The American journal of Chinese medicine最新文献_第2页

Ophiopogonin D from Ophiopogon japonicas-induced USP25 Activity to Reduce Ferroptosis of Macrophage in Acute Lung Injury by the Inhibition of Bound Rac1 and Nox1 Complex. 麦冬皂苷D通过抑制结合的Rac1和Nox1复合物，诱导USP25活性降低急性肺损伤巨噬细胞铁下垂

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-03-19 DOI: 10.1142/S0192415X25500193

Zhichen Pu, Yingjing Gui, Wenhui Wang, Yinping Shui, Haitang Xie, Min Zhao

{"title":"Ophiopogonin D from Ophiopogon japonicas-induced USP25 Activity to Reduce Ferroptosis of Macrophage in Acute Lung Injury by the Inhibition of Bound Rac1 and Nox1 Complex.","authors":"Zhichen Pu, Yingjing Gui, Wenhui Wang, Yinping Shui, Haitang Xie, Min Zhao","doi":"10.1142/S0192415X25500193","DOIUrl":"10.1142/S0192415X25500193","url":null,"abstract":"Acute lung injury (ALI) can lead to severe respiratory system damage, characterized by extensive inflammation and lung tissue injury. Ophiopogonin D (OD), from Ophiopogon japonicus, has pharmacological effects such as anti-inflammatory and anti-oxidant, hypoglycemic, anti-aging, and immune regulation properties. This study attempts to identify the protective mechanism of OD against ALI by the inhibition of ferroptosis of macrophages. The tissue-specific expression of USP25 in patients with COVID-19 was evaluated using single-cell data from the China National GeneBank and the GSE147507 dataset from Gene Expression Omnibus (GEO). C57BL/6 mice, Murine bone marrow derived macrophages (BMDM) or RAW264.7 cells were induced by Lipopolysaccharide (LPS). OD prevented ALI, and reduced inflammation levels and oxidative stress in mice models. OD significantly decreased the number of monocyte/macrophages (CD11b [Formula: see text]Ly6G-cells) in the peritoneal cavity after ALI induction. OD-mitigated inflammation and oxidative stress of macrophages in the ALI model. OD-reduced ferroptosis of macrophages in a model of ALI through the inhibition of ROS-induced mitochondrial damage. USP25 is significantly expressed in macrophages in patients with COVID-19 using single-cell analysis. OD-suppressed Rac1/NOX1-derived ROS to reduce the mitochondrial damage of macrophages in a model of ALI by the induction of USP25 activity. OD-identified USP25 at 907-VAL and 975-ARG in an ALI model to suppress USP25 Ubiquitination. OD from Ophiopogon japonicus induces USP25 activity to reduce ferroptosis of macrophages in ALI by binding the Rac1 and Nox1 complex. Therefore, it can be concluded that OD may be a potential therapeutic drug for the treatment of ALI.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"501-522"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653031","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

Targeting EGFR-Mcl-1 Axis by Piperlongumine as a Novel Strategy for Non-Small Cell Lung Cancer Therapy. 哌隆明靶向EGFR-Mcl-1轴治疗非小细胞肺癌的新策略

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-03-27 DOI: 10.1142/S0192415X25500235

Wen Liu, Zhibin Jiang, Ruirui Wang, Xiongjian Zhang, Xiaoqing Jiang, Can Chen, Pengfei Guo, Ming Yi, Wei Li

{"title":"Targeting EGFR-Mcl-1 Axis by Piperlongumine as a Novel Strategy for Non-Small Cell Lung Cancer Therapy.","authors":"Wen Liu, Zhibin Jiang, Ruirui Wang, Xiongjian Zhang, Xiaoqing Jiang, Can Chen, Pengfei Guo, Ming Yi, Wei Li","doi":"10.1142/S0192415X25500235","DOIUrl":"10.1142/S0192415X25500235","url":null,"abstract":"Non-small cell lung cancer (NSCLC) is a malignancy that faces serious resistance challenges in treatment. In this study, we identified Piperlongumine as a promising therapeutic candidate to overcome Osimertinib resistance in NSCLC. We systematically investigated the inhibitory effect of Piperlongumine on NSCLC cells and confirmed that it could effectively inhibit the in vitro kinase activity of wild-type (WT), exon 19 deletion, and L858R/T790M-mutated EGFR. We also found that Piperlongumine-induced intrinsic apoptosis by interfering with the EGFR signaling pathway, which was characterized by the down-regulation of the anti-apoptotic protein Mcl-1. Further mechanistic studies revealed that Piperlongumine-induced degradation of Mcl-1 was dependent on the Akt-GSK3β signaling pathway. Additionally, Piperlongumine-promoted interaction between Mcl-1 and β-TRCP, thereby enhancing β-TRCP-mediated ubiquitination and the degradation of Mcl-1. Furthermore, Piperlongumine significantly inhibited tumor growth in both Osimertinib-sensitive and resistant NSCLC xenograft models. These findings highlight the potential of Piperlongumine as an effective agent in overcoming EGFR-targeted therapy resistance and suggest new avenues for its clinical application in NSCLC treatment.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"597-619"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143722899","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

Gambogic Acid Induces Ferroptosis via miR-1291/FOXA2 Axis in Gastric Cancer. 藤黄酸通过miR-1291/FOXA2轴诱导胃癌铁下垂。

The American journal of Chinese medicine Pub Date : 2025-01-01 DOI: 10.1142/S0192415X25500363

Chun-Mei Qian, Liu Yang, Yi-Ying Wang, Zi-Liang Wang, Zi-Hang Xu, Mi-Die Xu, Xing Zhang, Xiao-Yu Wang

{"title":"Gambogic Acid Induces Ferroptosis via miR-1291/FOXA2 Axis in Gastric Cancer.","authors":"Chun-Mei Qian, Liu Yang, Yi-Ying Wang, Zi-Liang Wang, Zi-Hang Xu, Mi-Die Xu, Xing Zhang, Xiao-Yu Wang","doi":"10.1142/S0192415X25500363","DOIUrl":"https://doi.org/10.1142/S0192415X25500363","url":null,"abstract":"Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, posing a significant threat to human health. Recently, gambogic acid (GA) has garnered attention for its anticancer properties in GC. However, it remains unclear whether GA can regulate other forms of cell death beyond apoptosis. In this study, we found that GA inhibited proliferation and induced ferroptosis in GC cells. Western blot analysis was employed to assess ferroptosis and endoplasmic reticulum (ER) stress-related proteins, as well as forkhead box A2 (FOXA2) expression. Additionally, malondialdehyde (MDA) and glutathione (GSH) levels were measured following GA treatment, and quantitative real-time polymerase chain reaction (RT-qPCR) was used to evaluate miR-1291 expression. Our findings revealed that GA treatment elevated reactive oxygen species (ROS) levels and promoted intracellular Fe[Formula: see text], MDA, and GSH accumulation. Furthermore, GA upregulated SLC7A11 and ferritin expression while suppressing glutathione peroxidase 4 (GPX4) in AGS and HGC27 cells, suggesting its role in ferroptosis induction. Notably, GA increased miR-1291 levels and downregulated FOXA2 expression. Subsequent analyses showed FOXA2 as a direct target of miR-1291. Functional experiments involving miR-1291 and FOXA2 knockdown or overexpression further suggested that the miR-1291/FOXA2 axis mediates ferroptosis. Finally, tumor xenograft models showed that GA effectively inhibited tumor growth by inducing ferroptosis. In conclusion, our study provides compelling evidence that GA induces ferroptosis in GC through the miR-1291/FOXA2 axis, highlighting its potential as a novel therapeutic strategy and preventive target for gastric cancer treatment.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"951-971"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082979","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

Panax notoginseng Saponins Alleviate Inflammatory Bowel Disease via Alteration of Gut Microbiota-Bile Acid Metabolism. 三七皂苷通过改变肠道微生物-胆汁酸代谢减轻炎症性肠病。

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-03-29 DOI: 10.1142/S0192415X25500223

Lin Wang, Li Shao, Yong-Chao Gao, Jing Liu, Xu-Dong Li, Jie Zhou, Shuang-Feng Li, Yue-Lin Song, Bo Liu, Wei Zhang, Wei-Hua Huang

{"title":"Panax notoginseng Saponins Alleviate Inflammatory Bowel Disease via Alteration of Gut Microbiota-Bile Acid Metabolism.","authors":"Lin Wang, Li Shao, Yong-Chao Gao, Jing Liu, Xu-Dong Li, Jie Zhou, Shuang-Feng Li, Yue-Lin Song, Bo Liu, Wei Zhang, Wei-Hua Huang","doi":"10.1142/S0192415X25500223","DOIUrl":"10.1142/S0192415X25500223","url":null,"abstract":"Bile acid metabolism mediated by gut microbiota is significantly related to immunity regulation that plays an important role in the development and treatment of inflammatory bowel disease (IBD). Our previous study has demonstrated that Panax notoginseng saponins (PNS) alleviate colitis due to the regulation of T helper 17/Regulatory T cells (Th17/Treg) balance via gut microbiota. However, the effects and mechanism of PNS on colitis pertinent to bile acid metabolism mediated by gut microbiota remain elusive. This study aims to investigate the anti-colitis mechanism of PNS by regulating the Th17/Treg balance pertinent to gut microbiota-bile acid metabolism. Results showed that PNS significantly decreased the relative abundance of Allobaculum, Dubosiella, Muribaculum, and Alistipes, and up-regulated the relative contents of conjugated bile acids, such as TCA and TCDCA. Fecal microbiota transplantation (FMT) showed that the gut microbiota remodeled by PNS had a regulatory effect on bile acid metabolism, and up-regulated the relative contents of TCA and TCDCA, which alleviated IBD and promoted Treg cell expression in vivo and in vitro. Taken together, PNS could reshape the profiling of gut microbiota to generate more TCA and TCDCA, which improve the balance of Th17/Treg to exert anti-IBD effects.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"567-596"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756715","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

Geniposide Suppresses Tumor Progression Through DUOX1-Mediated Ferroptosis in Hepatocellular Carcinoma. 京尼平苷通过duox1介导的肝癌铁下垂抑制肿瘤进展。

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-07-07 DOI: 10.1142/S0192415X25500600

Mei Luo, Yuelian Wang, Xiaodong Liu, Lin Liu, Li Zhu, Guo Chen, Qing Ye, Chengshi He, Xujue Xiao, Jike Li

{"title":"Geniposide Suppresses Tumor Progression Through DUOX1-Mediated Ferroptosis in Hepatocellular Carcinoma.","authors":"Mei Luo, Yuelian Wang, Xiaodong Liu, Lin Liu, Li Zhu, Guo Chen, Qing Ye, Chengshi He, Xujue Xiao, Jike Li","doi":"10.1142/S0192415X25500600","DOIUrl":"10.1142/S0192415X25500600","url":null,"abstract":"Among the spectrum of digestive system cancers, hepatocellular carcinoma (HCC) poses a particularly formidable challenge due to its poor prognosis. Geniposide, an iridoid glucoside extracted from the fruit of Gardenia jasminoides Ellis, exhibits a diverse array of biological activities. The goal of this study is to delineate the specific roles and underlying mechanisms of geniposide on the progression of HCC. Cell viability, apoptosis and migration of Huh7 and HepG2 cells were, respectively, assessed via CCK-8, flow cytometry and trans-well assays. The level of reactive oxygen species (ROS) was assessed with a dihydroethidium (DHE) probe. The measurement of mitochondrial membrane potential (MMP) was conducted using JC-1 staining. Ferroptosis-related markers were evaluated by Western Blot assay. Transcriptome sequencing was performed in HCC cells both treated and untreated with geniposide. In vivo experiments were applied with the subcutaneous xenograft tumor model. In vitro experiments revealed that geniposide exerted a concentration-dependent suppression on cell viability and migration, concurrently eliciting apoptosis in HCC cells. Ferroptosis was identified as the main form of geniposide-induced cell death in HCC. Geniposide promoted the iron ions levels, ROS accumulation, and the expression of ferroptosis markers, which were partially reversed by the addition of deferoxamine (DFO, ferroptosis inhibitor). Intersection analysis was applied between upregulated genes of HCC cells and ferroptosis-related genes. DUOX1 was proven to be involved in geniposide-mediated roles in HCC. In vivo experiments further clarified the suppressive effects of geniposide on tumors. Geniposide treatment increased intracellular iron ions and induced ferroptosis in HCC. Geniposide attenuated tumor progression and oxidative stress via DUOX1-mediated ferroptosis.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1573-1589"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577485","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

The Role of Traditional Chinese Medicine in Targeting NF-[Formula: see text]B Ubiquitination Against Ischemic Stroke. 中药靶向NF- B泛素化对缺血性脑卒中的作用。

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-07-16 DOI: 10.1142/S0192415X25500521

Jieyu Ding, Yi Qiu, Fang Yan, Xi Peng

{"title":"The Role of Traditional Chinese Medicine in Targeting NF-[Formula: see text]B Ubiquitination Against Ischemic Stroke.","authors":"Jieyu Ding, Yi Qiu, Fang Yan, Xi Peng","doi":"10.1142/S0192415X25500521","DOIUrl":"https://doi.org/10.1142/S0192415X25500521","url":null,"abstract":"Ischemic Stroke (IS) is a severe neurological disease with high mortality rates worldwide, involving a complex cascade reaction in which the ubiquitination process of nuclear factor kappa B (NF-[Formula: see text]B) pathway has been proposed as a therapeutic target for IS on account of the fact that NF-[Formula: see text]B can be suppressed by the Ubiquitin-Proteasome System (UPS). This review systematically discusses the epidemiology of IS, the NF-[Formula: see text]B signaling pathway, and the anti-inflammatory and anti-apoptotic effects that TCM monomers and formulations exert by regulating the ubiquitination process of the NF-[Formula: see text]B signaling pathway. We initially offer an overview of the incidence and treatment of IS, following which the canonical pathway and non-canonical pathway of NF-[Formula: see text]B are introduced. Next, the ubiquitination mechanisms of NF-[Formula: see text]B when using traditional Chinese medicine (TCM) to treat IS were highlighted. We also discussed the involvement of MyD88, an upstream protein, in the herb-based treatment of IS. Finally, we proposed future research directions for screening advantageous herbal components. Given previous research, we anticipate that TCM drugs will present promising candidates for IS treatment in clinical medicine.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 5","pages":"1355-1378"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710425","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

Role of Traditional Chinese Medicine in Lung Cancer Management: A Review. 中医药在肺癌治疗中的作用综述

The American journal of Chinese medicine 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

{"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":"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.","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

Chinese Medicine for the Treatment of Liver Cirrhosis: The Mechanism of Cellular Autophagy. 中药治疗肝硬化：细胞自噬的机制。

The American journal of Chinese medicine Pub Date : 2025-01-01 Epub Date: 2025-03-12 DOI: 10.1142/S0192415X25500168

Shihao Zheng, Tianyu Xue, Qiuyue Wang, Pingxin Zhang, Wenying Qi, Chengyuan Xue, Xiaoke Li, Hongbo Du, Peng Zhang, Xiaobin Zao, Yongan Ye

{"title":"Chinese Medicine for the Treatment of Liver Cirrhosis: The Mechanism of Cellular Autophagy.","authors":"Shihao Zheng, Tianyu Xue, Qiuyue Wang, Pingxin Zhang, Wenying Qi, Chengyuan Xue, Xiaoke Li, Hongbo Du, Peng Zhang, Xiaobin Zao, Yongan Ye","doi":"10.1142/S0192415X25500168","DOIUrl":"10.1142/S0192415X25500168","url":null,"abstract":"Liver cirrhosis is a critical stage in the progression of various chronic liver diseases, often leading to severe complications such as ascites, hepatic encephalopathy, and a high mortality rate, and it thus poses a serious threat to patient life. The activation of hepatic stellate cells is a central driver of disease progression. Cellular autophagy, a lysosome-mediated degradation process, plays a key role in maintaining cellular function and dynamic homeostasis. Research has shown that autophagy is closely associated with proteins like LC3, Beclin-1, P62, and mTOR, and is regulated through signaling pathways such as PI3K/Akt/mTOR, Ras/Raf/MEK/ERK, and AMPK/mTOR. Additionally, the relationship between autophagy and apoptosis, as well as between autophagy and exosomes, has been further demonstrated. While modern medicine has made progress in treating cirrhosis, it still faces significant limitations. By contrast, numerous studies have demonstrated the efficacy of traditional Chinese medicine in preventing and treating liver cirrhosis by regulating autophagy, with fewer adverse effects. Chinese herbal monomers and formulations can modulate various autophagy-related signaling pathways, including PI3K/Akt/mTOR, Ras/Raf/MEK/ERK, and AMPK/mTOR, and influence key autophagy proteins such as LC3 and Beclin-1. This modulation inhibits hepatic stellate cell activation, reduces extracellular matrix deposition, and exerts anticirrhotic effects. Moreover, Chinese medicine appears to reduce adverse reactions in cirrhosis treatment and lower the risk of disease recurrence. This review explores the mechanisms of autophagy in the prevention and treatment of liver cirrhosis through Chinese medicine, offering new insights for the development of Chinese medicinal therapies for cirrhosis and their rational clinical application.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"409-433"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607612","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

Puerarin Alleviates Alcoholic Liver Disease via Suppressing Lipolysis Induced by Sympathetic Outflow. 葛根素通过抑制交感神经流出诱导的脂肪分解缓解酒精性肝病。

The American journal of Chinese medicine Pub Date : 2025-01-01 DOI: 10.1142/S0192415X25500326

Ke Zheng, Liu Yang, Rui-Shuo Zhang, Yi-Han Qian, Yu-Ge Zhou, Wei-Fan Huang, Jia-Cheng Lin, Yan-Jun Shi, Xiao-Ni Kong

{"title":"Puerarin Alleviates Alcoholic Liver Disease via Suppressing Lipolysis Induced by Sympathetic Outflow.","authors":"Ke Zheng, Liu Yang, Rui-Shuo Zhang, Yi-Han Qian, Yu-Ge Zhou, Wei-Fan Huang, Jia-Cheng Lin, Yan-Jun Shi, Xiao-Ni Kong","doi":"10.1142/S0192415X25500326","DOIUrl":"https://doi.org/10.1142/S0192415X25500326","url":null,"abstract":"The aim of this study was to evaluate the therapeutic effect of puerarin (PUE) on alcoholic liver disease (ALD) and elucidate the potential mechanism from the perspective of lipolysis and hepatic steatosis. Assessment of PUE efficacy against ALD was performed using serum biochemical parameters and the histological examination of liver and adipose tissue via Hematoxylin and eosin (H&E) staining. The potential mechanisms underlying the amelioration of ALD by PUE were investigated using Western blotting (WB) analysis and immunofluorescence (IHC) staining. We demonstrated that PUE attenuated steatosis in ALD by alleviating ethanol-induced liver damage and lipid accumulation, suppressing the expression of lipid synthesis genes, upregulating the expression of lipid metabolism genes, and reducing lipolysis by inhibiting adipose triglyceride lipase (ATGL) activation and the phosphorylation of hormone-sensitive lipase (HSL). In conclusion, PUE ameliorates ALD by inhibiting the sympathetic outflow-mediated activation of key lipolysis enzymes ATGL and HSL. These findings provide a solid theoretical foundation for the potential application of PUE in the clinical treatment of ALD.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"863-888"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082984","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

Traditional Chinese Medicine Formulae and Chinese Patent Medicines for the Treatment of Diabetic Kidney Disease: Efficacies and Mechanisms. 治疗糖尿病肾病的中药方剂与中成药：疗效与机制。

The American journal of Chinese medicine Pub Date : 2025-01-01 DOI: 10.1142/S0192415X25500260

Haoyu Li, Huan Chen, Renhao Gao, Mingjing Yin, Fang Huang

{"title":"Traditional Chinese Medicine Formulae and Chinese Patent Medicines for the Treatment of Diabetic Kidney Disease: Efficacies and Mechanisms.","authors":"Haoyu Li, Huan Chen, Renhao Gao, Mingjing Yin, Fang Huang","doi":"10.1142/S0192415X25500260","DOIUrl":"https://doi.org/10.1142/S0192415X25500260","url":null,"abstract":"Diabetic kidney disease is one of the most significant comorbidities of diabetic patients, and has become the second cause of end-stage renal disease. Current clinical management programs have difficulty in reducing morbidity and poor prognosis, and thus new treatment options and concepts need to be developed. Traditional Chinese medicine formulae and Chinese patent medicines contain a variety of medicinal flavors, laying the material foundation for the multi-target, multi-level therapeutic features. This study describes the main pathologic features of DKD as well as its pathogenesis. Additionally, the categorization of TCM according to its different therapeutic mechanisms is discussed, and the signaling pathways targeted and corresponding biological effects are described in detail. For example, TCM formulae can alleviate oxidative stress through pathways such as Nrf2 and NOX4, can inhibit the development of inflammation through pathways such as TGF-β and NF-κB, and can ameliorate DKD by inhibiting endoplasmic reticulum stress and apoptosis. Moreover, it highlights the superior efficacy of the combined application of TCM formulae and Western medicine over Western medicine alone, which can compensate for the shortcomings of existing DKD treatment methods to a certain extent. TCM formulae and CPMs are promising candidates for the auxiliary treatment of DK, however, the lack of clarity regarding the active ingredients intensifies the difficulty of integrating TCM formulae and CPMs into clinical practice. Further research is warranted to explore the material basis and molecular mechanisms of action of TCM formulae against DKD.","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":"53 3","pages":"675-707"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083045","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