The American journal of Chinese medicine最新文献

{"title":"Nanoformulated Curcumin Ameliorates Ulcerative Colitis via Gut Microbiota Modulation and Barrier Function Restoration.","authors":"Yin-Zhuo Xie, Chen-Xi Sun, Tian-Tian Fu, Zheng Jin, Nonthaneth Nalinratana, Pornchai Rojsitthisak, Kai Zhao, Jing-Sheng Hua, Fang-Yi Pei, Xiao-Hua Wang","doi":"10.1142/S0192415X26500837","DOIUrl":"https://doi.org/10.1142/S0192415X26500837","url":null,"abstract":"<p><p>The gut microbiota is increasingly recognized as a key mediator of the anticolitis effects of curcumin (CUR). However, the clinical translation of this promising activity is severely hampered by CUR's low solubility and poor bioavailability. Although nanoencapsulation represents a promising strategy to address these limitations, the preventive effect of nanocurcumin (nano-CUR) against colitis remains largely unexplored. The present study aimed to elucidate the preventive effects of nano-CUR on intestinal barrier function, gut microbiota composition, and metabolic profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis. The results demonstrated that pre-supplementation of nano-CUR significantly ameliorated disease severity, attenuated intestinal barrier disruption, and suppressed colonic inflammation in mice with DSS-induced colitis. Mechanistically, integrated 16S rRNA sequencing and untargeted metabolomics demonstrated that nano-CUR-restored microbial homeostasis and enhanced the production of short-chain fatty acids, linking microbial shifts to anti-inflammatory outcomes. Fecal microbiota transplantation (FMT) further validated the causal role of the nano-CUR-remodeled microbiota in conferring protection. Collectively, these findings decipher the mechanism by which nano-CUR interacts with the gut microbiota, confirming that dietary nano-CUR consumption protects against ulcerative colitis by modulating the gut microbiome and its metabolic output.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-26"},"PeriodicalIF":5.5,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172276","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}

{"title":"Fucoidan Modulates USP22/HIF-1α Against Ferroptosis in Diabetic Nephropathy.","authors":"Xiaofeng Xu, Tong Wang, Haomiao Li, Xinyue Liu, Jie Bai, Wei-Kun Qu","doi":"10.1142/S0192415X26500825","DOIUrl":"https://doi.org/10.1142/S0192415X26500825","url":null,"abstract":"<p><p>Ubiquitin-specific protease 22 (USP22), which was found to serve as a specific deubiquitinase of hypoxia-inducible factor-1α (HIF-1α), plays an important role in diabetic nephropathy (DN) pathological mechanisms, but currently available therapies remain insufficient to fully arrest its progression. Fucoidan (FO), a marine-derived fucose-rich sulfated polysaccharide, has been reported to treat acute renal damage and chronic renal failure by ameliorating ferroptosis. But whether FO could modulate USP22/HIF-1α in the pathogenesis of DN is unknown. Here, db/db mice were treated with the USP22 inhibitor S02 or FO for 13 weeks, and renal injury was subsequently characterized through biochemical, histological, and molecular analyses. S02 or FO administration markedly alleviated renal structural injury, improved fasting blood glucose and renal functional indices, and reduced oxidative stress, iron deposition, and the expression of profibrotic and proinflammatory mediators in diabetic kidneys. Mechanistically, protective effects were associated with suppression of USP22 by deubiquitinating HIF-1α, and amelioration of ferroptosis-related renal damage. Notably, inhibition of USP22 by FO recapitulated the renoprotective phenotype. Together, these findings suggest that FO mitigates DN by constraining USP22/HIF-1α-driven ferroptotic and oxidative injury, thereby supporting its potential as a natural therapeutic candidate for DN.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-22"},"PeriodicalIF":5.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129645","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}

{"title":"Anemoside B4 from <i>Pulsatilla chinensis</i> Ameliorates Ulcerative Colitis by Inhibiting Inflammatory Responses via the Modulation of the Gut Microbiota-Immune Interplay.","authors":"Li-Rong Deng, Yi-Ming Zhong, Shu-Fen Zhu, Zi-Yi Wu, Fang-Jun Chen, Chang-Yin Huang, Qian-Yan Wu, Brian Tomlinson, Hwei-Ee Tan, Yan-Hong Li","doi":"10.1142/S0192415X26500849","DOIUrl":"https://doi.org/10.1142/S0192415X26500849","url":null,"abstract":"<p><p>We previously demonstrated that anemoside B4 (AB4) exerts a beneficial effect in a dextran sulfate sodium (DSS)-induced murine model of ulcerative colitis (UC). In this study, we further explored the mechanism of AB4 against UC from the perspective of gut microbiota-immune interplay. The gut microbiota was depleted in two DSS-induced colitis models to investigate the modulatory effects of the gut microbiome on immune responses and the activity of AB4. In parallel, adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into Rag1-deficient (<i>Rag1</i>^-/-) mice was used to elucidate the alterations in the gut microbiota associated with immune-mediated colitis as well as the modulation by AB4. qPCR, ELISA and western blotting were used to determine the inflammatory responses of mice with colitis, while immunohistochemistry and flow cytometry were employed to determine the CD4[Formula: see text] T cell function and the underlying mechanism. Metagenomic sequencing analysis was used to detect changes in the intestinal microbiota. The depletion of the gut microbiota attenuated disease severity and immune responses in mice with DSS-induced acute and chronic colitis. Notably, the inhibitory effects of orally administered AB4 on colitis progression and immune responses were abrogated. In addition, colitis induced by adoptive transfer of CD4[Formula: see text]CD62L[Formula: see text] T cells into <i>Rag1</i>^-/- mice was accompanied by CD4[Formula: see text] T cell engraftment and alterations in gut microbiota. Remarkably, all these pathological changes were significantly attenuated by AB4. Crucially, we found that AB4 suppresses the proliferation, migration, and differentiation of CD4[Formula: see text] T cells, which provides a mechanistic basis for its immunosuppressive effects. Collectively, these findings indicate that the gut microbiota and the immune system, particularly CD4[Formula: see text] T cells, interact with each other in the initiation of colitis. We show that, by targeting this gut microbiota-immune interplay, AB4 is a promising therapeutic strategy for UC.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-29"},"PeriodicalIF":5.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169531","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}

{"title":"Targeting Ferroptosis with Natural Products: A Promising Strategy for Neurodegenerative Diseases.","authors":"Weiyi Guan, Xinyue Zhang, Zhenru Liu, Yuting Ouyang, Xiaohu Li, Hongfeng Xu, Shujia Huang, Yanan Hu","doi":"10.1142/S0192415X26500758","DOIUrl":"https://doi.org/10.1142/S0192415X26500758","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) are chronic disorders characterized by progressive neuronal damage, neuronal loss, and gradual decline in neural function. They commonly present with cognitive impairment or motor dysfunction, seriously reducing patients' quality of life. Ferroptosis is a form of cell death marked by excessive iron accumulation, lipid peroxidation (LPO), and disrupted anti-oxidant defenses. It can aggravate neuronal injury and contributes to the onset and progression of NDDs. This paper reviews recent advances in the neuroprotective effects of natural compounds through ferroptosis regulation. Based on recent cellular and animal studies on natural compounds, ferroptosis, and neuronal damage, we summarized the pharmacological features and potential mechanisms of phenethyl glycosides, polyphenols, flavonoids, and other natural compounds. Available evidence shows that natural compounds, including salidroside (SAL), forsythoside A (FA), syringin, tenuifolin (Ten), tannic acid (TA), eriodictyol, quercetin (QCT), epigallocatechin-3-gallate (EGCG), emodin, and Herpotrichone A (He-A), can alleviate neuronal injury to varying extents by reducing abnormal iron accumulation. Some compounds also suppress ferroptosis by modulating intracellular anti-oxidant defense pathways and restoring glutathione (GSH)-related protective enzyme functions. Overall, natural products offer the advantage of multi-target and multi-step intervention in neural injury and show great potential for delaying neurodegeneration progression. However, current evidence mainly comes from cell and animal studies, while clinical research remains limited. Moreover, some compounds still face problems such as low bioavailability and incompletely understood mechanisms. Future studies should strengthen clinical translation and validation, clarify safety, effective dosages, and targets, and improve clinical applicability through strategies such as structural optimization.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-30"},"PeriodicalIF":5.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167611","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}

{"title":"Isoliquiritigenin Triggers HMOX1-Driven Ferroptosis to Suppress Non-Small Cell Lung Cancer.","authors":"Yi-Jie Wang, Feng Liang, Ya-Ting Deng, Zhuo Li, Yuan Wang, Tao Li, Xin Chen, Ling Qiao, Wei Wang","doi":"10.1142/S0192415X26500850","DOIUrl":"10.1142/S0192415X26500850","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related death, and new treatment strategies are needed. Ferroptosis is an iron-dependent cell death driven by lipid peroxidation, and targeting ferroptosis has become a new strategy for anti-NSCLC. Isoliquiritigenin (ISL) is a bioactive natural flavonoid with antitumor potential, but its mechanism of ferroptosis in NSCLC remains to be elucidated. We investigated the effects of ISL on cell viability, proliferation, colony formation, cell cycle and cell death in NSCLC cells. Quantitative proteomic and bioinformatics analyses identified enriched pathways and key molecular targets. The effect of ISL on ferroptosis markers was also assessed. The regulatory effects of ISL on the main target proteins and key signaling pathways were verified by molecular docking, CETSA, co-immunoprecipitation, siRNA knockdown, overexpression and Western blotting. The antitumor effect of ISL and its synergistic effect with cisplatin <i>in vivo</i> were evaluated. The safety of ISL was also evaluated. ISL significantly inhibited NSCLC cell proliferation, arrested cell cycle in S phase, and induced cell death. Further investigation revealed that ferroptosis was the major cell death pathway, and this process was achieved by up-regulation of the protein HMOX1. In addition, the iron homeostasis disrupted by ISL was somewhat restored after administration of the iron chelator DFO, attenuating its mediated ferroptosis. Mechanistically, we verified that binding of ISL to Nrf2 activates Nrf2, upregulates HMOX1, inhibits CP, and disrupts iron homeostasis, thereby triggering ferroptosis. <i>In vivo</i>, ISL inhibited tumor growth in A549 xenograft mice without significant organ toxicity. Meanwhile, ISL can synergistically increase the antitumor efficacy of cisplatin, accompanied by more obvious ferroptosis changes in NSCLC. ISL induces ferroptosis by activating the Nrf2/HMOX1/CP pathway, leading to iron overload, thus exerting an effective antitumor effect on NSCLC. These findings indicate that ISL is a promising antitumor agent targeting ferroptosis, and also provide part of the preliminary mechanistic basis for its clinical development.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-31"},"PeriodicalIF":5.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129678","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}

{"title":"Decoding Ginsenosides: The Structural and Therapeutic Core of Ginseng.","authors":"Ka Iong Chan, Xintong Han, Siyuan Chen, Dianxin Cui, Sio I Chan, Wenying Zheng, Simin Chen, Lihua Shen, Wanyu Li, Yu Fan, Guodong Li, Milen I Georgiev, Wen Tan, Zhangfeng Zhong","doi":"10.1142/S0192415X26500746","DOIUrl":"https://doi.org/10.1142/S0192415X26500746","url":null,"abstract":"<p><p>Ginseng (<i>Panax ginseng</i> C.A. Meyer), a highly valued traditional herb in traditional medicine, exerts its major health benefits through ginsenosides - its core bioactive triterpenoid saponins. With a characteristic steroidal structure, ginsenosides interact with cell membranes, receptors, and signaling cascades to produce diverse pharmacological effects. This review summarizes the pharmacological properties, molecular mechanisms, structure-activity relationships, and advanced delivery strategies of key ginsenosides, including Rb1, Rg1, Rg3, Rh2, compound K (CK), and Rd. These compounds exhibit potent anti-oxidant, anti-inflammatory, cardioprotective, neuroprotective, antidiabetic, anti-obesity, anticancer, and anti-aging activities, acting through well-characterized pathways such as PI3K/Akt, Nrf2/ARE, AMPK, MAPK, and NF-[Formula: see text]B. Notably, their bioactivity is strongly governed by the number and position of sugar moieties: ginsenosides with fewer glycosyl groups (e.g., Rg3, Rh2, and CK) generally display higher potency <i>in vitro</i> and <i>in vivo</i>, whereas multi-glycosylated forms like Rb1 and Rc show milder effects. Despite their promising efficacy, poor oral bioavailability, rapid metabolism, and nonspecific tissue distribution remain major hurdles for clinical translation. To overcome these limitations, recent nanotechnology-based delivery systems have been developed, including liposomes, polymeric nanoparticles, inorganic nanocarriers, self-assembled micelles, and exosome-based platforms, to enhance solubility, prolong circulation, enable targeted delivery, and improve therapeutic outcomes. By integrating current knowledge on ginsenoside pharmacology and formulation engineering, this work supports their translational research and clinical application as multi-target agents for treating inflammatory, metabolic, cardiovascular, neurodegenerative, and malignant disorders.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-48"},"PeriodicalIF":5.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149129660","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}

{"title":"Tanshinone IIA Ameliorates Sleep Deprivation-Induced Cognitive Impairment: Involvement of Gut Microbiota and the TLR4/NF-κB Signaling Pathway.","authors":"Chao Yin, Meiya Zhang, Shunbo Zhang, Tian Ren, Li Ding, Ping Wang, Qiuyun You","doi":"10.1142/S0192415X26500801","DOIUrl":"https://doi.org/10.1142/S0192415X26500801","url":null,"abstract":"<p><p>Previous studies have indicated that <i>Salvia miltiorrhiza</i> Bunge (Danshen, DS) improves sleep deprivation (SD)-induced cognitive deficits, suggesting that tanshinone IIA (Tan IIA) may be a key pharmacodynamic substance. However, the mechanism behind this remains unclear. This study aims to evaluate the protective effects of Tan IIA on learning and memory abilities in SD model rats and to explore its potential mechanisms related to gut microbiota. The Morris water maze (MWM) test was used to assess cognitive function, while Hematoxylin and Eosin (H&E) staining, Nissl staining, immunofluorescence, and Alcian blue-periodic acid Schiff (AB-PAS) staining were employed to examine histopathology and barrier proteins. Enzyme-linked immunosorbent assay (ELISA), Western blot, and 16S rRNA microbiome sequencing were used to explore the mechanism of Tan IIA in the SD rat model. Tan IIA significantly protected cognitive function in SD model rats, rescued the BBB function (ZO-1 and Occludin), reduced hippocampal inflammation and neuronal death, and alleviated hippocampal microglial inflammatory activation and Aβ42 deposition. Additionally, Tan IIA treatment markedly reduced systemic inflammation (serum TNF-α, IL-1β, and IL-6), intestinal inflammation, and intestinal barrier disruption (MUC-2, ZO-1, and Occludin). 16S rRNA microbiome sequencing indicated that the therapeutic effects of Tan IIA were associated with gut microbiota regulation, reducing lipopolysaccharide (LPS) production and leakage, thereby modulating abnormal expression of the TLR4/NF-κB signaling pathways and the abnormal expression of downstream inflammatory cytokines (TNF-α, IL-1β, IL-6) and enzymes (iNOS and COX2). In conclusion, Tan IIA protects cognitive function in SD rats through anti-inflammatory mechanisms, in part by reshaping the gut microbiota and modulating the TLR4/NF-κB signaling pathway, providing a theoretical basis for the clinical application of Tan IIA in the prevention and treatment of SD-related cognitive impairment.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-30"},"PeriodicalIF":5.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121272","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}

{"title":"The Therapeutic Potential of Berberine in Treating Diabetes and Its Complications: Molecular Mechanisms and Future Perspectives.","authors":"Yile Liao, Yu Gui, Tongyi Li, Qian Zhou, Xiangyan Chen, Qiu Chen","doi":"10.1142/S0192415X26500795","DOIUrl":"https://doi.org/10.1142/S0192415X26500795","url":null,"abstract":"<p><p>Diabetes mellitus (DM), a chronic metabolic disorder characterized by persistent hyperglycemia, poses a significant global health burden. Berberine (BBR), a natural isoquinoline alkaloid derived from medicinal plants such as Coptidis Rhizoma, has shown therapeutic promise for DM and its complications. Preclinical and clinical studies have revealed that BBR exerts multi-target effects, including remodeling the gut microbiome, promoting insulin secretion, ameliorating insulin resistance, and inhibiting hepatic gluconeogenesis. Its protective mechanisms against diabetic complications, such as nephropathy, cardiomyopathy, and retinopathy, involve modulating key pathways like AMPK/SIRT1, PI3K/Akt, and TGF-[Formula: see text]/Smad, which attenuate oxidative stress, inflammation, and fibrosis. Despite its low oral bioavailability, a wide array of formulation strategies, including polymer nanocarriers, lipid-based nanocarriers, mixed micelles, and absorption enhancer, have improved systemic exposure in preclinical models, although clinical translation remains limited. This review synthesizes evidence from the past decade spanning preclinical mechanisms, randomized controlled trials, pharmacokinetics and nanoformulation strategies, concluding that BBR is a promising candidate for complementary therapy, although the supporting clinical evidence remains limited. Further studies are warranted to clarify its mechanisms, and optimize its delivery. In particular, larger and longer-term trials, along with systematic pharmacokinetic-pharmacodynamic studies of BBR and its metabolites, are needed to confirm its efficacy and long-term safety.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-34"},"PeriodicalIF":5.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121303","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}

{"title":"Recent Advances in Natural Product Interventions on Cardiovascular Disease: The Role of Programmed Cell Death.","authors":"Liping Yang, Huiping Wei, Zhaodi Yang, Yushuan Gong, Xinyue Liu, Baomei Xu, Yunyan Lu","doi":"10.1142/S0192415X2650076X","DOIUrl":"https://doi.org/10.1142/S0192415X2650076X","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain one of the leading causes of morbidity and mortality worldwide, with cardiomyocyte death playing an important role in myocardial injury, pathological cardiac remodeling, and the progression of heart failure. Programmed cell death (PCD), including apoptosis, pyroptosis, ferroptosis, cuproptosis, and disulfidptosis, plays an essential role in maintaining cellular homeostasis; however, its aberrant activation or dysregulation can contribute to cardiovascular injury and disease progression. Increasing evidence indicates that these PCD pathways are not independent but form a complex regulatory network through shared mechanisms, including mitochondrial dysfunction, oxidative stress, inflammatory activation, and metabolic imbalance, thereby contributing collectively to the development and progression of CVDs. Therefore, targeting PCD-related pathways has emerged as a promising therapeutic strategy. Natural products and their bioactive constituents can exert cardioprotective effects by regulating PCD-related signaling networks through multiple targets and pathways, thereby alleviating cardiomyocyte death, oxidative stress, inflammation, and cardiac dysfunction. Representative bioactive compounds, including salvianolic acid B, resveratrol, quercetin, and astragaloside IV, have demonstrated potential to modulate PCD-related signaling pathways in experimental models of CVDs. This review summarizes the molecular mechanisms and pathological roles of apoptosis, pyroptosis, ferroptosis, cuproptosis, and disulfidptosis in CVDs, elucidates the regulatory crosstalk among different PCD pathways, and systematically reviews the research progress on the cardioprotective effects of natural products and their bioactive constituents through targeting PCD. In conclusion, natural products targeting dysregulated PCD pathways may represent a promising multi-target therapeutic strategy for cardiovascular protection; however, current evidence is derived predominantly from preclinical studies, and further in-depth mechanistic investigations and high-quality clinical studies are warranted to validate their therapeutic potential and clinical translational value.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-33"},"PeriodicalIF":5.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121167","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}

{"title":"Curcumin from Turmeric Alleviates Lipid Metabolism: Network Pharmacology and Cellular Validation.","authors":"Li-Sha Niu, Yi-Zhe Zhang, Feng-Yang Wu, Wen-Hui Qi, Chi Ren, Yi-Shuo Xu, Yu-Tao Yang, Zhi-Sheng Zhang","doi":"10.1142/S0192415X26500813","DOIUrl":"https://doi.org/10.1142/S0192415X26500813","url":null,"abstract":"<p><p>Curcumin, the primary active compound in turmeric, a widely used medicinal and edible herb in traditional Chinese medicine, exhibits beneficial effects against lipid metabolic dysfunction (LMD). Nevertheless, its comprehensive regulatory network and precise mechanisms remain unclear. In this study, network pharmacology, molecular docking, and <i>in vitro</i> cellular assays were integrated to elucidate the targets and mechanisms by which curcumin acts against LMD. Seven hub targets were identified: AKT1, ALB, INS, IL6, TP53, TNF, and PPARG. Kyoto Encyclopedia of Genes and Genomes analysis revealed significant enrichment of these hub targets in multiple pathways, with a notable emphasis on non-alcoholic fatty liver disease. Molecular docking confirmed that curcumin exhibited a favorable binding affinity to the hub targets. Cellular experiments using oleic acid-induced human hepatocellular carcinoma HepG2 cells demonstrated that curcumin markedly reduced triglyceride and total cholesterol levels, alleviated lipid droplet accumulation, and significantly modulated the mRNA expression of genes involved in lipid metabolism, anti-oxidant defense, and inflammation. These findings were consistent with predictions from network pharmacology. In summary, curcumin may alleviate OA-induced LMD by synergistically modulating lipid metabolism, inhibiting oxidative damage, and diminishing inflammation. This study provides a comprehensive theoretical basis for the application of curcumin in LMD intervention.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"1-20"},"PeriodicalIF":5.5,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121130","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}