular endothelial cells by supporting cell proliferation and inhibiting cell apoptosis. These results were consistent with the known mechanism of nimodipine action, thus confirming that the multicellular network can be used to study the transmission of drug effects among cells.\u0000 \u0000 \u0000 \u0000 This study lays a foundation for the analysis of the transmission of drug effects in multi-cells, tissues, organs, and other spatial scales through multicellular co-culture experiments, based on a multicellular communication network. In addition, it provides a biological network model for the analysis of TCM action mechanisms.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141107838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-18DOI: 10.4103/wjtcm.wjtcm_70_24
Xin Zhang, Jian-Li Ge, Kun Su, Jian-Ming He, Min-Mei Zhang, Jing Zhang, Yun-Long Ma, Yun-Chao Sun, Xin-Qiang Chu
The objective of the study was to explore the regulatory mechanism of the Xiaozheng Tongluo method on lipid metabolism in liver tissue based on the sterol regulatory element-binding protein-2/(SREBP2)/3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)/low-density lipoprotein receptor (LDLR) signaling pathway. C57BL/6 mice were selected as the blank group. The apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into the model group, traditional Chinese medicine (TCM) group, and control group. The general condition of the mice was determined by the mouse’s state and liver weight. Liver hematoxylin and eosin staining and Oil Red O staining were used to observe the pathological changes and lipid droplet deposition of the liver. The protein expression levels of SREBP2, HMGCR, and LDLR were detected by Western blotting and polymerase chain reaction. (1) The rats in the model group were in poor condition, and their liver weight increased significantly. Compared with the model group, the condition of the TCM group and the control group improved to varying degrees, and their liver weight decreased significantly. (2) Compared with the normal group, the hepatocytes in the model group were arranged in a disorderly manner, and the red-stained lipids of stem cells increased significantly. Compared with the model group, the degree of liver lesions in the control group and TCM group was reduced, and the red-stained lipid of hepatocytes was significantly reduced. (3) Compared with the blank group, the expression of SREBP2 and HMGCR protein in the model group increased significantly, and the expression of LDLR protein decreased significantly (P < 0.05). Compared with the model group, the expression of SREBP2 and HMGCR protein in the TCM group decreased significantly, and the expression of LDLR protein increased significantly (P < 0.05). The method detailed in this paper can increase the expression of SREBP2 and HMGCR protein and decrease the expression of LDLR protein, thus regulating liver cholesterol metabolism and delaying the progression of atherosclerosis.
本研究的目的是基于固醇调节元件结合蛋白-2/（SREBP2）/3-羟基-3-甲基戊二酰辅酶A还原酶（HMGCR）/低密度脂蛋白受体（LDLR）信号通路，探讨小青龙汤法对肝组织脂质代谢的调控机制。 C57BL/6 小鼠为空白组。将载脂蛋白 E 缺乏（ApoE-/-）小鼠随机分为模型组、中药组和对照组。小鼠的一般状况由小鼠的状态和肝脏重量决定。肝脏苏木精、伊红染色和油红 O 染色用于观察肝脏的病理变化和脂滴沉积。通过 Western 印迹和聚合酶链反应检测 SREBP2、HMGCR 和 LDLR 的蛋白表达水平。 (1) 模型组大鼠状况不佳，肝脏重量明显增加。与模型组相比，中药组和对照组的病情均有不同程度的改善，肝脏重量明显减轻。(2）与正常组相比，模型组肝细胞排列紊乱，干细胞红染脂质明显增加。与模型组相比，对照组和中药组肝脏病变程度减轻，肝细胞红染脂质明显减少。(3）与空白组相比，模型组 SREBP2 和 HMGCR 蛋白表达明显增加，LDLR 蛋白表达明显减少（P < 0.05）。与模型组相比，中药组的 SREBP2 和 HMGCR 蛋白表达明显降低，LDLR 蛋白表达明显升高（P < 0.05）。 本文详述的方法可增加SREBP2和HMGCR蛋白的表达，降低LDLR蛋白的表达，从而调节肝脏胆固醇代谢，延缓动脉粥样硬化的进展。
{"title":"Regulatory Mechanism of Xiaozheng Tongluo Method on Hepatic Lipid Metabolism in ApoE-/- Mice: Insights from the Sterol Regulatory Element-binding Protein-2/3-hydroxy-3-methylglutaryl Coenzyme A Reductase/Low-density Lipoprotein Receptor Signaling Pathway","authors":"Xin Zhang, Jian-Li Ge, Kun Su, Jian-Ming He, Min-Mei Zhang, Jing Zhang, Yun-Long Ma, Yun-Chao Sun, Xin-Qiang Chu","doi":"10.4103/wjtcm.wjtcm_70_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_70_24","url":null,"abstract":"\u0000 \u0000 \u0000 The objective of the study was to explore the regulatory mechanism of the Xiaozheng Tongluo method on lipid metabolism in liver tissue based on the sterol regulatory element-binding protein-2/(SREBP2)/3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)/low-density lipoprotein receptor (LDLR) signaling pathway.\u0000 \u0000 \u0000 \u0000 C57BL/6 mice were selected as the blank group. The apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into the model group, traditional Chinese medicine (TCM) group, and control group. The general condition of the mice was determined by the mouse’s state and liver weight. Liver hematoxylin and eosin staining and Oil Red O staining were used to observe the pathological changes and lipid droplet deposition of the liver. The protein expression levels of SREBP2, HMGCR, and LDLR were detected by Western blotting and polymerase chain reaction.\u0000 \u0000 \u0000 \u0000 (1) The rats in the model group were in poor condition, and their liver weight increased significantly. Compared with the model group, the condition of the TCM group and the control group improved to varying degrees, and their liver weight decreased significantly. (2) Compared with the normal group, the hepatocytes in the model group were arranged in a disorderly manner, and the red-stained lipids of stem cells increased significantly. Compared with the model group, the degree of liver lesions in the control group and TCM group was reduced, and the red-stained lipid of hepatocytes was significantly reduced. (3) Compared with the blank group, the expression of SREBP2 and HMGCR protein in the model group increased significantly, and the expression of LDLR protein decreased significantly (P < 0.05). Compared with the model group, the expression of SREBP2 and HMGCR protein in the TCM group decreased significantly, and the expression of LDLR protein increased significantly (P < 0.05).\u0000 \u0000 \u0000 \u0000 The method detailed in this paper can increase the expression of SREBP2 and HMGCR protein and decrease the expression of LDLR protein, thus regulating liver cholesterol metabolism and delaying the progression of atherosclerosis.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141125348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NOD-like receptor protein 3 (NLRP3)-mediated pyroptosis is pivotal in the pathological development of cerebral ischemia/reperfusion injury (CIRI). Although previous research has shown that electroacupuncture (EA) can alleviate CIRI through sirtuin-1 (SIRT1), the mechanism has not been well elucidated. Our study aimed to clarify whether the neuroprotective functions of EA are related to the reduction in NLRP3-mediated pyroptosis through the SIRT1 pathway. Rats received daily pretreatment with EA for 5 consecutive days before undergoing middle cerebral artery occlusion surgery. The Longa score was used to assess neurologic function. Infarct volume and morphological alterations were analyzed using 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin staining. In addition, neuronal pyroptosis was identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling/caspase-1 and neuronal nuclear antigen/caspase-1 immunofluorescence double staining. Levels of expression of pyroptosis markers were assessed by Western blotting and enzyme-linked immunosorbent assay. EA improved deficits in neurologic function and minimized cerebral infarct volume. Mechanistically, a number of neuronal pyroptotic cells and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD, and gasdermin D in the cerebral cortex were markedly reduced by EA treatment, and conversely, SIRT1 levels were increased. Notably, the specific SIRT1 inhibitor, EX527, reversed the effects of EA. EA potentially exerts a neuroprotective effect against CIRI through the SIRT1 pathway in NLRP3-mediated pyroptosis.
NOD样受体蛋白3（NLRP3）介导的热蛋白沉积是脑缺血再灌注损伤（CIRI）病理发展的关键。尽管之前的研究表明电针（EA）可以通过sirtuin-1（SIRT1）缓解CIRI，但其机制尚未得到很好的阐明。我们的研究旨在阐明 EA 的神经保护功能是否与通过 SIRT1 途径减少 NLRP3 介导的热蛋白沉积有关。 大鼠在接受大脑中动脉闭塞手术前连续5天每天接受EA预处理。Longa 评分用于评估神经功能。用2,3,5-三苯基氯化四氮唑和苏木精及伊红染色分析梗死体积和形态学改变。此外，通过末端脱氧核苷酸转移酶介导的dUTP-生物素缺口端标记/caspase-1和神经元核抗原/caspase-1免疫荧光双重染色，确定了神经元的脓毒症。通过 Western 印迹法和酶联免疫吸附试验评估了热蛋白沉积标记物的表达水平。 EA改善了神经功能缺损，最大程度地缩小了脑梗塞体积。从机理上讲，EA治疗后大脑皮层中神经元凋亡细胞的数量和NLRP3、含有CARD的凋亡相关斑点样蛋白和gasdermin D的蛋白水平明显降低，相反，SIRT1的水平升高。值得注意的是，特异性 SIRT1 抑制剂 EX527 逆转了 EA 的作用。 EA可能通过SIRT1途径在NLRP3介导的热蛋白沉积过程中对CIRI发挥神经保护作用。
{"title":"Electroacupuncture Ameliorates Cerebral Ischemia-reperfusion Injury by Inhibiting Pyroptosis through the Sirtuin-1 Pathway","authors":"Ya-Nan Luo, Rong-Hua Xu, Zhi-Tao Feng, Song-bai Yang, Ya-Guang Huang, Zhi-Gang Mei","doi":"10.4103/wjtcm.wjtcm_77_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_77_24","url":null,"abstract":"\u0000 \u0000 \u0000 NOD-like receptor protein 3 (NLRP3)-mediated pyroptosis is pivotal in the pathological development of cerebral ischemia/reperfusion injury (CIRI). Although previous research has shown that electroacupuncture (EA) can alleviate CIRI through sirtuin-1 (SIRT1), the mechanism has not been well elucidated. Our study aimed to clarify whether the neuroprotective functions of EA are related to the reduction in NLRP3-mediated pyroptosis through the SIRT1 pathway.\u0000 \u0000 \u0000 \u0000 Rats received daily pretreatment with EA for 5 consecutive days before undergoing middle cerebral artery occlusion surgery. The Longa score was used to assess neurologic function. Infarct volume and morphological alterations were analyzed using 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin staining. In addition, neuronal pyroptosis was identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling/caspase-1 and neuronal nuclear antigen/caspase-1 immunofluorescence double staining. Levels of expression of pyroptosis markers were assessed by Western blotting and enzyme-linked immunosorbent assay.\u0000 \u0000 \u0000 \u0000 EA improved deficits in neurologic function and minimized cerebral infarct volume. Mechanistically, a number of neuronal pyroptotic cells and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD, and gasdermin D in the cerebral cortex were markedly reduced by EA treatment, and conversely, SIRT1 levels were increased. Notably, the specific SIRT1 inhibitor, EX527, reversed the effects of EA.\u0000 \u0000 \u0000 \u0000 EA potentially exerts a neuroprotective effect against CIRI through the SIRT1 pathway in NLRP3-mediated pyroptosis.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140971993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The objective of this study was to summarize the research context, hotspots, and the development trend of Huoxue lishui method in ophthalmology in the past decade by reviewing the relevant publications. Relevant publications on the application of Huoxue lishui method in ophthalmology from January 1, 2011, to December 31, 2021, in databases such as CNKI, VIP, and Wanfang were retrieved. The analysis of coauthorship, keyword co-occurrence, keyword clustering, keyword emergence, and keyword timeline map of the publications was done with bibliometrics tools CiteSpace and VOSviewer. A total of 100 publications were included in the analysis. The year 2020 saw the publication of most papers concerning the application of Huoxue lishui method in ophthalmology. High-frequency words are macular edema, Huoxue lishui, diabetic macular edema, Huoxue lishui method, Huoxue lishui formula, and promoting Qi and nourishing Yin. Three research hotspots were identified through keyword clustering analysis. Keyword emergence analysis and keyword timeline map indicated that a combined treatment of Huoxue lishui method and promoting Qi and nourishing Yin and diabetic ophthalmology is predicted to be research frontiers. Through the use of knowledge maps, this article reveals the research status in this field in the past decade and highlights the major directions, research hotspots, and development trends, providing references for further research in this field.
{"title":"Research Atlas Analysis on the Application of Huoxue Lishui Method (Promoting Blood Circulation and Diuresis) in Ophthalmology Based on VOSviewer’s and CiteSpace’s Methods","authors":"Qian Luo, Ze-Qi Li, Xiao-Huan Zhang, Yi-Jing Yang, Jing Lu, Qing-Hua Peng","doi":"10.4103/wjtcm.wjtcm_59_24","DOIUrl":"https://doi.org/10.4103/wjtcm.wjtcm_59_24","url":null,"abstract":"\u0000 \u0000 \u0000 The objective of this study was to summarize the research context, hotspots, and the development trend of Huoxue lishui method in ophthalmology in the past decade by reviewing the relevant publications.\u0000 \u0000 \u0000 \u0000 Relevant publications on the application of Huoxue lishui method in ophthalmology from January 1, 2011, to December 31, 2021, in databases such as CNKI, VIP, and Wanfang were retrieved. The analysis of coauthorship, keyword co-occurrence, keyword clustering, keyword emergence, and keyword timeline map of the publications was done with bibliometrics tools CiteSpace and VOSviewer.\u0000 \u0000 \u0000 \u0000 A total of 100 publications were included in the analysis. The year 2020 saw the publication of most papers concerning the application of Huoxue lishui method in ophthalmology. High-frequency words are macular edema, Huoxue lishui, diabetic macular edema, Huoxue lishui method, Huoxue lishui formula, and promoting Qi and nourishing Yin. Three research hotspots were identified through keyword clustering analysis. Keyword emergence analysis and keyword timeline map indicated that a combined treatment of Huoxue lishui method and promoting Qi and nourishing Yin and diabetic ophthalmology is predicted to be research frontiers.\u0000 \u0000 \u0000 \u0000 Through the use of knowledge maps, this article reveals the research status in this field in the past decade and highlights the major directions, research hotspots, and development trends, providing references for further research in this field.\u0000","PeriodicalId":23692,"journal":{"name":"World Journal of Traditional Chinese Medicine","volume":null,"pages":null},"PeriodicalIF":4.4,"publicationDate":"2024-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140999230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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