Archives of Pharmacal Research最新文献

{"title":"Exploring NNMT: from metabolic pathways to therapeutic targets","authors":"Jeongwoo Park,&nbsp;Eun Jin Shin,&nbsp;Tae Hyun Kim,&nbsp;Ji Hye Yang,&nbsp;Sung Hwan Ki,&nbsp;Keon Wook Kang,&nbsp;Kyu Min Kim","doi":"10.1007/s12272-024-01519-9","DOIUrl":"10.1007/s12272-024-01519-9","url":null,"abstract":"<div><p>Cellular metabolism-related epigenetic modulation plays a pivotal role in the maintenance of cellular homeostasis. Nicotinamide <i>N</i>-methyltransferase (NNMT) serves as a crucial link between cellular metabolism and epigenetics by catalyzing nicotinamide methylation using the universal methyl donor S-adenosyl-L-methionine. This direct connection bridges the methylation-mediated one-carbon metabolism with nicotinamide adenine dinucleotide levels. Numerous studies have revealed tissue-specific differences in NNMT expression and activity, indicating that its varied physiological and pathological roles depend on its distribution. In this review, we provide an overview of the NNMT involvement in various pathological conditions, including cancer, liver disease, obesity, diabetes, brain disease, pulmonary disease, cardiovascular disease, and kidney disease. By synthesizing this information, our article aims to enhance our understanding of the cellular mechanisms underlying NNMT biology related to diverse diseases and lay the molecular groundwork for developing therapeutic strategies for pharmacological interventions.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 12","pages":"893 - 913"},"PeriodicalIF":6.9,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738302","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":"Curcumin targets CXCL16-mediated podocyte injury and lipid accumulation in diabetic kidney disease treatment","authors":"Ying Chen,&nbsp;Jun Tao,&nbsp;Yijun He,&nbsp;Xudong Hou,&nbsp;Ji Fang,&nbsp;Jiebo Huang,&nbsp;Li Wang,&nbsp;Junlong Shen,&nbsp;Bingbing Zhu,&nbsp;Niansong Wang,&nbsp;Aili Cao","doi":"10.1007/s12272-024-01521-1","DOIUrl":"10.1007/s12272-024-01521-1","url":null,"abstract":"<div><p>Among the complications of diabetes, diabetic kidney disease (DKD) frequently emerges, typified by the detrimental effects on renal function, manifesting through inflammation, dysregulated lipid metabolism, and harm to podocytes. Existing research underscores the significance of the soluble form of C-X-C chemokine ligand 16 (CXCL16) within the context of renal impairments. However, whether CXCL16 is involved in the pathogenesis of DKD remains elusive. We report that CXCL16 levels in the serum and kidneys of individuals with DKD were elevated and correlated with various lipid parameters. The expression of CXCL16 in human podocytes subjected to high glucose or palmitic acid induction and exogenous CXCL16 administration in these cells were examined. Higher CXCL16 levels were linked to abnormal lipid metabolism. Exogenous CXCL16 administration induced lipid droplets, microfilament disorganization, apoptosis, oxidative stress, and inflammation, inhibited PPAR γ, up-regulated COX2 expression, and inhibited Nrf2 translocation in podocytes. Molecular analysis revealed that Curcumin (Cur), a polyphenolic compound derived from <i>Curcuma longa</i> and an Nrf2 agonist, targets the ATP-binding pocket of CXCL16, inhibiting its kinase activity. Meanwhile, Cur therapy alleviated podocyte injury, lipid accumulation, improved glomerulopathy, and reduced albuminuria. Furthermore, after silencing CXCL16 expression in podocytes using siRNA, the effects of exogenous CXCL16 were nullified, and Cur no longer exhibited any significant impact. Thus, CXCL16 participates in the pathogenesis of DKD. Inhibition of CXCL16 has shown promising results in experimental models, suggesting its beneficial effects in ameliorating DKD.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 12","pages":"924 - 939"},"PeriodicalIF":6.9,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738301","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":"Prediction of human pharmacokinetic parameters incorporating SMILES information","authors":"Jae-Hee Kwon,&nbsp;Ja-Young Han,&nbsp;Minjung Kim,&nbsp;Seong Kyung Kim,&nbsp;Dong-Kyu Lee,&nbsp;Myeong Gyu Kim","doi":"10.1007/s12272-024-01520-2","DOIUrl":"10.1007/s12272-024-01520-2","url":null,"abstract":"<div><p>This study aimed to develop a model incorporating natural language processing analysis for the simplified molecular-input line-entry system (SMILES) to predict clearance (CL) and volume of distribution at steady state (V_d,ss) in humans. The construction of CL and V_d,ss prediction models involved data from 435 to 439 compounds, respectively. In machine learning, features such as animal pharmacokinetic data, in vitro experimental data, molecular descriptors, and SMILES were utilized, with XGBoost employed as the algorithm. The ChemBERTa model was used to analyze substance SMILES, and the last hidden layer embedding of ChemBERTa was examined as a feature. The model was evaluated using geometric mean fold error (GMFE), r², root mean squared error (RMSE), and accuracy within 2- and 3-fold error. The model demonstrated optimal performance for CL prediction when incorporating animal pharmacokinetic data, in vitro experimental data, and SMILES as features, yielding a GMFE of 1.768, an r² of 0.528, an RMSE of 0.788, with accuracies within 2-fold and 3-fold error reaching 75.8% and 81.8%, respectively. The model's performance in V_d,ss prediction was optimized by leveraging animal pharmacokinetic data and in vitro experimental data as features, yielding a GMFE of 1.401, an r² of 0.902, an RMSE of 0.413, with accuracies within 2-fold and 3-fold error reaching 93.8% and 100%, respectively. This study has developed a highly predictive model for CL and V_d,ss. Specifically, incorporating SMILES information into the model has predictive power for CL.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 12","pages":"914 - 923"},"PeriodicalIF":6.9,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715310","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":"Donepezil improves skeletal muscle insulin resistance in obese mice via the AMPK/FGF21-mediated suppression of inflammation and ferroptosis","authors":"Hyeon Ji Gwon,&nbsp;Wonjun Cho,&nbsp;Sung Woo Choi,&nbsp;Do Su Lim,&nbsp;Esra Çinar Tanriverdi,&nbsp;A. M. Abd El-Aty,&nbsp;Ji Hoon Jeong,&nbsp;Tae Woo Jung","doi":"10.1007/s12272-024-01518-w","DOIUrl":"10.1007/s12272-024-01518-w","url":null,"abstract":"<div><p>Donepezil has traditionally been used in Alzheimer’s disease treatment and is known for its ability to alleviate neural inflammation and apoptosis. However, its impact on insulin signaling remains unexplored. This study sought to elucidate the novel role of donepezil in mitigating skeletal muscle insulin resistance under hyperlipidemic conditions. Western blot analysis was used to assess the expression of various proteins of interest, whereas a glucose uptake assay was performed in skeletal muscle cells via commercially available kits. An in vitro model of obesity was developed using palmitate. These in vitro findings were corroborated in vivo via insulin resistance models established through high-fat diet (HFD) feeding in mice. Intraperitoneal glucose tolerance tests and insulin tolerance tests were performed on the experimental mice. The results revealed that donepezil treatment improved insulin signaling and inflammation in palmitate-treated C2C12 myocytes and the skeletal muscle of HFD-fed mice. Notably, donepezil treatment augmented FGF21 expression and AMPK phosphorylation in the myocytes and skeletal muscle of HFD-fed mice. Knockdown of FGF21 or AMPK via siRNA reversed the effects of donepezil on insulin signaling and inflammation in cultured myocytes. We also found that donepezil ameliorated skeletal muscle insulin resistance via the FGF21-mediated suppression of ferroptosis under hyperlipidemic conditions. These findings suggest that donepezil enhances the FGF21/AMPK axis, thereby mitigating inflammation and insulin resistance in skeletal muscle. This study introduces a novel therapeutic approach for treating Alzheimer’s disease patients with insulin resistance.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 12","pages":"940 - 953"},"PeriodicalIF":6.9,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708869","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":"Saponins as potential novel NLRP3 inflammasome inhibitors for inflammatory disorders","authors":"Jiamei Tang,&nbsp;Yaxiao Liu,&nbsp;Ying Wu,&nbsp;Shixing Li,&nbsp;Dongdong Zhang,&nbsp;Haifang Wang,&nbsp;Wei Wang,&nbsp;Xiaomei Song,&nbsp;Yuze Li","doi":"10.1007/s12272-024-01517-x","DOIUrl":"10.1007/s12272-024-01517-x","url":null,"abstract":"<div><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-1<i>β</i>, 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><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 10-11","pages":"757 - 792"},"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,&nbsp;Ci-Jheng Hong,&nbsp;Chen-Shen Wang,&nbsp;Ching-Ping Yang","doi":"10.1007/s12272-024-01514-0","DOIUrl":"10.1007/s12272-024-01514-0","url":null,"abstract":"<div><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></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 10-11","pages":"829 - 853"},"PeriodicalIF":6.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12272-024-01514-0.pdf","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":"OA","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,&nbsp;Jianfeng Ding,&nbsp;Jie Huang,&nbsp;Zhao Hu,&nbsp;Fa Jin,&nbsp;Keren Wu","doi":"10.1007/s12272-024-01516-y","DOIUrl":"10.1007/s12272-024-01516-y","url":null,"abstract":"<div><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></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 10-11","pages":"793 - 811"},"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,&nbsp;Dung Van Nguyen,&nbsp;Yujin Jin,&nbsp;Lila Kim,&nbsp;Kyung-Sun Heo","doi":"10.1007/s12272-024-01515-z","DOIUrl":"10.1007/s12272-024-01515-z","url":null,"abstract":"<div><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></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 10-11","pages":"854 - 869"},"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,&nbsp;Yujeong Lee,&nbsp;Seonguk Yang,&nbsp;Eun Ji Gong,&nbsp;Jaehoon Kim,&nbsp;Nam-Chul Ha,&nbsp;Dong-Gyu Jo,&nbsp;Mark P. Mattson,&nbsp;Jaewon Lee","doi":"10.1007/s12272-024-01513-1","DOIUrl":"10.1007/s12272-024-01513-1","url":null,"abstract":"<div><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></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"47 10-11","pages":"812 - 828"},"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}