Phytotherapy Research最新文献

{"title":"Epigenetic Insights Into Aging: Emerging Roles of Natural Products in Therapeutic Interventions.","authors":"Yutong Pang, Huan Zhang, Huimin Li, Xiaojue Wang, Panjian Wei, Ling Yi, Shuye Lin","doi":"10.1002/ptr.70003","DOIUrl":"10.1002/ptr.70003","url":null,"abstract":"<p><p>Aging is a significant contributor to numerous diseases and presents serious challenges to public health. Consequently, investigating the underlying mechanisms of aging and developing effective interventions to combat its effects have become increasingly important, as achieving healthy aging has emerged as a growing priority. A primary characteristic of aging is the epigenetic changes that occur within the genome. Epigenetic regulation, functioning as a reversible mechanism, closely links gene composition to phenotype and plays a crucial role in reversing aging in response to environmental stimuli. Epigenetics involves modifying phenotype or gene expression by regulating posttranscriptional levels without altering the DNA sequence. These mechanisms are vital to the aging process and are anticipated to become key targets for delaying aging and improving or preventing age-related diseases in the future. Recent studies have indicated that natural product therapy has emerged as one of the most promising strategies for mitigating the effects of aging. The application of natural products acting via the epigenetic regulation in therapy is particularly flexible and controllable, facilitating practical use while reducing the risk of drug resistance and enhancing host immune responses. This article reviews the current research status and advancements in epigenetic pathways within the realm of anti-aging drugs, proposing future research directions and potential development trends. The aim is to provide a reference for researchers in the field of epigenetics while offering ideas and suggestions for subsequent studies.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Compound K Mitigates Mitochondrial Fission Through Bile Acid Receptors/YAP Signaling to Counteract Podocyte Injury in Lupus Nephritis.","authors":"Ying Li, Ziyu Song, Sumei Xu, Ke Xu, Wangda Xu, Li Xu, Fengyuan Tian","doi":"10.1002/ptr.8492","DOIUrl":"https://doi.org/10.1002/ptr.8492","url":null,"abstract":"<p><p>Irreversible renal damage in lupus nephritis (LN) results from critical podocyte injury. Disruption in the actin cytoskeleton initiates mitochondrial fission to exacerbate podocyte injury. While ginsenoside compound K (CK) alleviates podocyte injury in lupus-prone mice, its mechanism in regulating mitochondrial dynamics underlying remains elusive. Based on the open-source single-cell RNA sequencing dataset, this study clarified CK's role in alleviating podocyte injury in MRL/lpr mice by regulating cytoskeleton-mediated mitochondrial fission and elucidated the molecular mechanisms underlying the BA receptor-YAP axis. MRL/lpr mice were administered CK (20 or 40 mg/kg) for 10 weeks. Renal function and pathological changes were evaluated, along with renal metabolite profiles and metabolomics analysis. We analyzed publicly available single-cell RNA sequencing data to specifically profile gene mapping and enrichment analysis during immune-mediated renal injury. Furthermore, podocyte-based in vitro assays were conducted to investigate the impact of the BA receptors-YAP axis on mitochondrial dynamics. CK effectively cleared anti-dsDNA antibodies, attenuated systemic inflammation, and improved renal function through resolving immune complex deposition. Mechanistically, CK restored actin cytoskeleton integrity via Rho GTPase regulation and reshaped BA metabolism to activate TGR5/FXR receptors in podocytes. This dual action suppressed DRP1 s616 phosphorylation, inhibiting excessive mitochondrial fission, regulating while enhancing TFAM-mediated mtDNA replication for mitochondrial homeostasis. Concurrently, CK attenuated podocyte apoptosis through Hippo signaling inhibition and YAP activation. In conclusion, CK ameliorates podocyte injury by preventing excessive mitochondrial fission through the BA receptors-YAP axis, thus providing a potential therapy for LN.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing Dietary Phytochemicals to Modulate Signaling Pathways in Cancer Chemoprevention-A Review.","authors":"Kritika Pandit, Chandni Garg, Aashaq H Bhat, Renu Bhardwaj, Satwinderjeet Kaur","doi":"10.1002/ptr.8524","DOIUrl":"https://doi.org/10.1002/ptr.8524","url":null,"abstract":"<p><p>Cancer chemoprevention involves the use of natural or synthetic agents to delay, suppress, or reverse cancer progression. Among natural sources, phytochemicals derived from medicinal plants have garnered significant attention due to their potent biological effects on human health, particularly in combating various cancer types. These compounds offer a promising alternative to traditional therapeutic approaches by targeting key mechanisms involved in cancer development. Their natural origin, minimal side effects, and diverse modes of action make them valuable candidates for cancer prevention strategies. This review highlights the diverse mechanisms by which plant-derived compounds exert chemopreventive effects, including cell cycle arrest, induction of apoptosis, and activation of autophagy. Additionally, it explores their ability to reverse adverse epigenetic modifications, enhance the expression of phase II detoxification enzymes, and modulate critical signaling pathways involved in tumor progression. Understanding these molecular mechanisms is essential for optimizing the therapeutic potential of phytochemicals and expanding their clinical applications. By emphasizing the multifaceted role of phytochemicals in cancer chemoprevention, the review underscores their significance in developing novel anticancer therapeutics. These plant-derived compounds hold great promise in shaping future cancer treatment paradigms through their ability to modulate key cellular processes and signaling pathways. Addressing existing research gaps could pave the way for more extensive studies and clinical trials, ultimately leading to the development of effective, plant-based anticancer therapies.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xanthohumol Alleviates Inflammatory Bowel Disease-Associated Osteoporosis via Regulating Gut Microbial Metabolites.","authors":"Weiqing Fan, Tianshuang Xia, Yiping Jiang, Kun Li, Jianyong Han, Ruiqing Zhu, Yue Hu, Jianyong Zhu, Hua Nian, Hailiang Xin","doi":"10.1002/ptr.70001","DOIUrl":"https://doi.org/10.1002/ptr.70001","url":null,"abstract":"<p><p>Patients with inflammatory bowel disease (IBD) frequently experience osteoporosis (OP) due to factors such as chronic inflammation, malnutrition, and corticosteroid use. However, there is currently a lack of effective pharmacological interventions for the prevention and treatment of IBD-associated OP. Xanthohumol (XAN), a natural flavonoid compound isolated from hops, has shown beneficial effects on both inflammation and osteoporosis. This study aimed to explore the therapeutic effects and potential mechanisms of XAN from hops on IBD-associated OP based on gut microbiota. The IBD-associated OP model was constructed by free drinking of dextran sulfate sodium (DSS). Therapeutic effects of XAN were investigated through disease activity index (DAI) scoring, colon pathology, mucosal barrier function, inflammatory factors, bone metabolism indicators, and femoral Micro-CT. Mechanisms of XAN regulating gut microbiota were preliminarily elucidated by 16S rDNA sequencing and non-targeted metabolomics. XAN could effectively alleviate colonic tissue inflammation and protect the intestinal mucosal barrier, further improve colonic pathological damage, and reduce the DAI scoring in DSS mice. It also exerted anti-IBD-associated OP effects by reducing serum inflammatory factors IL-6, IL-17A, and TNF-α, inhibiting serum CTX-I expression, promoting serum OPG expression, regulating calcium-phosphorus balance, and improving bone density and morphology. More importantly, 16S rDNA sequencing and untargeted metabolomics showed that XAN increased the abundance and diversity of the gut microbiota in DSS mice. By altering the abundance of specific bacterial taxa such as Turicibacter, norank_f__norank_o__Clostridia_UCG-014, norank_f__Muribaculaceae, and Faecalibaculum, XAN changed the metabolites of gut microbiota, thereby regulating the tryptophan (Trp) metabolism pathway, as well as improving the intestinal mucosal barrier and bone metabolism. XAN can improve the pathological injury of the colon and bone loss caused by IBD. The mechanism is to regulate Trp metabolism by intervening in gut microbiota, thereby protecting intestinal mucosal barrier function and promoting bone formation.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochanin a Alleviated Doxorubicin-Induced Cardiotoxicity but Did not Interfere With the Antitumor Effect of Doxorubicin.","authors":"Yijin Yang, Zhenyu Feng, Fengying Zhou, Xuyang Sun, Jinshu Shang, Ningning Zhang, Yunlong Xia, Yunpeng Xie","doi":"10.1002/ptr.8525","DOIUrl":"https://doi.org/10.1002/ptr.8525","url":null,"abstract":"<p><strong>Background and aim: </strong>Doxorubicin (DOX)-induced cardiotoxicity (DIC) by the chemotherapeutic drug seriously affects the prognosis of patients with cancer. Therefore, it is significant to actively explore the underlying mechanisms of DIC and develop safe and effective adjuvant therapies to improve DIC. As a traditional Chinese medicine monomer, BCA can treat cardiovascular diseases. However, whether BCA is able to inhibit DOX-induced myocardial injury without affecting its anticancer effect is unclear.</p><p><strong>Experimental procedure: </strong>We divided tumor-bearing mice into four groups, constructed a heart failure model by administering DOX, and treated with BCA. Histopathological staining was performed (WGA, HE, IF, IHC, etc.), WB, qPCR, and serum detection of SOD and MDA. In vitro experiments, the effects of BCA and DOX in both kinds of cells were demonstrated by various experiments in primary cardiomyocytes and tumor cells panc02 of neonatal rats.</p><p><strong>Key results: </strong>The results showed that BCA could inhibit DOX-induced abnormal cardiac function in mice, improve heart failure, and inhibit the expression of ANP and BNP. It inhibited the level of myocardial oxidative stress and reduced the number of myocardial vacuolation and the degree of myocardial fibrosis in mice. BCA reduced DOX-induced oxidative stress in NRCMs. In terms of tumors, BCA cooperates with DOX to inhibit the occurrence and development of panc02 and reduce the body weight of tumors. It inhibited the expression of PCNA and promoted the expression of BAX. In vitro experiments, BCA cooperated with DOX to inhibit the proliferation and metastasis of panc02.</p><p><strong>Conclusions and implications: </strong>To sum up, BCA can affect the occurrence and development of DOX-induced myocardial injury through multiple targets and pathways and does not interfere with the anti-tumor effect of DOX. This study seeks new drugs for DOX-induced myocardial injury and provides new ideas for the treatment of inhibiting DOX-induced myocardial injury and the research of related diseases.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isoferulic Acid Mitigates Acute Lung Injury Induced by Sepsis Through the Inhibition of JAK2.","authors":"Tong Xu, Honglin Xu, Jiayi Zhang, Guanghong Chen, Xin Han, Guoyong Zhang, Changlei Hu, Mingjie Pang, Jian Gan, Yue Hua, Bin Liu, Yingchun Zhou","doi":"10.1002/ptr.8526","DOIUrl":"https://doi.org/10.1002/ptr.8526","url":null,"abstract":"<p><p>Sepsis-induced acute lung injury (ALI), among the most severe organ damages, induces irreversible lung injuries and results in a high mortality rate. The occurrence of ALI is highly correlated with the out-of-control inflammatory factors. Therefore, inflammatory inhibition is a crucial measure for treating sepsis-induced ALI. Isoferulic acid (IFA) possesses effective anti-inflammatory effects; however, its role in ALI and its molecular mechanisms remain to be further explored. This work focused on analyzing the possible role of IFA in combating sepsis-induced IFA and exploring the associated mechanisms. CLP mice and LPS-induced RAW264.7 cells were employed as the in vivo and in vitro experimental models. Effects of IFA on inflammation and its mechanisms were assessed using network pharmacology, molecular docking, surface plasmon resonance imaging (SPRi), qRT-PCR, ELISA, immunofluorescence analysis, and Western blot. According to in vivo and in vitro experimental results, IFA down-regulated inflammatory factors TNF-α, IL-6, and IL-1β in CLP mice and LPS-exposed RAW264.7 cells. IFA treatment significantly improved the sepsis-induced inflammation and protected lung function. Furthermore, as revealed by network pharmacology analysis, JAK2 was an important target for the interaction between IFA and ALI. Moreover, molecular docking and SPR results demonstrated a close binding between IFA and JAK2. Further research revealed that IFA suppressed JAK2/STAT3 pathway activation; besides, the therapeutic effect of IFA on ALI was not enhanced by incubation with the JAK2 inhibitor (AG490). Our results offer the preliminary evidence that IFA can restore the impaired function of CLP mice and RAW264.7 cells by alleviating the sepsis-induced inflammation. Additionally, IFA mitigates the sepsis-induced ALI through inhibiting JAK2/STAT3 pathway activation. Therefore, IFA may potentially be used to treat sepsis-induced lung injury.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jatrorrhizine Alleviates Calcific Aortic Valve Disease via Interfering With Glycolysis Targeting ALDOA K42 Lactylation.","authors":"Jiaqin Wu, Sixiang Wang, Pengfei Gao, Shunshun Wang, Huiming Yu, Qianqian Du, Minfu Liu, Shuwan Hou, Shan Jiang, Huajiao Xu, Siyi Ye, Fan Feng, Chunli Wang, Kang Xu","doi":"10.1002/ptr.8504","DOIUrl":"https://doi.org/10.1002/ptr.8504","url":null,"abstract":"<p><p>Calcific aortic valve disease (CAVD) is a common cardiovascular disorder. It is characterized by the thickening, fibrosis, and mineralization of aortic valve leaflets. These pathological changes can progress to heart failure if not managed effectively. Current surgical or transcatheter aortic valve replacement options exist, yet no pharmacotherapy has been established to impede CAVD advancement. Prior research by our team spotlighted the significance of lactate-derived protein lactylation (Kla) in initiating valve calcification. In this study, we aim to uncover the anti-calcification capacity of jatrorrhizine (JAT) and dissect its novel molecular underpinnings. The multi-omics analyses were used to indicate that JAT affects the glycolysis of hVICs, thus exerting a therapeutic effect on CAVD. Then, molecular docking, immunoprecipitation, and site mutation were used to demonstrate that JAT can reduce the lactylation of ALDOA at the K42 site by binding to the lactyltransferases KAT5, thereby affecting its enzymatic stability and downstream metabolic pathways. JAT impeded CAVD by perturbing glycolysis and Kla. Notably, a decline in non-histone Kla modification was linked to JAT inhibition of the osteogenic phenotype. ALDOA Kla, among glycolytic rate-limiting enzymes, is a prime target of JAT anti-calcification action. Crucially, the ALDOA K42la site was correlated with JAT-induced suppression of Runx2 expression. JAT treatment effectively curbed osteogenic differentiation in human aortic valve interstitial cells (hVICs) and mitigated CAVD progression in mice. our findings pioneer the revelation that JAT mitigates calcification by targeting ALDOA K42la to interfere with glycolysis, suggesting its potential as a potent preventative agent against CAVD. JAT alleviates calcific aortic valve disease via interfering with glycolysis targeting ALDOA K42 lactylation.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Piperine Improves DSS-Induced Colitis in Mice via Inhibition of Inflammation and Modulation of Gut Microbiota.","authors":"Yeye Hu, Yanting Wang, Haoyang Gao, Guigui Yang, Jing Xie, Ziliang He, Shenghui Lv, Fenglin Gu, Chaoqing Huang, Weicheng Hu","doi":"10.1002/ptr.8491","DOIUrl":"https://doi.org/10.1002/ptr.8491","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a global health concern with limited therapeutic options. Previous studies have demonstrated that piperine exhibited anti-inflammatory effects both in vitro and in vivo. However, its potential to ameliorate colitis in mice through modulation of gut microbiota has not been explored. This study aimed to investigate the role of gut microbiota in the protective effects of piperine against colitis using a dextran sulfate sodium (DSS)-induced mouse model. Mice were administered piperine (12.5 and 25 mg/kg) prior to DSS exposure. Fecal microbiota transplantation (FMT) was then performed, after which we evaluated colitis symptoms, inflammation levels, and intestinal barrier function. Subsequently, 16S rDNA-based high-throughput sequencing was employed to analyze the microbial composition of the mouse cecal contents. Piperine administration increased the colon length, decreased the spleen index, and improved colon histopathology. Furthermore, piperine modulated inflammatory responses by inhibiting NF-κB signaling, thereby reducing the release of pro-inflammatory cytokines and mediators. It also enhanced intestinal barrier integrity by increasing the expression of claudin-1, claudin-3, ZO-1, occludin, and mucin 2. Notably, the 16S rDNA sequencing results revealed that piperine increased the abundance of Dubosiella in the gut. Piperine effectively protected mice from DSS-induced colitis, suppressed inflammation, and improved poor intestinal barrier function. It reshaped the intestinal microbiota, ultimately alleviating DSS-induced colitis in mice. Our research highlighted the significant role of gut microbiota in the piperine-mediated alleviation of intestinal damage and suggested its therapeutic potential for promoting gut health and reducing the risk of colitis.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144209158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sinomenine Ameliorates Liver Fibrosis by Blocking TGF-β/SMAD and c-JUN Signaling.","authors":"Yichao Du, Junjie Bai, Tingting Ma, Ziming Wu, Pengru Wang, Xiaolin Zhong, Wenguang Fu, Shuixiang He","doi":"10.1002/ptr.8502","DOIUrl":"https://doi.org/10.1002/ptr.8502","url":null,"abstract":"<p><p>Liver fibrosis, a pivotal pathological feature in the progression of chronic liver injury, currently lacks effective therapies. Sinomenine (SIN), a bioactive alkaloid derived from traditional Chinese medicine, demonstrates diverse pharmacological properties. However, its therapeutic potential and mechanisms in liver fibrosis remain inadequately characterized. This study investigates the anti-fibrotic effects of SIN and its underlying molecular mechanisms. The anti-fibrotic efficacy of SIN was evaluated in two murine models of liver fibrosis induced by carbon tetrachloride (CCl₄) or bile duct ligation (BDL), along with transforming growth factor-beta 1 (TGF-β1)-stimulated rat hepatic stellate cells (HSC-T6). Serum biochemical markers, histopathological analyses (Hematoxylin-Eosin, Sirius red, and Masson's trichrome staining), immunofluorescence, and immunohistochemistry were employed to assess hepatic injury and collagen deposition. Western blotting elucidated molecular mechanisms. SIN administration significantly attenuated hepatic injury in CCl₄- or BDL-induced mice, as evidenced by reduced transaminase levels and improved histopathological features. In both in vivo and in vitro models, SIN suppressed fibrogenesis by decreasing collagen deposition and downregulating expression of α-smooth muscle actin (α-SMA), matrix metalloproteinase 2 (MMP2), and collagen I. Mechanistically, SIN inhibited the TGF-β/SMAD pathway through reduced phosphorylation of SMAD2/3 and attenuated c-JUN signaling via diminished phosphorylated c-JUN levels. Pretreatment with TP0427736 (a SMAD2/3 inhibitor) or SP600125 (a c-JUN inhibitor) synergistically enhanced SIN-mediated α-SMA suppression in HSC-T6 cells. SIN ameliorates liver fibrosis through inhibition of TGF-β/SMAD and c-JUN signaling pathways. These findings position SIN as a promising therapeutic candidate for liver fibrotic disorders.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Efficacy of Curcumin, Resveratrol, Silymarin, and Berberine on Cardio-Metabolic Risk Factors Among Patients With Type 2 Diabetes Mellitus: A Systemic Review and Bayesian Network Meta-Analysis.","authors":"Runyu Miao, Boxun Zhang, Danni Zhou, Mengjiao Kang, Jiaxing Tian, Linhua Zhao, Xiaolin Tong","doi":"10.1002/ptr.8431","DOIUrl":"https://doi.org/10.1002/ptr.8431","url":null,"abstract":"<p><p>The comprehensive management of cardiovascular risk factors, including blood glucose, blood lipids, and blood pressure in type 2 diabetes mellitus (T2DM), is essential to prevent cardiovascular complications. Consequently, there is an urgent need to explore improved clinical treatment strategies by comparing the efficacy of various interventions. To assess the efficacy of herbal phytochemicals in regulating cardio-metabolic risk factors among patients with T2DM. A systematic literature review of the English language literature from inception to March 31, 2024, was conducted using PubMed, Embase, and Cochrane Library databases. The included literature focused on treating patients with T2DM using herbal phytochemicals. ADDIS and Revman were used to conduct Bayesian network and pairwise meta-analyses, respectively, and the surface under the cumulative ranking curve was used to obtain the ranking order of different herbal phytochemicals. This study included 17 studies involving 1,337 participants. Resveratrol was generally the most effective, followed by silymarin. Compared with the placebo, resveratrol significantly improved HOMA-IR, total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), systolic blood pressure (SBP), and diastolic blood pressure (DBP) (P < 0.05); silymarin significantly improved fasting plasma glucose (FPG), HOMA-IR, and hemoglobin A1c (HbA1c) (P < 0.05). For HbA1c, silymarin was more effective than resveratrol (MD -2.08, 95%Cl -3.50 to -0.72) (P < 0.05). For body mass index (BMI), curcumin was more effective than resveratrol (MD -1.27, 95%Cl -2.43 to -0.03) (P < 0.05). Curcumin, resveratrol, silymarin, and berberine can effectively improve cardio-metabolic risk factors in T2DM, and different herbal phytochemicals have different clinical advantages. The therapeutic potential of resveratrol is significant in the regulation of blood glucose, blood lipids, and body weight, silymarin exhibited the best effect in reducing blood glucose, berberine could lower blood glucose and regulate blood lipids, and curcumin had a definite therapeutic effect on weight loss. However, further validation of these findings is necessary through extensive clinical studies with larger sample sizes.</p>","PeriodicalId":20110,"journal":{"name":"Phytotherapy Research","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}