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Role of Traditional Chinese Medicine in Lung Cancer Management: A Review.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500053
Zhijing Rao, Zhongqi Wang, Haibin Deng, Wan Su, Xiaowei Huang, Zhenye Xu

With the continuous advancements in modern medicine, significant progress has been made in the treatment of lung cancer. Current standard treatments, such as surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy, have notably improved patient survival. However, the adverse effects associated with these therapies limit their use and impact the overall treatment process. Traditional Chinese medicine (TCM) has shown holistic, multi-target, and multi-level therapeutic effects. Numerous studies have highlighted the importance of TCM's role in the comprehensive management of lung cancer, demonstrating its benefits in inhibiting tumor growth, reducing complications, mitigating side effects, and enhancing the efficacy of conventional treatments. Here, we review the main mechanisms of TCM in combating lung cancer, inducing cancer cell cycle arrest and apoptosis. These include inhibiting lung cancer cell growth and proliferation, inhibiting cancer cell invasion and metastasis, suppressing angiogenesis and epithelial-mesenchymal transition (EMT), and modulating antitumor inflammatory responses and immune evasion. This paper aims to summarize recent advancements in the application of TCM for lung cancer, emphasizing its unique advantages and distinctive features. In promoting the benefits of TCM, we seek to provide valuable insights for the integrated treatment of lung cancer.

{"title":"Role of Traditional Chinese Medicine in Lung Cancer Management: A Review.","authors":"Zhijing Rao, Zhongqi Wang, Haibin Deng, Wan Su, Xiaowei Huang, Zhenye Xu","doi":"10.1142/S0192415X25500053","DOIUrl":"10.1142/S0192415X25500053","url":null,"abstract":"<p><p>With the continuous advancements in modern medicine, significant progress has been made in the treatment of lung cancer. Current standard treatments, such as surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy, have notably improved patient survival. However, the adverse effects associated with these therapies limit their use and impact the overall treatment process. Traditional Chinese medicine (TCM) has shown holistic, multi-target, and multi-level therapeutic effects. Numerous studies have highlighted the importance of TCM's role in the comprehensive management of lung cancer, demonstrating its benefits in inhibiting tumor growth, reducing complications, mitigating side effects, and enhancing the efficacy of conventional treatments. Here, we review the main mechanisms of TCM in combating lung cancer, inducing cancer cell cycle arrest and apoptosis. These include inhibiting lung cancer cell growth and proliferation, inhibiting cancer cell invasion and metastasis, suppressing angiogenesis and epithelial-mesenchymal transition (EMT), and modulating antitumor inflammatory responses and immune evasion. This paper aims to summarize recent advancements in the application of TCM for lung cancer, emphasizing its unique advantages and distinctive features. In promoting the benefits of TCM, we seek to provide valuable insights for the integrated treatment of lung cancer.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"97-117"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advances in Pharmacological Research on Icaritin: A Comprehensive Review.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500089
Ran Guo, Zhiping Yan, Rui Wang, Tongxuan Guo, Hao Li, Minyu Kong, Wenzhi Guo

Epimedium has been widely used in traditional Chinese medicine for several thousands of years. This plant is known for tonifying kidney Yang, strengthening muscles and bones, and dispelling wind and dampness. It is worth noting that icaritin, a prenylated flavonoid isolated from Epimedium, has received increasing attention in recent years due to its wide range of pharmacological activities. Icaritin exhibits significant therapeutic potential against various diseases, such as osteoporosis, tumors (hepatocellular carcinoma, stomach cancer, breast cancer, and glioblastoma), cerebral ischemia skin injury, thrombocytopenia, and systemic lupus erythematosus. We review the pharmacological activities of icaritin and its potential molecular mechanisms for the treatment of related diseases. The data suggest that icaritin can have the pharmacological effects of mediating Wnt/[Formula: see text]-catenin, IL-6/JAK2/STAT3, AMPK/mTOR, PTEN/AKT, MAPK, NF-[Formula: see text]B, and other signaling pathways. This paper also discusses the progress of clinical trials of icaritin. Icaritin was approved by the State Food and Drug Administration in January 2022 for the treatment of advanced HCC, and has various clinical drug prospects. Although it has some disadvantages, including poor solubility, and low bioavailability, icaritin is still a prospective candidate for the development of naturally derived drugs, especially in the treatment of tumors and inflammatory diseases. This review aims to update and deepen the understanding of icaritin, and provide a theoretical basis for its further study.

{"title":"Advances in Pharmacological Research on Icaritin: A Comprehensive Review.","authors":"Ran Guo, Zhiping Yan, Rui Wang, Tongxuan Guo, Hao Li, Minyu Kong, Wenzhi Guo","doi":"10.1142/S0192415X25500089","DOIUrl":"10.1142/S0192415X25500089","url":null,"abstract":"<p><p><i>Epimedium</i> has been widely used in traditional Chinese medicine for several thousands of years. This plant is known for tonifying kidney Yang, strengthening muscles and bones, and dispelling wind and dampness. It is worth noting that icaritin, a prenylated flavonoid isolated from <i>Epimedium</i>, has received increasing attention in recent years due to its wide range of pharmacological activities. Icaritin exhibits significant therapeutic potential against various diseases, such as osteoporosis, tumors (hepatocellular carcinoma, stomach cancer, breast cancer, and glioblastoma), cerebral ischemia skin injury, thrombocytopenia, and systemic lupus erythematosus. We review the pharmacological activities of icaritin and its potential molecular mechanisms for the treatment of related diseases. The data suggest that icaritin can have the pharmacological effects of mediating Wnt/[Formula: see text]-catenin, IL-6/JAK2/STAT3, AMPK/mTOR, PTEN/AKT, MAPK, NF-[Formula: see text]B, and other signaling pathways. This paper also discusses the progress of clinical trials of icaritin. Icaritin was approved by the State Food and Drug Administration in January 2022 for the treatment of advanced HCC, and has various clinical drug prospects. Although it has some disadvantages, including poor solubility, and low bioavailability, icaritin is still a prospective candidate for the development of naturally derived drugs, especially in the treatment of tumors and inflammatory diseases. This review aims to update and deepen the understanding of icaritin, and provide a theoretical basis for its further study.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"179-203"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Therapeutic Effects of Natural Products in the Treatment of Chronic Diseases: The Role in Regulating KEAP1-NRF2 Pathway.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500041
Yaling Li, Xijia Wang, Shuyue Li, Lei Wang, Ningning Ding, Yali She, Changtian Li

Oxidative stress represents a pivotal mechanism in the pathogenesis of numerous chronic diseases. The Kelch-like ECH-associated protein 1-transcription factor NF-E2 p45-related factor 2 (KEAP1-NRF2) pathway plays a crucial role in maintaining redox homeostasis and regulating a multitude of biological processes such as inflammation, protein homeostasis, and metabolic homeostasis. In this paper, we present the findings of recent studies on the KEAP1-NRF2 pathway, which have revealed that it is aberrantly regulated and induces oxidative stress injury in a variety of diseases such as neurodegenerative diseases, cardiovascular diseases, metabolic diseases, respiratory diseases, digestive diseases, and cancer. Given this evidence, targeting KEAP1-NRF2 represents a highly promising avenue for developing therapeutic strategies for chronic diseases, and thus the development of appropriate therapeutic strategies based on the targeting of the NRF2 pathway has emerged as a significant area of research interest. This paper highlights an overview of current strategies to modulate KEAP1-NRF2, as well as recent advances in the use of natural compounds and traditional Chinese medicine, with a view to providing meaningful guidelines for drug discovery and development targeting KEAP1-NRF2. Additionally, it discusses the challenges associated with harnessing NRF2 as a therapeutic target.

{"title":"Therapeutic Effects of Natural Products in the Treatment of Chronic Diseases: The Role in Regulating KEAP1-NRF2 Pathway.","authors":"Yaling Li, Xijia Wang, Shuyue Li, Lei Wang, Ningning Ding, Yali She, Changtian Li","doi":"10.1142/S0192415X25500041","DOIUrl":"10.1142/S0192415X25500041","url":null,"abstract":"<p><p>Oxidative stress represents a pivotal mechanism in the pathogenesis of numerous chronic diseases. The Kelch-like ECH-associated protein 1-transcription factor NF-E2 p45-related factor 2 (KEAP1-NRF2) pathway plays a crucial role in maintaining redox homeostasis and regulating a multitude of biological processes such as inflammation, protein homeostasis, and metabolic homeostasis. In this paper, we present the findings of recent studies on the KEAP1-NRF2 pathway, which have revealed that it is aberrantly regulated and induces oxidative stress injury in a variety of diseases such as neurodegenerative diseases, cardiovascular diseases, metabolic diseases, respiratory diseases, digestive diseases, and cancer. Given this evidence, targeting KEAP1-NRF2 represents a highly promising avenue for developing therapeutic strategies for chronic diseases, and thus the development of appropriate therapeutic strategies based on the targeting of the NRF2 pathway has emerged as a significant area of research interest. This paper highlights an overview of current strategies to modulate KEAP1-NRF2, as well as recent advances in the use of natural compounds and traditional Chinese medicine, with a view to providing meaningful guidelines for drug discovery and development targeting KEAP1-NRF2. Additionally, it discusses the challenges associated with harnessing NRF2 as a therapeutic target.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"67-96"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Hepatic Oxidative Metabolite of Palmatine Ameliorates DSS-Induced Ulcerative Colitis by Regulating Macrophage Polarization Through AMPK/NF-κB Pathway.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500119
Qi-Ting Huang, Xing-Dong Ma, Jia-Na Zhang, Wei-Xiong Lin, Xue-Xia Shen, Zhuo-Wen Huang, Xia Zhang, Xiao-Yan Wu, Yao-Xing Dou, Zi-Ren Su, Ji-Yan Su, Yu-Cui Li, Yu-Hong Liu, You-Liang Xie, Rong-Feng Lin, Hai-Yang Huang, Qi-Hui Zhang, Xiao-Qi Huang

Palmatine (PAL) and berberine are both classified as protoberberine alkaloids, derived from several traditional Chinese herbs such as Coptis chinensis Franch. and Phellodendron chinense Schneid. These compounds are extensively used in treating dysentery and colitis. PAL is one of the crucial quality markers for these plants in the Chinese Pharmacopoeia. A key metabolite of PAL, 8-Oxypalmatine (OPAL), shows favorable anti-inflammatory activity and better safety compared to PAL, though its mechanisms in ulcerative colitis (UC) are not fully understood. This study used a dextran sodium sulfate-induced colitis mouse model to explore OPAL's effects. The results indicated that OPAL provided superior therapeutic effects to those of PAL, alleviating colitis symptoms and reducing colon inflammation by modulating pro-inflammatory (tumor necrosis factor-α, interleukin-1β, and interleukin-6) and anti-inflammatory (transforming growth factor-β and interleukin-10) cytokines. Additionally, OPAL helped rebuild the mucus barrier and upregulated tight junction proteins, thereby restoring intestinal integrity. Notably, OPAL inhibited the M1 macrophages infiltration while promoting M2 macrophage distribution in the colon. Its role in fostering M2 polarization and modulating the inflammatory cytokine profile was further confirmed in vitro. Importantly, the anti-inflammatory effects were primarily linked to AMP-activated protein kinase activation, which subsequently inhibited the nuclear factor-kappa B pathway. These findings highlight OPAL as a crucial active metabolite responsible for the therapeutic effects of PAL against UC, emphasizing its potential as a novel treatment for this condition.

{"title":"A Hepatic Oxidative Metabolite of Palmatine Ameliorates DSS-Induced Ulcerative Colitis by Regulating Macrophage Polarization Through AMPK/NF-κB Pathway.","authors":"Qi-Ting Huang, Xing-Dong Ma, Jia-Na Zhang, Wei-Xiong Lin, Xue-Xia Shen, Zhuo-Wen Huang, Xia Zhang, Xiao-Yan Wu, Yao-Xing Dou, Zi-Ren Su, Ji-Yan Su, Yu-Cui Li, Yu-Hong Liu, You-Liang Xie, Rong-Feng Lin, Hai-Yang Huang, Qi-Hui Zhang, Xiao-Qi Huang","doi":"10.1142/S0192415X25500119","DOIUrl":"10.1142/S0192415X25500119","url":null,"abstract":"<p><p>Palmatine (PAL) and berberine are both classified as protoberberine alkaloids, derived from several traditional Chinese herbs such as <i>Coptis chinensis</i> Franch. and <i>Phellodendron</i> <i>chinense</i> Schneid. These compounds are extensively used in treating dysentery and colitis. PAL is one of the crucial quality markers for these plants in the Chinese Pharmacopoeia. A key metabolite of PAL, 8-Oxypalmatine (OPAL), shows favorable anti-inflammatory activity and better safety compared to PAL, though its mechanisms in ulcerative colitis (UC) are not fully understood. This study used a dextran sodium sulfate-induced colitis mouse model to explore OPAL's effects. The results indicated that OPAL provided superior therapeutic effects to those of PAL, alleviating colitis symptoms and reducing colon inflammation by modulating pro-inflammatory (tumor necrosis factor-α, interleukin-1β, and interleukin-6) and anti-inflammatory (transforming growth factor-β and interleukin-10) cytokines. Additionally, OPAL helped rebuild the mucus barrier and upregulated tight junction proteins, thereby restoring intestinal integrity. Notably, OPAL inhibited the M1 macrophages infiltration while promoting M2 macrophage distribution in the colon. Its role in fostering M2 polarization and modulating the inflammatory cytokine profile was further confirmed <i>in</i> <i>vitro</i>. Importantly, the anti-inflammatory effects were primarily linked to AMP-activated protein kinase activation, which subsequently inhibited the nuclear factor-kappa B pathway. These findings highlight OPAL as a crucial active metabolite responsible for the therapeutic effects of PAL against UC, emphasizing its potential as a novel treatment for this condition.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"285-307"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advancements in the Research of Astragalus membranaceus for the Treatment of Colorectal Cancer.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500065
Qiwen Lu, Jiaxin Jiang, Xi Wang, Rongling Wang, Xuan Han

Colorectal cancer, characterized by its high incidence, concealed early symptoms, and poor prognosis at advanced stages, ranks as the third leading cause of cancer-related deaths worldwide. Astragalus membranaceus (AM) refers to the dried roots of Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao and Astragalus membranaceus (Fisch.) Bge. In the theory of Traditional Chinese Medicine (TCM), it is believed to have the functions of tonifying qi and lifting yang, as well as generating body fluids and nourishing blood. It can effectively treat cancer caused by the deficiency of vital energy and susceptibility to external diseases. Modern research has confirmed that the active components of AM, including Astragalus polysaccharides, flavonoids (formononetin and calycosin), Astragalus saponins (Astragaloside I and Astragaloside III), and Astragalus nanovesicles, are effective in the treatment of colorectal cancer. The mechanisms mainly involve inducing apoptosis, inhibiting tumor angiogenesis and the metastasis of cancer cells, regulating the cell cycle and tumor microenvironment, and reversing drug resistance. Moreover, it offers a synergistic enhancement when used in combination with chemotherapy, radiotherapy, targeted therapy, or surgical treatment. AM also has great potential in treating colorectal cancer when combined with other herbs. This review summarizes the relevant research findings on the treatment of colorectal cancer with AM, as well as its main pharmacological effects and molecular mechanisms, aiming to provide guidance for the development of new drugs, and offer direction for the conduct of more related research and promoting the development and application of AM.

{"title":"Advancements in the Research of <i>Astragalus membranaceus</i> for the Treatment of Colorectal Cancer.","authors":"Qiwen Lu, Jiaxin Jiang, Xi Wang, Rongling Wang, Xuan Han","doi":"10.1142/S0192415X25500065","DOIUrl":"10.1142/S0192415X25500065","url":null,"abstract":"<p><p>Colorectal cancer, characterized by its high incidence, concealed early symptoms, and poor prognosis at advanced stages, ranks as the third leading cause of cancer-related deaths worldwide. <i>Astragalus membranaceus</i> (AM) refers to the dried roots of <i>Astragalus membranaceus</i> (Fisch.) Bge. var. <i>mongholicus</i> (Bge.) Hsiao and <i>Astragalus membranaceus</i> (Fisch.) Bge. In the theory of Traditional Chinese Medicine (TCM), it is believed to have the functions of tonifying qi and lifting yang, as well as generating body fluids and nourishing blood. It can effectively treat cancer caused by the deficiency of vital energy and susceptibility to external diseases. Modern research has confirmed that the active components of AM, including <i>Astragalus</i> polysaccharides, flavonoids (formononetin and calycosin), <i>Astragalus</i> saponins (Astragaloside I and Astragaloside III), and <i>Astragalus</i> nanovesicles, are effective in the treatment of colorectal cancer. The mechanisms mainly involve inducing apoptosis, inhibiting tumor angiogenesis and the metastasis of cancer cells, regulating the cell cycle and tumor microenvironment, and reversing drug resistance. Moreover, it offers a synergistic enhancement when used in combination with chemotherapy, radiotherapy, targeted therapy, or surgical treatment. AM also has great potential in treating colorectal cancer when combined with other herbs. This review summarizes the relevant research findings on the treatment of colorectal cancer with AM, as well as its main pharmacological effects and molecular mechanisms, aiming to provide guidance for the development of new drugs, and offer direction for the conduct of more related research and promoting the development and application of AM.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"119-146"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ameliorative Effect of Glycyrrhizic Acid on Diosbulbin B-Induced Liver Injury and Its Mechanism. 甘草酸对薯蓣皂苷b所致肝损伤的改善作用及其机制。
Pub Date : 2025-01-01 Epub Date: 2025-01-17 DOI: 10.1142/S0192415X25500120
Xin Wang, Lei-Lei Shi, Yu-Han Zhang, Hong-Zhe Zhu, Shan-Shan Cao, Yong Shi, Hui-Zi Shangguan, Ji-Ping Liu, Yun-Dong Xie

This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) - induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment. After the experiment, the pharmacodynamics and mechanisms of GL in ameliorating DB-induced liver injury were explored using biochemical indexes, non-targeted metabolomics, targeted metabolomics, Western blotting analysis of protein expression, 16S rDNA sequencing, and Spearman correlation analysis. The results show reduced liver function indices and improved DB-induced hepatic pathological changes. It also attenuated DB-induced hepatic inflammation and oxidative stress. Hepatic metabolomics revealed that GL regulated ABC transporters and bile secretion. Targeted bile acid (BA) metabolomics and Western blotting demonstrated that GL improved DB-induced reduction in BA efflux by regulating FXR-mediated efflux transporters. Furthermore, analysis of 16S rDNA gene sequencing revealed that GL effectively restored the relative abundance of beneficial bacteria, reduced the relative abundance of harmful bacteria, and reinstated the structure of the intestinal flora. Additionally, correlation analyses between BA and intestinal flora indicated that Firmicutes, Bacteroidota, TDGA, DGA, UDGA, GDGA, THDGA, and HDGA could serve as major markers for DB-induced liver injury. In conclusion, GL significantly improved DB-induced liver injury by increasing the expression of Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1, promoting BA efflux, regulating intestinal flora, and alleviating inflammation and oxidative stress.

本研究旨在阐明甘草酸(GL)对薯蓣皂苷B (DB)诱导的小鼠肝损伤的保护作用,并探讨其作用机制。通过给药15 d建立小鼠肝损伤模型。同时给予小鼠GL治疗。实验结束后,通过生化指标、非靶向代谢组学、靶向代谢组学、蛋白表达Western blotting分析、16S rDNA测序和Spearman相关分析,探讨GL改善db诱导肝损伤的药效学和机制。结果显示,大鼠肝功能指数降低,肝脏病理改变改善。它还能减轻db诱导的肝脏炎症和氧化应激。肝脏代谢组学显示GL调节ABC转运蛋白和胆汁分泌。靶向胆汁酸(BA)代谢组学和Western blotting表明,GL通过调节fxr介导的外排转运蛋白,改善了db诱导的BA外排减少。此外,16S rDNA基因测序分析显示,GL有效地恢复了有益菌的相对丰度,降低了有害菌的相对丰度,恢复了肠道菌群的结构。此外,BA与肠道菌群的相关性分析表明,厚壁菌门(Firmicutes)、拟杆菌门(Bacteroidota)、TDGA、DGA、UDGA、GDGA、THDGA和HDGA可能是db诱导肝损伤的主要标志物。综上所述,GL通过增加Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1的表达,促进BA外排,调节肠道菌群,减轻炎症和氧化应激,显著改善了db诱导的肝损伤。
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引用次数: 0
Gut Microbiota and Osteoarthritis: From Pathogenesis to Novel Therapeutic Opportunities.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X2550003X
Yujiang Xi, Zhifeng Wang, Yuanyuan Wei, Niqin Xiao, Li Duan, Ting Zhao, Xiaoyu Zhang, Liping Zhang, Jian Wang, Zhaofu Li, Dongdong Qin

Osteoarthritis (OA) is the most common chronic degenerative joint disease, characterized by cartilage damage, synovial inflammation, subchondral bone sclerosis, marginal bone loss, and osteophyte development. Clinical manifestations include inflammatory joint pain, swelling, osteophytes, and limitation of motion. The pathogenesis of osteoarthritis has not yet been fully uncovered. With ongoing research, however, it has been gradually determined that OA is not caused solely by mechanical injury or aging, but rather involves chronic low-grade inflammation, metabolic imbalances, dysfunctional adaptive immunity, and alterations in central pain processing centers. The main risk factors for OA include obesity, age, gender, genetics, and sports injuries. In recent years, extensive research on gut microbiota has revealed that gut dysbiosis is associated with some common risk factors for OA, and that it may intervene in its pathogenesis through both direct and indirect mechanisms. Therefore, gut flora imbalance as a pathogenic factor in OA has become a hotspot topic of research, with potential therapeutic connotations. In this paper, we review the role of the gut microbiota in the pathogenesis of OA, describe its relationship with common OA risk factors, and address candidate gut microbiota markers for OA diagnosis. In addition, with focus on OA therapies, we discuss the effects of direct and indirect interventions targeting the gut microbiota, as well as the impact of gut bacteria on the efficacy of OA drugs.

{"title":"Gut Microbiota and Osteoarthritis: From Pathogenesis to Novel Therapeutic Opportunities.","authors":"Yujiang Xi, Zhifeng Wang, Yuanyuan Wei, Niqin Xiao, Li Duan, Ting Zhao, Xiaoyu Zhang, Liping Zhang, Jian Wang, Zhaofu Li, Dongdong Qin","doi":"10.1142/S0192415X2550003X","DOIUrl":"10.1142/S0192415X2550003X","url":null,"abstract":"<p><p>Osteoarthritis (OA) is the most common chronic degenerative joint disease, characterized by cartilage damage, synovial inflammation, subchondral bone sclerosis, marginal bone loss, and osteophyte development. Clinical manifestations include inflammatory joint pain, swelling, osteophytes, and limitation of motion. The pathogenesis of osteoarthritis has not yet been fully uncovered. With ongoing research, however, it has been gradually determined that OA is not caused solely by mechanical injury or aging, but rather involves chronic low-grade inflammation, metabolic imbalances, dysfunctional adaptive immunity, and alterations in central pain processing centers. The main risk factors for OA include obesity, age, gender, genetics, and sports injuries. In recent years, extensive research on gut microbiota has revealed that gut dysbiosis is associated with some common risk factors for OA, and that it may intervene in its pathogenesis through both direct and indirect mechanisms. Therefore, gut flora imbalance as a pathogenic factor in OA has become a hotspot topic of research, with potential therapeutic connotations. In this paper, we review the role of the gut microbiota in the pathogenesis of OA, describe its relationship with common OA risk factors, and address candidate gut microbiota markers for OA diagnosis. In addition, with focus on OA therapies, we discuss the effects of direct and indirect interventions targeting the gut microbiota, as well as the impact of gut bacteria on the efficacy of OA drugs.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"43-66"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Korean Red Ginseng Marc-Derived Gintonin Improves Alzheimer's Cognitive Dysfunction by Upregulating LPAR1.
Pub Date : 2025-01-01 Epub Date: 2025-02-17 DOI: 10.1142/S0192415X25500028
Yujeong Ha, Rami Lee, Seung Ho Jeon, Ji-Hun Kim, Hyo-Sung Jo, Tae Woo Kwon, Sung-Hee Hwang, Jong Kil Lee, Seung-Yeol Nah, Ik-Hyun Cho

Ginseng is a well-established functional food for brain health. However, its active ingredients have not yet been identified. Gintonin is a promising compound isolated from white/red ginseng. Its lysophosphatidic acid (LPA) is an exogenous G protein-coupled LPA receptor (LPAR) agonist. Korean red ginseng marc (KRGM) is a by-product after KRG extractions. In a previous study, we demonstrated that KRGM-derived gintonin (KRGM-G) contains LPA C[Formula: see text], a major functional component of both white and red ginseng. [Formula: see text] transgenic mice and SH-SY5Y cells were used to determine molecular mechanisms involved in KRGM-G-mediated anti-Alzheimer's disease (AD) effects. KRGM-G improved cognition impairment associated with alleviation of amyloid-β accumulation in the brain (hippocampus and cortex) in [Formula: see text] mice. KRGM-G inhibited activation of inflammatory cells (Iba-1-positive microglia and GFAP-positive astrocyte) and expression of pro-inflammatory mediators (IL-1β, IL-6, iNOS, or NO) in the brains of [Formula: see text] mice, increased the viability of H2O2-induced SH-SY5Y cells, and down-regulated the p38 MAPK, NF-κB p65, and STAT3 signaling pathways. KRGM-G also prevented the formation of reactive oxygen species and stimulated the Nrf2-HO-1/4-HNE signaling pathway in the brains of [Formula: see text] mice and SH-SY5Y cells. Interestingly, these positive effects of KRGM-G on AD-related symptoms and immunopathology were associated with up-regulation of LPAR1 in the brains of [Formula: see text] mice. These results suggest that KRGM-G might improve AD-related cognitive dysfunction by stimulating the anti-oxidant pathway (Nrf2) and inhibiting inflammatory pathways (p38/NF-κB/STAT3) through LPAR1.

{"title":"Korean Red Ginseng Marc-Derived Gintonin Improves Alzheimer's Cognitive Dysfunction by Upregulating LPAR1.","authors":"Yujeong Ha, Rami Lee, Seung Ho Jeon, Ji-Hun Kim, Hyo-Sung Jo, Tae Woo Kwon, Sung-Hee Hwang, Jong Kil Lee, Seung-Yeol Nah, Ik-Hyun Cho","doi":"10.1142/S0192415X25500028","DOIUrl":"10.1142/S0192415X25500028","url":null,"abstract":"<p><p>Ginseng is a well-established functional food for brain health. However, its active ingredients have not yet been identified. Gintonin is a promising compound isolated from white/red ginseng. Its lysophosphatidic acid (LPA) is an exogenous G protein-coupled LPA receptor (LPAR) agonist. Korean red ginseng marc (KRGM) is a by-product after KRG extractions. In a previous study, we demonstrated that KRGM-derived gintonin (KRGM-G) contains LPA C[Formula: see text], a major functional component of both white and red ginseng. [Formula: see text] transgenic mice and SH-SY5Y cells were used to determine molecular mechanisms involved in KRGM-G-mediated anti-Alzheimer's disease (AD) effects. KRGM-G improved cognition impairment associated with alleviation of amyloid-β accumulation in the brain (hippocampus and cortex) in [Formula: see text] mice. KRGM-G inhibited activation of inflammatory cells (Iba-1-positive microglia and GFAP-positive astrocyte) and expression of pro-inflammatory mediators (IL-1β, IL-6, iNOS, or NO) in the brains of [Formula: see text] mice, increased the viability of H<sub>2</sub>O<sub>2</sub>-induced SH-SY5Y cells, and down-regulated the p38 MAPK, NF-κB p65, and STAT3 signaling pathways. KRGM-G also prevented the formation of reactive oxygen species and stimulated the Nrf2-HO-1/4-HNE signaling pathway in the brains of [Formula: see text] mice and SH-SY5Y cells. Interestingly, these positive effects of KRGM-G on AD-related symptoms and immunopathology were associated with up-regulation of LPAR1 in the brains of [Formula: see text] mice. These results suggest that KRGM-G might improve AD-related cognitive dysfunction by stimulating the anti-oxidant pathway (Nrf2) and inhibiting inflammatory pathways (p38/NF-κB/STAT3) through LPAR1.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"17-41"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Berberine Inhibited SASP-Related Inflammation through RXRα/PPARγ/NEDD4 Pathway in Atherosclerosis. 小檗碱通过动脉粥样硬化中的RXR[公式:见文]/PPAR[公式:见文]/NEDD4通路抑制sasp相关炎症。
Pub Date : 2025-01-01 Epub Date: 2025-01-22 DOI: 10.1142/S0192415X25500107
Yinghong Zheng, Jiayuan Kou, Xi Gao, Jinxiang Guo, Qian Liu, Huiwen Ren, Tielei Gao, Qianbing Wang, Yajie Zhao, Yuqin Wang, Hong Li, Liming Yang

The accumulation of aging cells significantly contributes to chronic inflammatory diseases such as atherosclerosis. Human carotid artery single-cell sequencing has shown that large numbers of aging foam cells are present in the plaques of human patients. Berberine (BBR) has been shown to inhibit cell senescence, however, the mechanisms involved in its treatment of atherosclerotic senescence have not yet been determined. Changes in plaque morphology and blood chemistry were observed in ApoE[Formula: see text] mice fed with a high-fat diet before and after BBR treatment. Inflammatory proteins linked to the senescence-associated secretory phenotypes (SASP) were detected in RAW264.7 and peritoneal macrophage-derived foam cells. Smart-seq analysis was used to explore the pathways associated with BBR therapy for atherosclerosis. Finally, the effect of lentivirus-mediated knockdown of RXRα in macrophages in plaques on atherosclerosis treatment with BBR was determined. We found that BBR reduced inflammation linked to SASP in atherosclerosis through the RXRα/PPARγ/NEDD4 signaling pathway. BBR increased GATA4 binding to p62, promoted ubiquitination, and inhibited SASP-associated protein production in RAW264.7 and peritoneal macrophage-derived foam cells. Mechanistically, according to the Smart-seq results, BBR activated RXRα and PPARγ, synergistically increased NEDD4 transcription levels, and promoted ubiquitination-mediated degradation of the GATA4/p62 complex. Additionally, the anti-aging impact of BBR on atherosclerosis was negated when macrophage-specific RXRα was knocked down using lentivirus (pLVCD68-shRNA RXRα) in ApoE[Formula: see text] mice. BBR activated PPARγ through RXRα-PPARγ immune complex in macrophage-derived foam cells, increased NEDD4 transcriptional activity, promoted ubiquitination of GATA4-p62 complex, and inhibited SASP-related inflammation. These findings suggest the potential of BBR as a novel approach to addressing SASP-associated inflammation in atherosclerosis.

衰老细胞的积累是导致动脉粥样硬化等慢性炎症性疾病的重要因素。人类颈动脉单细胞测序显示,大量老化泡沫细胞存在于人类患者的斑块中。小檗碱(BBR)已被证明可以抑制细胞衰老,然而,其治疗动脉粥样硬化性衰老的机制尚未确定。在BBR治疗前后,观察高脂饮食喂养的ApoE小鼠斑块形态和血液化学的变化。在RAW264.7和腹膜巨噬细胞来源的泡沫细胞中检测到与衰老相关分泌表型(SASP)相关的炎症蛋白。Smart-seq分析用于探索与BBR治疗动脉粥样硬化相关的途径。最后,确定慢病毒介导的斑块内巨噬细胞RXR下调对BBR治疗动脉粥样硬化的影响。我们发现BBR通过RXR[公式:见文本]/PPAR[公式:见文本]/NEDD4信号通路减少动脉粥样硬化中与SASP相关的炎症。BBR增加了RAW264.7和腹腔巨噬细胞源性泡沫细胞中GATA4与p62的结合,促进了泛素化,并抑制了sasp相关蛋白的产生。在机制上,根据Smart-seq结果,BBR激活RXR[公式:见文]和PPAR[公式:见文],协同增加NEDD4转录水平,并促进泛素化介导的GATA4/p62复合物降解。此外,当使用慢病毒(pLVCD68-shRNA RXR[公式:见文])敲除ApoE小鼠巨噬细胞特异性RXR[公式:见文]时,BBR对动脉粥样硬化的抗衰老作用被否定。BBR通过RXR[公式:见文本]-PPAR[公式:见文本]激活巨噬细胞源性泡沫细胞中的PPAR[公式:见文本]免疫复合物,增加NEDD4转录活性,促进GATA4-p62复合物泛素化,抑制sasp相关炎症。这些发现提示BBR作为一种解决动脉粥样硬化中sasp相关炎症的新方法的潜力。
{"title":"Berberine Inhibited SASP-Related Inflammation through RXRα/PPARγ/NEDD4 Pathway in Atherosclerosis.","authors":"Yinghong Zheng, Jiayuan Kou, Xi Gao, Jinxiang Guo, Qian Liu, Huiwen Ren, Tielei Gao, Qianbing Wang, Yajie Zhao, Yuqin Wang, Hong Li, Liming Yang","doi":"10.1142/S0192415X25500107","DOIUrl":"10.1142/S0192415X25500107","url":null,"abstract":"<p><p>The accumulation of aging cells significantly contributes to chronic inflammatory diseases such as atherosclerosis. Human carotid artery single-cell sequencing has shown that large numbers of aging foam cells are present in the plaques of human patients. Berberine (BBR) has been shown to inhibit cell senescence, however, the mechanisms involved in its treatment of atherosclerotic senescence have not yet been determined. Changes in plaque morphology and blood chemistry were observed in ApoE[Formula: see text] mice fed with a high-fat diet before and after BBR treatment. Inflammatory proteins linked to the senescence-associated secretory phenotypes (SASP) were detected in RAW264.7 and peritoneal macrophage-derived foam cells. Smart-seq analysis was used to explore the pathways associated with BBR therapy for atherosclerosis. Finally, the effect of lentivirus-mediated knockdown of RXRα in macrophages in plaques on atherosclerosis treatment with BBR was determined. We found that BBR reduced inflammation linked to SASP in atherosclerosis through the RXRα/PPARγ/NEDD4 signaling pathway. BBR increased GATA4 binding to p62, promoted ubiquitination, and inhibited SASP-associated protein production in RAW264.7 and peritoneal macrophage-derived foam cells. Mechanistically, according to the Smart-seq results, BBR activated RXRα and PPARγ, synergistically increased NEDD4 transcription levels, and promoted ubiquitination-mediated degradation of the GATA4/p62 complex. Additionally, the anti-aging impact of BBR on atherosclerosis was negated when macrophage-specific RXRα was knocked down using lentivirus (pLVCD68-shRNA RXRα) in ApoE[Formula: see text] mice. BBR activated PPARγ through RXRα-PPARγ immune complex in macrophage-derived foam cells, increased NEDD4 transcriptional activity, promoted ubiquitination of GATA4-p62 complex, and inhibited SASP-related inflammation. These findings suggest the potential of BBR as a novel approach to addressing SASP-associated inflammation in atherosclerosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"251-283"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143019247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Pharmacokinetics and Biological Activities of Notoginsenoside R1: A Systematical Review.
Pub Date : 2025-01-01 Epub Date: 2025-01-29 DOI: 10.1142/S0192415X25500090
Chao Wen, Xiaofei Liao, Xinyun Ye, Wentao Lai

Panax notoginseng (PN) root is a renowned nutritional supplement, health food additive, and traditional medicine that maintains homeostasis within the human microcirculatory system. Notoginsenoside R1 (NG-R1), an active compound derived from PN root, has been reported to possess various pharmacological activities, including anti-inflammatory, antioxidant, anticancer, antimicrobial, and angiogenic effects. However, NG-R1's pharmacokinetic properties and pharmacological activities have not been systematically elucidated. In this paper, the pharmacokinetic properties of NG-R1, its pharmacological effects, mechanisms of actions, and structure-activity relationship have been reviewed. Notably, NG-R1 inhibits tumor necrosis factor α (TNF-α) expression, enhances the expression of nuclear factor erythroid 2-related factor 2 (NRF2), and enhances the expression of vascular endothelial growth factor receptor (VEGFR). The pharmacological effects of NG-R1 are associated with the modulation of several signaling pathways, such as mitogen-activated protein kinase (MAPK)/nuclear factor κ-B (NF-κB), NRF2/antioxidant response element (ARE), Wnt/β-catenin, and phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT). NG-R1 offers potentially protective effects against numerous diseases, including cardiovascular, neurological, renal, pulmonary, bone, and diabetes-related conditions. Although the pharmacological activities and diverse effects of NG-R1 have been demonstrated in various diseases, its clinical applications are limited by poor bioavailability. Several strategies have been explored to improve the pharmacokinetic profile of NG-R1, making it a promising candidate for drug development.

{"title":"Pharmacokinetics and Biological Activities of Notoginsenoside R1: A Systematical Review.","authors":"Chao Wen, Xiaofei Liao, Xinyun Ye, Wentao Lai","doi":"10.1142/S0192415X25500090","DOIUrl":"10.1142/S0192415X25500090","url":null,"abstract":"<p><p><i>Panax notoginseng</i> (PN) root is a renowned nutritional supplement, health food additive, and traditional medicine that maintains homeostasis within the human microcirculatory system. Notoginsenoside R1 (NG-R1), an active compound derived from PN root, has been reported to possess various pharmacological activities, including anti-inflammatory, antioxidant, anticancer, antimicrobial, and angiogenic effects. However, NG-R1's pharmacokinetic properties and pharmacological activities have not been systematically elucidated. In this paper, the pharmacokinetic properties of NG-R1, its pharmacological effects, mechanisms of actions, and structure-activity relationship have been reviewed. Notably, NG-R1 inhibits tumor necrosis factor α (TNF-α) expression, enhances the expression of nuclear factor erythroid 2-related factor 2 (NRF2), and enhances the expression of vascular endothelial growth factor receptor (VEGFR). The pharmacological effects of NG-R1 are associated with the modulation of several signaling pathways, such as mitogen-activated protein kinase (MAPK)/nuclear factor κ-B (NF-κB), NRF2/antioxidant response element (ARE), Wnt/β-catenin, and phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT). NG-R1 offers potentially protective effects against numerous diseases, including cardiovascular, neurological, renal, pulmonary, bone, and diabetes-related conditions. Although the pharmacological activities and diverse effects of NG-R1 have been demonstrated in various diseases, its clinical applications are limited by poor bioavailability. Several strategies have been explored to improve the pharmacokinetic profile of NG-R1, making it a promising candidate for drug development.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"205-249"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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The American journal of Chinese medicine
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