Pub Date : 2024-05-01Epub Date: 2023-11-24DOI: 10.1007/s11655-023-3653-9
Pu Chen, Jun Zhou, An-Min Ruan, Yu-Feng Ma, Qing-Fu Wang
Objective: To explore the mechanism of paeoniflorin (PF) on osteoarthritis (OA) synovial inflammation from network pharmacology to experimental pharmacology.
Methods: Targets of OA were constructed by detecting the database of network database platforms (Therapeutic Target database, DrugBank and GeneCards), and the targets of PF were constructed by PubChem and Herbal Ingredients' Targets database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of these co-targeted genes were conducted via Database for Annotation, Visualization, and Integrated Discovery (DAVID) database, and protein-protein interaction (PPI) networks were conducted via the search tool for the retrieval of interacting genes (STRING) database. Cell counting kit-8 (CCK-8) assay was performed to assess the potential toxicity of PF on human OA fibroblast-like synoviocytes (FLS), quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) and Western blot were used to verify the potential mechanism of PF in synovial inflammation.
Results: Twenty-six co-targeted genes were identified. GO enrichment results showed that these co-targeted genes were most likely localized in the cytoplasm, and the biological processes mainly involved 'cellular response to hypoxia' 'lipopolysaccharide (LPS)-mediated signaling pathway' and 'positive regulation of gene expression'. KEGG pathway analysis indicated that these co-targeted genes may function through pathways associated with 'hypoxia-inducible factor-1 (HIF-1) signaling pathway' and 'tumor-necrosis factor (TNF) signaling pathway'. The PPI network showed that the top 3 hub genes were TP53, TNF, and CASP3. Molecular docking results showed that PF was well docking with TNF. CCK-8 showed no potential toxicity of 10, 20 and 50 µmol/L PF on human OA FLS. And PF significantly decreased the expression levels of interleukin-1 β, interleukin-6, TNF-α matrix metalloproteinase 13 (MMP13), and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and TNF-α in LPS-induced OA FLS.
Conclusion: PF exhibited potent anti-inflammatory effect in OA synovial inflammation.
目的:从网络药理学和实验药理学两方面探讨芍药苷(PF)对骨关节炎(OA)滑膜炎症的作用机制。方法:通过检测网络数据库平台(Therapeutic Target database、DrugBank和GeneCards)的数据库构建OA的靶点,通过PubChem和Herbal Ingredients’Targets数据库构建PF的靶点。基因本体(GO)和京都基因与基因组百科全书(KEGG)通过Database for Annotation, Visualization, and Integrated Discovery (DAVID)数据库对这些共靶向基因进行分析,蛋白质-蛋白质相互作用(PPI)网络通过检索相互作用基因的搜索工具(STRING)数据库进行。采用细胞计数试剂盒-8 (CCK-8)法评估PF对人OA成纤维细胞样滑膜细胞(FLS)的潜在毒性,采用实时定量聚合酶链反应(qPCR)、酶联免疫吸附法(ELISA)和Western blot法验证PF在滑膜炎症中的潜在机制。结果:共鉴定出26个共靶基因。氧化石墨烯富集结果表明,这些共靶基因极有可能定位于细胞质中,其生物学过程主要涉及“细胞对缺氧的反应”、“脂多糖(LPS)介导的信号通路”和“基因表达的正向调节”。KEGG通路分析表明,这些共同靶向基因可能通过与“缺氧诱导因子-1 (HIF-1)信号通路”和“肿瘤坏死因子(TNF)信号通路”相关的途径发挥作用。PPI网络显示,前3位枢纽基因分别为TP53、TNF和CASP3。分子对接结果表明,PF与TNF对接良好。CCK-8在10、20和50µmol/L PF浓度下对人OA FLS无潜在毒性。PF显著降低了lps诱导的OA FLS中白细胞介素-1 β、白细胞介素-6、TNF-α基质金属蛋白酶13 (MMP13)以及具有血栓反应蛋白基元的崩解素和金属蛋白酶5 (ADAMTS5)和TNF-α的表达水平。结论:茯苓多糖对OA滑膜炎症有较强的抗炎作用。
{"title":"Paeoniflorin, the Main Monomer Component of Paeonia lactiflora, Exhibits Anti-inflammatory Properties in Osteoarthritis Synovial Inflammation.","authors":"Pu Chen, Jun Zhou, An-Min Ruan, Yu-Feng Ma, Qing-Fu Wang","doi":"10.1007/s11655-023-3653-9","DOIUrl":"10.1007/s11655-023-3653-9","url":null,"abstract":"<p><strong>Objective: </strong>To explore the mechanism of paeoniflorin (PF) on osteoarthritis (OA) synovial inflammation from network pharmacology to experimental pharmacology.</p><p><strong>Methods: </strong>Targets of OA were constructed by detecting the database of network database platforms (Therapeutic Target database, DrugBank and GeneCards), and the targets of PF were constructed by PubChem and Herbal Ingredients' Targets database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of these co-targeted genes were conducted via Database for Annotation, Visualization, and Integrated Discovery (DAVID) database, and protein-protein interaction (PPI) networks were conducted via the search tool for the retrieval of interacting genes (STRING) database. Cell counting kit-8 (CCK-8) assay was performed to assess the potential toxicity of PF on human OA fibroblast-like synoviocytes (FLS), quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) and Western blot were used to verify the potential mechanism of PF in synovial inflammation.</p><p><strong>Results: </strong>Twenty-six co-targeted genes were identified. GO enrichment results showed that these co-targeted genes were most likely localized in the cytoplasm, and the biological processes mainly involved 'cellular response to hypoxia' 'lipopolysaccharide (LPS)-mediated signaling pathway' and 'positive regulation of gene expression'. KEGG pathway analysis indicated that these co-targeted genes may function through pathways associated with 'hypoxia-inducible factor-1 (HIF-1) signaling pathway' and 'tumor-necrosis factor (TNF) signaling pathway'. The PPI network showed that the top 3 hub genes were TP53, TNF, and CASP3. Molecular docking results showed that PF was well docking with TNF. CCK-8 showed no potential toxicity of 10, 20 and 50 µmol/L PF on human OA FLS. And PF significantly decreased the expression levels of interleukin-1 β, interleukin-6, TNF-α matrix metalloproteinase 13 (MMP13), and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and TNF-α in LPS-induced OA FLS.</p><p><strong>Conclusion: </strong>PF exhibited potent anti-inflammatory effect in OA synovial inflammation.</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138298548","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}
Objective: To evaluate the efficacy of Guanxin Danshen Dripping Pill (GXDSDP) in treating anxiety and depression in patients with coronary heart disease (CHD).
Methods: A total of 1,428 patients diagnosed with CHD screened for anxiety, depression, and quality of life (QOL) at baseline received 0.4 g of GXDSDP treatment 3 times per day and returned for monthly reassessment. Patients were recruited after stable treatment for CHD and received assessment of General Anxiety Disorder-7 (GAD-7), Patient Health Questionnaire-9 (PHQ-9), and Seattle Angina Questionnaire (SAQ) for evaluating anxiety, depression, and QOL. Patients were followed up 3 times, once every 4 weeks, during outpatient visits for 12 weeks.
Results: At the third follow-up (F3), the anxiety symptom of 63.79% (673/1,055) of the patients improved to sub-clinical level, and the GAD-7 score improved significantly (8.11 vs. 3.87, P<0.01); 57.52% (585/1,017) patients' depressive symptoms improved to sub-clinical level, with a significant improvement in PHQ-9 score (8.69 vs. 4.41, P<0.01) at F3. All aspects of QOL significantly improved at the end of treatment compared to those at baseline (all P<0.01) as assessed by SAQ: physical limitation (31.17 vs. 34.14), anginal stability (2.74 vs. 4.14), anginal frequency (8.16 vs. 9.10), treatment satisfaction (13.43 vs. 16.29), and disease perception (8.69 vs. 11.02).
Conclusions: A fixed dosage of GXDSDP may be a potential treatment option for CHD patients comorbid with anxiety or depression. (Registration No. ChiCTR2100051523).
目的:评价冠心丹参滴丸治疗冠心病患者焦虑、抑郁的疗效。方法:共有1428名诊断为CHD的患者在基线时接受焦虑、抑郁和生活质量(QOL)筛查,每天3次接受0.4 g GXDSDP治疗,并返回每月重新评估。CHD稳定治疗后招募患者,并接受一般性焦虑障碍-7(GAD-7)、患者健康问卷-9(PHQ-9)和西雅图心绞痛问卷(SAQ)评估,以评估焦虑、抑郁和生活质量。患者随访3次,每4周随访一次,门诊随访12周。结果:在第三次随访(F3)中,63.79%(673/1055)的患者的焦虑症状改善到亚临床水平,GAD-7评分显著改善(8.11比3.87,P结论:固定剂量的GXDSDP可能是合并焦虑或抑郁的CHD患者的潜在治疗选择。
{"title":"Effect of Guanxin Danshen Dripping Pills on Coronary Heart Disease Comorbid with Depression or Anxiety: The ADECODE-Real World Study.","authors":"Shi-Hao Wu, Wei-Qi Shi, Yu-Hang Li, Ru-Hui Liu, Da-Yi Hu, Li-Qiang Zheng, Wen-Lin Ma","doi":"10.1007/s11655-023-3628-x","DOIUrl":"10.1007/s11655-023-3628-x","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the efficacy of Guanxin Danshen Dripping Pill (GXDSDP) in treating anxiety and depression in patients with coronary heart disease (CHD).</p><p><strong>Methods: </strong>A total of 1,428 patients diagnosed with CHD screened for anxiety, depression, and quality of life (QOL) at baseline received 0.4 g of GXDSDP treatment 3 times per day and returned for monthly reassessment. Patients were recruited after stable treatment for CHD and received assessment of General Anxiety Disorder-7 (GAD-7), Patient Health Questionnaire-9 (PHQ-9), and Seattle Angina Questionnaire (SAQ) for evaluating anxiety, depression, and QOL. Patients were followed up 3 times, once every 4 weeks, during outpatient visits for 12 weeks.</p><p><strong>Results: </strong>At the third follow-up (F3), the anxiety symptom of 63.79% (673/1,055) of the patients improved to sub-clinical level, and the GAD-7 score improved significantly (8.11 vs. 3.87, P<0.01); 57.52% (585/1,017) patients' depressive symptoms improved to sub-clinical level, with a significant improvement in PHQ-9 score (8.69 vs. 4.41, P<0.01) at F3. All aspects of QOL significantly improved at the end of treatment compared to those at baseline (all P<0.01) as assessed by SAQ: physical limitation (31.17 vs. 34.14), anginal stability (2.74 vs. 4.14), anginal frequency (8.16 vs. 9.10), treatment satisfaction (13.43 vs. 16.29), and disease perception (8.69 vs. 11.02).</p><p><strong>Conclusions: </strong>A fixed dosage of GXDSDP may be a potential treatment option for CHD patients comorbid with anxiety or depression. (Registration No. ChiCTR2100051523).</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72013711","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 : 2024-05-01Epub Date: 2023-09-26DOI: 10.1007/s11655-023-3649-5
Yu-Xuan Hu, Sheng-Lei Qiu, Ju-Ju Shang, Zi Wang, Xiao-Lei Lai
Although there have been significant advances in the treatment of heart failure in recent years, chronic heart failure remains a leading cause of cardiovascular disease-related death. Many studies have found that targeted cardiac metabolic remodeling has good potential for the treatment of heart failure. However, most of the drugs that increase cardiac energy are still in the theoretical or testing stage. Some research has found that botanical drugs not only increase myocardial energy metabolism through multiple targets but also have the potential to restore the balance of myocardial substrate metabolism. In this review, we summarized the mechanisms by which botanical drugs (the active ingredients/formulas/Chinese patent medicines) improve substrate utilization and promote myocardial energy metabolism by activating AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs) and other related targets. At the same time, some potential protective effects of botanical drugs on myocardium, such as alleviating oxidative stress and dysbiosis signaling, caused by metabolic disorders, were briefly discussed.
{"title":"Pharmacological Effects of Botanical Drugs on Myocardial Metabolism in Chronic Heart Failure.","authors":"Yu-Xuan Hu, Sheng-Lei Qiu, Ju-Ju Shang, Zi Wang, Xiao-Lei Lai","doi":"10.1007/s11655-023-3649-5","DOIUrl":"10.1007/s11655-023-3649-5","url":null,"abstract":"<p><p>Although there have been significant advances in the treatment of heart failure in recent years, chronic heart failure remains a leading cause of cardiovascular disease-related death. Many studies have found that targeted cardiac metabolic remodeling has good potential for the treatment of heart failure. However, most of the drugs that increase cardiac energy are still in the theoretical or testing stage. Some research has found that botanical drugs not only increase myocardial energy metabolism through multiple targets but also have the potential to restore the balance of myocardial substrate metabolism. In this review, we summarized the mechanisms by which botanical drugs (the active ingredients/formulas/Chinese patent medicines) improve substrate utilization and promote myocardial energy metabolism by activating AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs) and other related targets. At the same time, some potential protective effects of botanical drugs on myocardium, such as alleviating oxidative stress and dysbiosis signaling, caused by metabolic disorders, were briefly discussed.</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41171555","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 : 2024-05-01Epub Date: 2023-12-28DOI: 10.1007/s11655-023-3650-z
Tong-Tong Yue, Ying-Jie Cao, Ya-Xuan Cao, Wei-Xia Li, Xiao-Yan Wang, Chun-Ying Si, Han Xia, Ming-Jun Zhu, Jin-Fa Tang, He Wang
Objective: To investigate the main components and potential mechanism of Shuxuening Injection (SXNI) in the treatment of myocardial ischemia-reperfusion injury (MIRI) through network pharmacology and in vivo research.
Methods: The Traditional Chinese Medicine Systems Pharmacology (TCMSP) and PharmMapper databases were used to extract and evaluate the effective components of Ginkgo biloba leaves, the main component of SXNI. The Online Mendelian Inheritance in Man (OMIM) and GeneCards databases were searched for disease targets and obtain the drug target and disease target intersections. The active ingredient-target network was built using Cytoscape 3.9.1 software. The STRING database, Metascape online platform, and R language were used to obtain the key targets and signaling pathways of the anti-MIRI effects of SXNI. In order to verify the therapeutic effect of different concentrations of SXNI on MIRI in rats, 60 rats were first divided into 5 groups according to random number table method: the sham operation group, the model group, SXNI low-dose (3.68 mg/kg), medium-dose (7.35 mg/kg), and high-dose (14.7 mg/kg) groups, with 12 rats in each group. Then, another 60 rats were randomly divided into 5 groups: the sham operation group, the model group, SXNI group (14.7 mg/kg), SXNI+LY294002 group, and LY294002 group, with 12 rats in each group. The drug was then administered intraperitoneally at body weight for 14 days. The main biological processes were validated using in vivo testing. Evans blue/triphenyltetrazolium chloride (TTC) double staining, hematoxylin-eosin (HE) staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were used to investigate the efficacy and mechanism of SXNI in MIRI rats.
Results: Eleven core targets and 30 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were selected. Among these, the phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) pathway was closely related to SXNI treatment of MIRI. In vivo experiments showed that SXNI reduced the myocardial infarction area in the model group, improved rat heart pathological damage, and reduced the cardiomyocyte apoptosis rate (all P<0.01). After SXNI treatment, the p-PI3K/PI3K and p-AKT/AKT ratios as well as B-cell lymphoma-2 (Bcl-2) protein expression in cardiomyocytes were increased, while the Bax and cleaved caspase 3 protein expression levels were decreased (all P<0.05). LY294002 partially reversed the protective effect of SXNI on MIRI.
Conclusion: SXNI protects against MIRI by activating the PI3K/AKT signaling pathway.
{"title":"Shuxuening Injection Inhibits Apoptosis and Reduces Myocardial Ischemia-Reperfusion Injury in Rats through PI3K/AKT Pathway.","authors":"Tong-Tong Yue, Ying-Jie Cao, Ya-Xuan Cao, Wei-Xia Li, Xiao-Yan Wang, Chun-Ying Si, Han Xia, Ming-Jun Zhu, Jin-Fa Tang, He Wang","doi":"10.1007/s11655-023-3650-z","DOIUrl":"10.1007/s11655-023-3650-z","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the main components and potential mechanism of Shuxuening Injection (SXNI) in the treatment of myocardial ischemia-reperfusion injury (MIRI) through network pharmacology and in vivo research.</p><p><strong>Methods: </strong>The Traditional Chinese Medicine Systems Pharmacology (TCMSP) and PharmMapper databases were used to extract and evaluate the effective components of Ginkgo biloba leaves, the main component of SXNI. The Online Mendelian Inheritance in Man (OMIM) and GeneCards databases were searched for disease targets and obtain the drug target and disease target intersections. The active ingredient-target network was built using Cytoscape 3.9.1 software. The STRING database, Metascape online platform, and R language were used to obtain the key targets and signaling pathways of the anti-MIRI effects of SXNI. In order to verify the therapeutic effect of different concentrations of SXNI on MIRI in rats, 60 rats were first divided into 5 groups according to random number table method: the sham operation group, the model group, SXNI low-dose (3.68 mg/kg), medium-dose (7.35 mg/kg), and high-dose (14.7 mg/kg) groups, with 12 rats in each group. Then, another 60 rats were randomly divided into 5 groups: the sham operation group, the model group, SXNI group (14.7 mg/kg), SXNI+LY294002 group, and LY294002 group, with 12 rats in each group. The drug was then administered intraperitoneally at body weight for 14 days. The main biological processes were validated using in vivo testing. Evans blue/triphenyltetrazolium chloride (TTC) double staining, hematoxylin-eosin (HE) staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were used to investigate the efficacy and mechanism of SXNI in MIRI rats.</p><p><strong>Results: </strong>Eleven core targets and 30 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were selected. Among these, the phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) pathway was closely related to SXNI treatment of MIRI. In vivo experiments showed that SXNI reduced the myocardial infarction area in the model group, improved rat heart pathological damage, and reduced the cardiomyocyte apoptosis rate (all P<0.01). After SXNI treatment, the p-PI3K/PI3K and p-AKT/AKT ratios as well as B-cell lymphoma-2 (Bcl-2) protein expression in cardiomyocytes were increased, while the Bax and cleaved caspase 3 protein expression levels were decreased (all P<0.05). LY294002 partially reversed the protective effect of SXNI on MIRI.</p><p><strong>Conclusion: </strong>SXNI protects against MIRI by activating the PI3K/AKT signaling pathway.</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139048403","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}
Objective: To investigate the therapeutic efficacy of cinnamaldehyde (CA) on systemic Candida albicans infection in mice and to provide supportive data for the development of novel antifungal drugs.
Methods: Ninety BALB/c mice were randomly divided into 3 groups according to a random number table: CA treatment group, fluconazole (positive control) group, and Tween saline (negative control) group, with 30 mice in each group. Initially, all groups of mice received consecutive intraperitoneal injections of cyclophosphamide at 200 mg/kg for 2 days, followed by intraperitoneal injection of 0.25 mL C. albicans fungal suspension (concentration of 1.0 × 107 CFU/mL) on the 4th day, to establish an immunosuppressed systemic Candida albicans infection animal model. Subsequently, the mice were orally administered CA, fluconazole and Tween saline, at 240, 240 mg/kg and 0.25 mL/kg respectively for 14 days. After a 48-h discontinuation of treatment, the liver, small intestine, and kidney tissues of mice were collected for fungal direct microscopic examination, culture, and histopathological examination. Additionally, renal tissues from each group of mice were collected for (1,3)- β -D-glucan detection. The survival status of mice in all groups was monitored for 14 days of drug administration.
Results: The CA group exhibited a fungal clearance rate of C. albicans above 86.7% (26/30), significantly higher than the fluconazole group (60.0%, 18/30, P<0.01) and the Tween saline group (30.0%, 9/30, P<0.01). Furthermore, histopathological examination in the CA group revealed the disappearance of inflammatory cells and near-normal restoration of tissue structure. The (1,3)-β-D-glucan detection value in the CA group (860.55 ± 126.73 pg/mL) was significantly lower than that in the fluconazole group (1985.13 ± 203.56 pg/mL, P<0.01) and the Tween saline group (5910.20 ± 320.56 pg/mL, P<0.01). The mouse survival rate reached 90.0% (27/30), higher than the fluconazole group (60.0%, 18/30) and the Tween saline group (30.0%, 9/30), with a significant difference between the two groups (both P<0.01).
Conclusions: CA treatment exhibited significant therapeutic efficacy in mice with systemic C. albicans infection. Therefore, CA holds potential as a novel antifungal agent for targeted treatment of C. albicans infection.
{"title":"Effect of Cinnamaldehyde on Systemic Candida albicans Infection in Mice.","authors":"Xiao-Ru Guo, Xiao-Guang Zhang, Gang-Sheng Wang, Jia Wang, Xiao-Jun Liu, Jie-Hua Deng","doi":"10.1007/s11655-023-3754-5","DOIUrl":"https://doi.org/10.1007/s11655-023-3754-5","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the therapeutic efficacy of cinnamaldehyde (CA) on systemic Candida albicans infection in mice and to provide supportive data for the development of novel antifungal drugs.</p><p><strong>Methods: </strong>Ninety BALB/c mice were randomly divided into 3 groups according to a random number table: CA treatment group, fluconazole (positive control) group, and Tween saline (negative control) group, with 30 mice in each group. Initially, all groups of mice received consecutive intraperitoneal injections of cyclophosphamide at 200 mg/kg for 2 days, followed by intraperitoneal injection of 0.25 mL C. albicans fungal suspension (concentration of 1.0 × 10<sup>7</sup> CFU/mL) on the 4th day, to establish an immunosuppressed systemic Candida albicans infection animal model. Subsequently, the mice were orally administered CA, fluconazole and Tween saline, at 240, 240 mg/kg and 0.25 mL/kg respectively for 14 days. After a 48-h discontinuation of treatment, the liver, small intestine, and kidney tissues of mice were collected for fungal direct microscopic examination, culture, and histopathological examination. Additionally, renal tissues from each group of mice were collected for (1,3)- β -D-glucan detection. The survival status of mice in all groups was monitored for 14 days of drug administration.</p><p><strong>Results: </strong>The CA group exhibited a fungal clearance rate of C. albicans above 86.7% (26/30), significantly higher than the fluconazole group (60.0%, 18/30, P<0.01) and the Tween saline group (30.0%, 9/30, P<0.01). Furthermore, histopathological examination in the CA group revealed the disappearance of inflammatory cells and near-normal restoration of tissue structure. The (1,3)-β-D-glucan detection value in the CA group (860.55 ± 126.73 pg/mL) was significantly lower than that in the fluconazole group (1985.13 ± 203.56 pg/mL, P<0.01) and the Tween saline group (5910.20 ± 320.56 pg/mL, P<0.01). The mouse survival rate reached 90.0% (27/30), higher than the fluconazole group (60.0%, 18/30) and the Tween saline group (30.0%, 9/30), with a significant difference between the two groups (both P<0.01).</p><p><strong>Conclusions: </strong>CA treatment exhibited significant therapeutic efficacy in mice with systemic C. albicans infection. Therefore, CA holds potential as a novel antifungal agent for targeted treatment of C. albicans infection.</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847425","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 : 2024-04-27DOI: 10.1007/s11655-024-3806-5
Lin Liu, Xiao-Hui Fan, Xu-Dong Tang
The progression from gastric mucosal inflammation to cancer signifies a pivotal event in the trajectory of gastric cancer (GC) development. Chinese medicine (CM) exhibits unique advantages and holds significant promise in inhibiting carcinogenesis of the gastric mucosa. This review intricately examines the critical pathological events during the transition from gastric mucosal inflammation-cancer transformation (GMICT), with a particular focus on pathological evolution mechanisms of spasmolytic polypeptide-expressing metaplasia (SPEM). Moreover, it investigates the pioneering applications and advancements of CM in intervening within the medical research domain of precancerous transformations leading to GC. Furthermore, the analysis extends to major shortcomings and challenges confronted by current research in gastric precancerous lesions, and innovative studies related to CM are presented. We offer a highly succinct yet optimistic outlook on future developmental trends. This paper endeavors to foster a profound understanding of forefront dynamics in GMICT research and scientific implications of modernizing CM. It also introduces a novel perspective for establishing a collaborative secondary prevention system for GC that integrates both Western and Chinese medicines.
{"title":"Revolutionizing Gastric Cancer Prevention: Novel Insights on Gastric Mucosal Inflammation-Cancer Transformation and Chinese Medicine.","authors":"Lin Liu, Xiao-Hui Fan, Xu-Dong Tang","doi":"10.1007/s11655-024-3806-5","DOIUrl":"https://doi.org/10.1007/s11655-024-3806-5","url":null,"abstract":"<p><p>The progression from gastric mucosal inflammation to cancer signifies a pivotal event in the trajectory of gastric cancer (GC) development. Chinese medicine (CM) exhibits unique advantages and holds significant promise in inhibiting carcinogenesis of the gastric mucosa. This review intricately examines the critical pathological events during the transition from gastric mucosal inflammation-cancer transformation (GMICT), with a particular focus on pathological evolution mechanisms of spasmolytic polypeptide-expressing metaplasia (SPEM). Moreover, it investigates the pioneering applications and advancements of CM in intervening within the medical research domain of precancerous transformations leading to GC. Furthermore, the analysis extends to major shortcomings and challenges confronted by current research in gastric precancerous lesions, and innovative studies related to CM are presented. We offer a highly succinct yet optimistic outlook on future developmental trends. This paper endeavors to foster a profound understanding of forefront dynamics in GMICT research and scientific implications of modernizing CM. It also introduces a novel perspective for establishing a collaborative secondary prevention system for GC that integrates both Western and Chinese medicines.</p>","PeriodicalId":10005,"journal":{"name":"Chinese Journal of Integrative Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854361","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}