Archives of Pharmacal Research最新文献

{"title":"Saponins as potential novel NLRP3 inflammasome inhibitors for inflammatory disorders.","authors":"Jiamei Tang, Yaxiao Liu, Ying Wu, Shixing Li, Dongdong Zhang, Haifang Wang, Wei Wang, Xiaomei Song, Yuze Li","doi":"10.1007/s12272-024-01517-x","DOIUrl":"https://doi.org/10.1007/s12272-024-01517-x","url":null,"abstract":"<p><p>Nucleotide-binding domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) is a downstream protein from the pattern recognition receptor family that forms the NLRP3 inflammasome. The NLRP3 inflammasome releases caspase-1, IL-1β, and IL-18, contributing to inflammatory responses associated with diabetes mellitus, arthritis, and ischemia-reperfusion injury. Recent studies suggest that specific saponin monomers and extracts from traditional Chinese medicines can inhibit inflammatory responses and related pathways, including the production of inflammatory factors. MCC950 is one of the most influential and specific NLRP3 inhibitors. Comparative molecular docking studies have identified 22 of the 37 saponin components as more robust binders to NLRP3 than MCC950. Dioscin, polyphyllin H, and saikosaponin-a have the highest binding affinities and potential NLRP3 inhibitors, offering a theoretical basis for developing novel anti-inflammatory therapies.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulating versatile pathways using a cleavable PEG shell and EGFR-targeted nanoparticles to deliver CRISPR-Cas9 and docetaxel for triple-negative breast cancer inhibition.","authors":"Yu-Li Lo, Ci-Jheng Hong, Chen-Shen Wang, Ching-Ping Yang","doi":"10.1007/s12272-024-01514-0","DOIUrl":"https://doi.org/10.1007/s12272-024-01514-0","url":null,"abstract":"<p><p>Human antigen R (HuR), an RNA-binding protein, is implicated in regulating mRNA stability and translation in cancer, especially in triple-negative breast cancer (TNBC), a highly aggressive form. CRISPR/Cas9-mediated HuR knockout (HuR CRISPR) presents a promising genetic therapeutic approach, but it encounters transfection limitations. Docetaxel (DTX), an effective cytotoxic agent against metastatic breast cancer (BC), faces challenges related to vehicle-associated adverse events in DTX formulations. Therefore, we designed multifunctional nanoparticles with pH-sensitive PEG derivatives and targeting peptides to enable efficient HuR CRISPR and DTX delivery to human TNBC MDA-MB-231 cells and tumor-bearing mice. Our findings indicated that these nanoparticles displayed pH-responsive cytotoxicity, precise EGFR targeting, efficient tumor penetration, successful endosomal escape, and accurate nuclear and cytoplasmic localization. They also demonstrated the ability to spare normal cells and prevent hemolysis. Our study concurrently modulated multiple pathways, including EGFR, Wnt/β-catenin, MDR, and EMT, through the regulation of EGFR/PI3K/AKT, HuR/galectin-3/GSK-3β/β-catenin, and P-gp/MRPs/BCRP, as well as YAP1/TGF-β/ZEB1/Slug/MMPs. The combined treatment arrested the cell cycle at the G2 phase and inhibited EMT, effectively impeding tumor progression. Tissue distribution, biochemical assays, and histological staining revealed the enhanced safety profile of pH-responsive PEG- and peptide-modified nanoformulations in TNBC mice. The DTX-embedded and peptide-modified nanoparticles mitigated the side effects of DTX, enhanced cytotoxicity in TNBC MDA-MB-231 cells, and exhibited remarkable antitumor efficacy and safety in TNBC-bearing mice with HuR CRISPR deletion. Collectively, the combination therapy of DTX and CRISPR/Cas9 offers an effective platform for delivering antineoplastic agents and gene-editing systems to combat tumor resistance and progression in TNBC.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rg3 activates the immune function of CD8+ T cells via circFOXP1-miR-4477a-PD-L1 axis to induce ferroptosis in gallbladder cancer.","authors":"Zhipeng Ye, Jianfeng Ding, Jie Huang, Zhao Hu, Fa Jin, Keren Wu","doi":"10.1007/s12272-024-01516-y","DOIUrl":"https://doi.org/10.1007/s12272-024-01516-y","url":null,"abstract":"<p><p>Gallbladder cancer (GBC) is the most common and leading cause of cancer-associated mortality among biliary tract carcinomas worldwide and there is no specific drug for treatment. Activation of CD8+ T cell immune activity is one of the strategies to improve GBC treatment. This study is aimed to investigate the role of Ginsenoside Rg3 on CD8+ T cell activation and pathogenesis of GBC. In GBC cells, Rg3 administration led to the significant reduction of circFOXP1 and PD-L1 as measured by Quantitative real-time polymerase chain reaction (RT-qPCR) and Western blotting. Mechanistically, circFOXP1 acted as the sponge of miR-4477a to regulate PD-L1 expression as demonstrated by RNA pull-down assay and dual luciferase reporter assay. Rg3 treatment enhanced the activity of CD8+ T cells by inhibiting the circFOXP1/miR-4477a/PD-L1 signaling axis. Besides, Rg3 administration induced lipid oxidation and ROS reduction as detected by Flow cytometry, resulting in ferroptosis via the inactivation of circFOXP1/miR-4477a/PD-L1 axis. Ferroptosis inhibitor Fer-1 administration could reverse the beneficial effects caused by Rg3 treatment while ferroptosis inducer Erastin treatment enhanced the effects. Moreover, Rg3 gavage alleviated tumor growth and elevated ferroptosis and apoptosis in tumor tissues, which were prevented by PD-L1 overexpression. Furthermore, Rg3 was demonstrated to activate the function of CD8+ T cells via regulating the circFOXP1-miR-4477a-PD-L1 signaling axis in vivo. Rg3 inactivated the circFOXP1-miR-4477a-PD-L1 signaling axis to activate the immune function of CD8+ T cells, thereby inducing ferroptosis and apoptosis in GBC cells. This research recognizes the mechanism of Rg3-mediated anti-cancer effect and offers evidence for the potentiality of Rg3 in clinical application for GBC therapy.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential effects of a human milk oligosaccharide 6'-sialyllactose on angiotensin II-induced aortic aneurysm via p90RSK/TGF-β/SMAD2 signaling pathway.","authors":"Thuy Le Lam Nguyen, Dung Van Nguyen, Yujin Jin, Lila Kim, Kyung-Sun Heo","doi":"10.1007/s12272-024-01515-z","DOIUrl":"https://doi.org/10.1007/s12272-024-01515-z","url":null,"abstract":"<p><p>The aberrant phenotypic transformation of vascular smooth muscle cells (VSMCs) is a key factor in the formation of aortic aneurysm (AA). This study aimed to explore the effects of 6'-sialyllactose (6'-SL), a human milk oligosaccharide, on angiotensin II (Ang II)-induced VSMC dysfunction and AA formation both in vitro and in vivo. An AA model was established in male C57BL/6 mice challenged with Ang II via osmotic pumps and a lysyl oxidase inhibitor, β-aminopropionitrile (BAPN), in drinking water. The mice were administered with 6'-SL, FMK (a p90RSK inhibitor), or losartan (as a positive control). In vitro, VSMCs were pretreated with 6'-SL before Ang II stimulation. We found that p90RSK inhibition abolished Ang II/BAPN-induced thoracic AA and abdominal AA formation. Treatment with 100 mg/kg 6'-SL significantly attenuated Ang II/BAPN-induced aortic dilatation. 6'-SL attenuated Ang II-induced collagen deposition, calcification, and immune cell accumulation. Consistently, 6'-SL downregulated p-p90RSK, p90RSK, and p-SMAD2, and mitigated VSMC contractility loss, as indicated by α-SMA expression in vivo. Interestingly, Ang II-induced transforming growth factor-beta (TGF-β) signaling pathway was suppressed by p90RSK inhibition in VSMCs. 6'-SL treatment significantly reduced TGF-β/SMAD2 targets, including dedifferentiation markers such as osteopontin and vimentin, and elastin degradation factors MMP2 and MMP9. Overexpression of p90RSK in VSMCs enhanced TGF-β and abrogated the effects of 6'-SL. Furthermore, 6'-SL co-treatment abolished high phosphate-induced calcification in vitro via p90RSK/TGF-β signaling pathway. Altogether, our findings suggest that 6'-SL could be a potential therapeutic candidate for protecting against Ang II-induced AA formation by inhibiting the p90RSK/TGF-β/SMAD2 signaling pathway.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.","authors":"Eunjin Lee, Yujeong Lee, Seonguk Yang, Eun Ji Gong, Jaehoon Kim, Nam-Chul Ha, Dong-Gyu Jo, Mark P Mattson, Jaewon Lee","doi":"10.1007/s12272-024-01513-1","DOIUrl":"https://doi.org/10.1007/s12272-024-01513-1","url":null,"abstract":"<p><p>Tau hyperphosphorylation and accumulation in neurofibrillary tangles are closely associated with cognitive deficits in Alzheimer's disease (AD). Glycogen synthase kinase 3β (GSK3β) overexpression has been implicated in tau hyperphosphorylation, and many GSK3β inhibitors have been developed as potential therapeutic candidates for AD. However, the potent GSK3β inhibitors produced are prone to side effects because they can interfere with the basic functions of GSK3β. We previously found that when the phosphorylated PPPSPxS motifs in Wnt coreceptor LRP6 can directly inhibit GSK3β, and thus, we produced a novel GSK3β inhibitory peptide (GIP), specifically activated by Akt, by combining the PPPSPxS motif of LRP6 and the Akt targeted sequence (RxRxxS) of GSK3β. GIP effectively blocked GSK3β-induced tau phosphorylation in hippocampal homogenates and, when fused with a cell-permeable sequence, attenuated Aβ-induced tau phosphorylation in human neuroblastoma cells and inhibited cell death. An in vivo study using a 3 × Tg-AD mouse model revealed that intravenous GIP significantly reduced tau phosphorylation in the hippocampus without affecting Aβ plaque levels or neuroinflammation and ameliorated memory defects. The study provides a novel neuroprotective drug development strategy targeting tau hyperphosphorylation in AD.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paeonia genus: a systematic review of active ingredients, pharmacological effects and mechanisms, and clinical applications for the treatment of cancer","authors":"Xinrui Zhou,&nbsp;Aikebaier Alimu,&nbsp;Jiarui Zhao,&nbsp;Xinyi Xu,&nbsp;Xiaowen Li,&nbsp;He Lin,&nbsp;Zhe Lin","doi":"10.1007/s12272-024-01512-2","DOIUrl":"10.1007/s12272-024-01512-2","url":null,"abstract":"<div><p>The main active constituents of plants of the Paeonia genus are known to have antitumor activity. Hundreds of compounds with a wide range of pharmacological activities, including monoterpene glycosides, flavonoids, tannins, stilbenes, triterpenoids, steroids, and phenolic compounds have been isolated. Among them, monoterpenes and their glycosides, flavonoids, phenolic acids, and other constituents have been shown to have good therapeutic effects on various cancers, with the main mechanisms including the induction of apoptosis; the inhibition of tumor cell proliferation, migration, and invasion; and the modulation of immunity. In this study, many citations related to the traditional uses, phytochemical constituents, antitumor effects, and clinical applications of the Paeonia genus were retrieved from popular and widely used databases such as Web of Science, Science Direct, Google Scholar, and PubMed using different search strings. A systematic review of the antitumor constituents of the Paeonia genus and their therapeutic effects on various cancers was conducted and the mechanisms of action and pathways of these phytochemicals were summarised to provide a further basis for antitumor research.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 8-9","pages":"677 - 695"},"PeriodicalIF":6.9,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Osteogenic effect of an adiponectin-derived short peptide that rebalances bone remodeling: a potential disease-modifying approach for postmenopausal osteoporosis therapy","authors":"Swati Rajput,&nbsp;Chirag Kulkarni,&nbsp;Shivani Sharma,&nbsp;Manendra Singh Tomar,&nbsp;Shamima Khatoon,&nbsp;Arvind Gupta,&nbsp;Sabyasachi Sanyal,&nbsp;Ashutosh Shrivastava,&nbsp;Jimut Kanti Ghosh,&nbsp;Naibedya Chattopadhyay","doi":"10.1007/s12272-024-01509-x","DOIUrl":"10.1007/s12272-024-01509-x","url":null,"abstract":"<div><p>Adiponectin, an adipokine, regulates metabolic processes, including glucose flux, lipid breakdown, and insulin response, by activating adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2). We have previously shown that globular adiponectin (gAd), an endogenous form of adiponectin, has osteoanabolic and anti-catabolic effects in rodent models of postmenopausal osteopenia. Moreover, we reported the identification of a 13-mer peptide (ADP-1) from the collagen domain of adiponectin, which exhibited significant adiponectin-mimetic properties. Since the clinical development of gAd is constrained by its large size, here, we investigated the osteogenic property of ADP-1. ADP-1 induced osteoblast differentiation more potently than gAd. ADP-1 elicited osteoblast differentiation through two downstream pathways that involved the participation of adiponectin receptors. Firstly, it enhanced mitochondrial biogenesis and OxPhos, leading to osteoblast differentiation. Secondly, it activated the Akt-glycogen synthase kinase 3β-Wnt pathway, thereby increasing osteoblast differentiation. Additionally, ADP-1 suppressed the production of receptor–activator of nuclear kappa B ligand from osteoblasts, enabling it to act as a dual-action molecule (suppressing osteoclast function besides promoting osteoblast function). In osteopenic ovariectomized rats, ADP-1 increased bone mass and strength and improved trabecular integrity by stimulating bone formation and inhibiting bone resorption. Furthermore, by increasing ATP-producing intermediates within the tricarboxylic acid cycle in bones, ADP-1 likely fueled osteoblast function. Given its dual-action mechanism and high potency, ADP-1 offers a unique opportunity to address the unmet clinical need to reset the aberrant bone remodeling in osteoporosis to normalcy, potentially offering a disease-modifying impact.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 8-9","pages":"736 - 755"},"PeriodicalIF":6.9,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E3 ubiquitin ligase RNF180 mediates the ALKBH5/SMARCA5 axis to promote colon inflammation and Th17/Treg imbalance in ulcerative colitis mice","authors":"Kailing Wang,&nbsp;Fan Liu,&nbsp;Budumu Muchu,&nbsp;Jiawen Deng,&nbsp;Jing Peng,&nbsp;Yan Xu,&nbsp;Fujun Li,&nbsp;Miao Ouyang","doi":"10.1007/s12272-024-01507-z","DOIUrl":"10.1007/s12272-024-01507-z","url":null,"abstract":"<div><p>SMARCA5, a protein in the SWI/SNF family, has been previously implicated in the development of ulcerative colitis (UC) through methylation. However, the specific molecular mechanisms by which SMARCA5 contributes to colonic inflammation and the imbalance between Th17 and Treg cells remain unclear. This study was designed to explore these molecular mechanisms. A UC mouse model was established using dextran sulfate sodium induction, followed by measurements of mouse weight, disease activity index (DAI) score, colon length, pathological changes in the colon, and FITC-dextran concentration. The levels of IL-17a, IFN-γ, IL-6, TNF-α, TGF-β, and IL-10 were measured, along with the protein expression of ZO-1 and Occludin. Flow cytometry was used to assess the presence of IL-17 + CD4 + (Th17 +) cells and FOXP3 + CD25 + CD4 + (Treg +) cells in the spleen and mesenteric lymph nodes of UC mice. We observed that SMARCA5 and RNF180 were increased, while ALKBH5 was downregulated in UC mouse colon tissue. SMARCA5 or RNF180 knockdown or ALKBH5 overexpression ameliorated the colon inflammation and Th17/Treg cell imbalance in UC mice, shown by increased body weight, colon length, FOXP3 + CD25 + CD4 + T cells, and the levels of ZO-1, Occludin, TGF-β, IL-10, and FOXP3. It decreased DAI scores, IL-17 + CD4 + T cells, and levels of IL-17a, IFN-γ, IL-6, TNF-α, and ROR-γt. ALKBH5 inhibited SMARCA5 expression via m6A modification, while RNF180 reduced ALKBH5 expression via ubiquitination. Our findings indicate that RNF180 aggravated the colon inflammation and Th17/Treg cell imbalance in UC mice by regulating the ALKBH5/SMARCA5 axis.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 7","pages":"645 - 658"},"PeriodicalIF":6.9,"publicationDate":"2024-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141765055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antitumor activity of Polygonatum sibiricum polysaccharides","authors":"Weiwei Lai,&nbsp;Qian Ning,&nbsp;Guihua Wang,&nbsp;Yuan Gao,&nbsp;Shuxian Liao,&nbsp;Shengsong Tang","doi":"10.1007/s12272-024-01511-3","DOIUrl":"10.1007/s12272-024-01511-3","url":null,"abstract":"<div><p>Cancer is a global public health problem. Natural polysaccharides have been shown to enhance the effectiveness of cancer treatments. <i>Polygonatum sibiricum</i> (PS) has been used for millennia to treat diverse diseases. PS comprises numerous active constituents, including saponins, peptides, volatile oils, polysaccharides, and lectins. Many studies have highlighted the crucial role of polysaccharides in PS. Modern studies have shown that <i>Polygonatum sibiricum</i> polysaccharide (PSP) exhibits diverse pharmacological activities, including immunomodulatory, antitumor, antioxidant, and anti-aging effects. However, further study of the antitumor mechanisms is difficult because the activities of PSP are closely associated with its complex structural features and the different molecular weights of its components. Therefore, this review focuses on the research background and the extraction and purification of PSP. Studies related to the mechanism of the antitumor effects of PSP constituents of different molecular weights are also summarized, and perspectives on PSP research are presented.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 8-9","pages":"696 - 708"},"PeriodicalIF":6.9,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141765054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pentacyclic triterpenes, potential novel therapeutic approaches for cardiovascular diseases","authors":"Dewei Peng,&nbsp;Aizan Wang,&nbsp;Wei Shi,&nbsp;Li Lin","doi":"10.1007/s12272-024-01510-4","DOIUrl":"10.1007/s12272-024-01510-4","url":null,"abstract":"<div><p>Cardiovascular diseases (CVDs) involve dysfunction of the heart and blood vessels and have become major health concerns worldwide. Multiple mechanisms may be involved in the occurrence and development of CVDs. Although therapies for CVDs are constantly being developed and applied, the incidence and mortality of CVDs remain high. The roles of natural compounds in CVD treatment are being explored, providing new approaches for the treatment of CVD. Pentacyclic triterpenes are natural compounds with a basic nucleus of 30 carbon atoms, and they have been widely studied for their potential applications in the treatment of CVDs, to which various pharmacological activities contribute, including anti-inflammatory, antioxidant, and antitumor effects. This review introduces the roles of triterpenoids in the prevention and treatment of CVDs, summarizes their potential underlying mechanisms, and provides a comprehensive overview of the therapeutic potential of triterpenoids in the management of CVDs.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 8-9","pages":"709 - 735"},"PeriodicalIF":6.9,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}