Pharmacology最新文献

{"title":"Erratum.","authors":"","doi":"10.1159/000541793","DOIUrl":"10.1159/000541793","url":null,"abstract":"","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"63"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of Lipid Profile, Glucose Metabolism, and Leptin Levels following Citalopram Administration and High-Carbohydrate and High-Cholesterol Diet in Mice.","authors":"Tomáš Hammer, Hana Kotolová, Jiří Procházka, Michal Karpíšek","doi":"10.1159/000541229","DOIUrl":"10.1159/000541229","url":null,"abstract":"<p><strong>Introduction: </strong>Depression therapy has been linked to negative effects on energy metabolism, which can be attributed to various factors, including an ongoing inflammatory process commonly seen in metabolic disorders. Unhealthy lifestyle choices of patients and the impact of antidepressants on body weight and lipid and glucose metabolism also contribute to these metabolic side effects. Although not as pronounced as other psychopharmaceuticals, the increasing use of antidepressants raises concerns about their potential impact on public health. The study aimed to evaluate the short- and long-term effects of the antidepressant citalopram and its long-term combination with a special diet on metabolic parameters in mice.</p><p><strong>Methods: </strong>Animals were randomly divided into 5 groups - control, control + special diet, citalopram (10 mg/kg for 35 days), citalopram + special diet (10 mg/kg for 35 days), and citalopram (10 mg/kg for 7 days). After a described time of administration, animals were anesthetized, blood and fat and liver tissues were collected. Biochemical parameters of lipid metabolism (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides) and glucose were analyzed using spectrophotometry and relevant adipokines and cytokines were evaluated by ELISA.</p><p><strong>Results: </strong>After a week of application of citalopram, we observed dyslipidemia that persisted even at the end of the 5-week experiment. Furthermore, after 5 weeks of citalopram administration, we observed a significant decrease in body weight gain and decreased leptin levels. Changes in lipid metabolism, higher levels of adipokines leptin and PAI-1 were observed due to the special diet after 5 weeks.</p><p><strong>Conclusions: </strong>Our research suggests that the effects of citalopram and a diet on the metabolism of mice can be significant, both in the short term (1 week) and in the long term (5 weeks).</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"87-97"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11975319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Use of PCSK9 Inhibitors in the Prognosis of Patients with Acute Coronary Syndrome by Protecting Vascular Endothelial Function.","authors":"Linghao Xu, Yuanqi Wang, Yiqiong Wang, Liang Wang, Peizhao Du, Jing Cheng, Chunsheng Zhang, Tiantian Jiao, Lijian Xing, Md Sakibur Rahman Tapu, Haonan Jia, Jiming Li","doi":"10.1159/000540083","DOIUrl":"10.1159/000540083","url":null,"abstract":"<p><strong>Introduction: </strong>Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) has a protective effect on acute coronary syndrome (ACS). However, most studies have shown that this protective effect is based on a decrease in low-density lipoprotein cholesterol, while other mechanisms remain limited. This study aimed to determine whether PCSK9i can improve the prognosis of ACS patients by protecting endothelial function.</p><p><strong>Methods: </strong>A total of 113 ACS patients were enrolled and randomly assigned to PCSK9i group (PCSK9i combined with statins) and control group (statins only). Blood lipids and endothelial function indicators were measured and analyzed 6 weeks before and after treatment. The effect of PCSK9i on the expression and secretion of endothelial function indicators in vascular endothelial cells were studied by cell experiments.</p><p><strong>Results: </strong>After 6 weeks of treatment, endothelial function indicators such as nitric oxide (NO), thrombomodulin, intercellular cell adhesion molecule-1, endothelin-1, and flow-mediated vasodilation were significantly improved in PCSK9i group compared with control group. Only the changes of NO and von Willebrand factor were associated with blood lipid levels, whereas the changes of other endothelial function indicators were not significantly associated with blood lipid levels. PCSK9i reduced the incidence of major adverse cardiovascular events in patients with ACS compared to those in the control group. In cell experiments, PCSK9i treatment significantly ameliorated LPS induced endothelial injury in HUVECs.</p><p><strong>Conclusion: </strong>PCSK9i can protect vascular endothelial function partly independently of its lipid-lowering effect and ameliorate the prognosis of patients with ACS within 6 weeks. This mechanism may involve heat shock transcription factor 1/heat shock proteins -related signaling pathways. Early use of PCSK9i in patients with ACS should be strongly considered in clinical practice.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-14"},"PeriodicalIF":2.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141535081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Meta-Analysis Assessing the Therapeutic Efficacy and Safety of Anlotinib in Combination with Chemotherapy for Small Cell Lung Cancer.","authors":"Ting Gao, Peiwen Zhao, Xiaopeng He, Meng Zhao, Yajuan Shang, Xiaomin Si","doi":"10.1159/000542769","DOIUrl":"10.1159/000542769","url":null,"abstract":"<p><strong>Introduction: </strong>This meta-analysis aimed to assess the effectiveness and safety of combining anlotinib with chemotherapy in treating patients with small cell lung cancer (SCLC).</p><p><strong>Methods: </strong>We systematically searched a range of databases, including PubMed, Embase, Cochrane Library, and Web of Science, up to July 28, 2023, complemented by searches in Chinese databases such as CNKI, Wanfang, and VIP, through July 4, 2023. The outcomes analyzed were objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), median PFS (mPFS), overall survival (OS), vascular endothelial growth factor (VEGF) levels, and the adverse events.</p><p><strong>Results: </strong>The analysis, which integrated data from 16 studies encompassing 1,083 patients, demonstrated that the combined treatment of anlotinib and chemotherapy significantly outperformed either anlotinib or chemotherapy alone in enhancing the ORR, DCR, and mPFS. Furthermore, this combination therapy also resulted in improved PFS, 1-year and 2-year overall OS, and reduced levels of VEGF) compared to chemotherapy alone, with all comparisons reaching statistical significance (p < 0.05). The combination of anlotinib with chemotherapy exhibited a considerably elevated risk of developing leukopenia (RR: 1.41, 95% CI: 1.09-1.82, p = 0.008). The subgroup analyses indicated the anlotinib plus etoposide group and anlotinib plus irinotecan were superior to the etoposide and the irinotecan groups, respectively, in terms of ORR outcome and DCR outcome. The subgroup analysis revealed that the combination of anlotinib and etoposide significantly increased the risk of thrombocytopenia and myelosuppression compared to etoposide alone. In patients with a history of one or an unspecified number of chemotherapy cycles, the integration of anlotinib into the chemotherapy regimen improved DCR. Conversely, in those who had undergone more than two prior treatment cycles, the risk of myelosuppression was heightened with the addition of anlotinib. Lastly, the risk of gastrointestinal adverse events was increased in patients receiving more than two treatment cycles of anlotinib plus chemotherapy compared to anlotinib monotherapy.</p><p><strong>Conclusion: </strong>The findings of this investigation imply that the integration of anlotinib into chemotherapy regimens may enhance PFS, ORR, DCR, and OS in SCLC patients. This meta-analysis presents novel therapeutic prospects for SCLC, suggesting that the synergistic approach of anlotinib and chemotherapy could markedly enhance treatment outcomes for this patient population.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-23"},"PeriodicalIF":2.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142814087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-Treated Adipose Mesenchymal Stem Cells Derived Exosomes Enhance the Therapeutic Effects on Unilateral Ureteral Obstruction Mice.","authors":"Chi Zhang, Longjun Cai, Meimei Ma, Xiaohui Xie, Junsheng Wang, Yuanyuan Zhang","doi":"10.1159/000542609","DOIUrl":"10.1159/000542609","url":null,"abstract":"<p><strong>Introduction: </strong>The exosomes from adipose-derived mesenchymal stem cells (AMSCs) had therapeutic effects. However, whether the exosomes derived from hypoxia-treated AMSCs could improve renal functions in unilateral ureteral obstruction (UUO) mice remains unclear.</p><p><strong>Methods: </strong>The exosomes were characterized using a transmission electron microscope and Western blot. Its size distribution was determined using the Zetasizer Nano ZS analysis system. The differentiation ability was assessed by alkaline phosphatase and oil red staining. Consequently, the function of exosomes in inhibiting inflammatory factors was evaluated using an enzyme-linked immunosorbent assay, and apoptosis inhibition was evaluated by Western blot. Finally, the function of exosomes to ameliorate kidney fibrosis was evaluated using quantitative reverse transcription polymerase chain reaction, Western blot, hematoxylin-eosin staining, and Masson staining.</p><p><strong>Results: </strong>The cultured AMSCs could differentiate into osteoblast and adipocyte. Meanwhile, the cultured AMSCs could effectively secrete the exosomes, which were characterized by around 110 nm diameter and surface marker expression. Exosomes derived from hypoxia-treated AMSCs improved renal functions in UUO mice. The mechanism exploration revealed that exosomes could decrease the TNF-α and IL-6 and inhibit cell apoptosis. Finally, the fibrosis-associated protein was reversed, and the renal dysfunctions were ameliorated in UUO mice.</p><p><strong>Conclusion: </strong>The exosomes derived from the hypoxia-treated AMSCs have a better effect than those from normal AMSCs in ameliorating renal dysfunctions in UUO mice.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-13"},"PeriodicalIF":2.9,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eleclazine Suppresses Ventricular Fibrillation in Failing Rabbit Hearts with Ischemia-Reperfusion Injury Undergoing Therapeutic Hypothermia.","authors":"Hui-Ling Lee, Po-Cheng Chang, Hung-Ta Wo, Hao-Tien Liu, Ming-Shien Wen, Chung-Chuan Chou","doi":"10.1159/000542292","DOIUrl":"10.1159/000542292","url":null,"abstract":"<p><strong>Introduction: </strong>Eleclazine is a highly selective late sodium current inhibitor, possibly effective in reducing ventricular fibrillation (VF) in heart failure (HF) with ischemia-reperfusion (IR) injury. The electrophysiological effects of eleclazine at therapeutic hypothermia (TH) are unknown. We investigated the effects of eleclazine in suppressing VF in failing rabbit hearts with IR injury undergoing TH.</p><p><strong>Method: </strong>HF was induced by right ventricular pacing. An IR model was created using coronary artery ligation for 60 min, followed by reperfusion for 30 min. Hearts were excised and Langendorff-perfused for optical mapping and electrophysiological studies. Electrophysiological studies were repeated after TH (33°C) for 30 min or eleclazine (1 μm) infusion for 20 min.</p><p><strong>Results: </strong>In failing IR-injured hearts, eleclazine reduced action potential duration (APD) dispersion and accelerated intracellular Ca2+ uptake to suppress arrhythmogenic alternans but also exacerbated rate-dependent conduction slowing, resulting in neutral effects on VF inducibility at normothermia. TH increased VF severity. Eleclazine after TH ameliorated TH-induced APD dispersion and further depressed conduction to reduce VF inducibility and severity. TH after eleclazine also slowed conduction to a greater extent to reduce VF inducibility and severity by extrastimulus pacing. In control IR-injured hearts, eleclazine increased VF severity by dynamic pacing at normothermia, which was counteracted by TH.</p><p><strong>Conclusions: </strong>Eleclazine does not prevent VF at normothermia but reduces VF inducibility and severity by extrastimulus pacing at TH in isolated failing hearts with regional IR injury.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-14"},"PeriodicalIF":2.9,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142522754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UCF101 Rescues against Diabetes-Evoked Cardiac Remodeling and Contractile Anomalies through AMP-Activated Protein Kinase-Mediated Induction of Mitophagy.","authors":"Zhiqiang Zhuang, Yuxi Zhu, Jun Tao, Yandong Liu, Jie Lin, Chunjie Yang, Chule Dong, Xing Qin, Qun Li, Russel J Reiter, Guizhen Wang, Zhaohui Pei, Jun Ren","doi":"10.1159/000541569","DOIUrl":"10.1159/000541569","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetes mellitus is known to provoke devastating anomalies in myocardial structure and function, while effective therapeutic regimen is still lacking. The selective protease inhibitor UCF101 (5-[5-(2-nitrophenyl) furfuryl iodine]-1,3-diphenyl-2-thiobarbituric acid) has been shown to fend off ischemic heart injury, although its impact on diabetic cardiomyopathy remains elusive.</p><p><strong>Methods: </strong>Our present work was conducted to examine the effect of UCF101 on experimental diabetes-evoked cardiac geometric and functional abnormalities as well as mechanisms involved. Adult mice were made diabetic using streptozotocin (STZ, 50 mg/kg, i.p., for 5 days) while receiving UCF101 (7.15 mg/kg, i.p.).</p><p><strong>Results: </strong>STZ evoked cardiac hypertrophy, interstitial fibrosis, mitochondrial ultrastructural damage, oxidative stress, dampened autophagy (LC3B, Beclin 1, elevated p62), mitophagy (FUNDC1 and Parkin with upregulated TOM20), increased left ventricular end systolic diameter, reduced fractional shortening, ejection fraction, cardiomyocyte shortening capacity, velocities of shortening/re-lengthening, and rise in intracellular Ca2+ in conjunction with elongated diastole and intracellular Ca2+ removal, the responses were overtly reconciled by UCF101 with little effects from UCF101 itself. Levels of cell injury markers Omi/HtrA2, TNFα, and stress signaling (JNK, ERK, p38) were overtly enhanced along with compromised phosphorylation of cellular fuel AMP-activated protein kinase (AMPK) (Thr172) and cell survival molecule GSK3β, as well as downregulated SERCA2a and elevated phospholamban, the effect was reversed by UCF101 (except for SERCA2a). AMPK knockout, pharmacological inhibition, the mitophagy inhibitor liensinine, and parkin knockout nullified UCF101-offered cardioprotection in diabetes. UCF101 reversed STZ-induced upregulation in the AMPK degrading enzymes PP2A and PP2C.</p><p><strong>Conclusion: </strong>These findings suggest that UCF101 rescues diabetes-mediated alterations in cardiac structure and function, likely through AMPK-mediated regulation of mitophagy.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-14"},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tanshinone IIA Inhibits Hydrogen Peroxide-Induced Ferroptosis in Melanocytes through Activating Nrf2 Signaling Pathway.","authors":"Xiaosha Li, Shiyang Tang, Haizhen Wang, Xin Li","doi":"10.1159/000541177","DOIUrl":"10.1159/000541177","url":null,"abstract":"<p><strong>Introduction: </strong>Melanocyte ferroptosis has been proven to contribute to the development of vitiligo. Tanshinone IIA (TSA), a Chinese herbal extract, has been shown to inhibit vitiligo progression. Whether TSA regulates ferroptosis in melanocytes remains unclear.</p><p><strong>Methods: </strong>Hydrogen peroxide (H2O2) was used to induce melanocytes to stimulate vitiligo cell model in vitro. Cell proliferation was examined by 5-ethynyl-2'-deoxyuridine assay. The levels of malondialdehyde, reactive oxygen species, glutathione peroxidase, and iron were detected by corresponding commercial kit. The protein levels of ferroptosis-related markers and Nrf2 pathway-related markers were examined using western blot and immunofluorescence staining. Cell viability and cytotoxicity were analyzed using Cell Counting Kit-8 assay and lactate dehydrogenase detection. Mitochondrial morphology was examined using a transmission electron microscope.</p><p><strong>Results: </strong>After H2O2 treatment, melanocyte proliferation was reduced, while oxidative stress and ferroptosis were enhanced. TSA treatment could inhibit ferroptosis in H2O2-induced melanocytes. Besides, TSA could activate Nrf2 pathway and promote Nrf2 nuclear translocation, and Nrf2-specific inhibitor (ML385) also reversed the inhibitory effect of TSA on H2O2-induced melanocyte ferroptosis.</p><p><strong>Conclusion: </strong>Our data showed that TSA alleviated H2O2-induced melanocyte ferroptosis via activating Nrf2 pathway.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"1-10"},"PeriodicalIF":2.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142472877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional Chinese Medicine Monomers Are Potential Candidate Drugs for Cancer-Induced Cardiac Cachexia.","authors":"Zhizheng Li,Xinyi Peng,Xinyi Zhu,Michail Spanos,Lan Wu","doi":"10.1159/000540915","DOIUrl":"https://doi.org/10.1159/000540915","url":null,"abstract":"BACKGROUNDCardiovascular diseases are now the second leading cause of death among cancer patients. Heart injury in patients with terminal cancer can lead to significant deterioration of left ventricular morphology and function. This specific heart condition is known as cancer-induced cardiac cachexia (CICC) and is characterized by cardiac dysfunction and wasting. However, an effective pharmacological treatment for CICC remains elusive.SUMMARYThe development and progression of CICC are closely related to pathophysiological processes, such as protein degradation, oxidative responses, and inflammation. Traditional Chinese medicine (TCM) monomers offer unique advantages in reversing heart injury, which is the end-stage manifestation of CICC except the regular treatment. This review outlines significant findings related to the impact of eleven TCM monomers, namely Astragaloside IV, Ginsenosides Rb1, Notoginsenoside R1, Salidroside, Tanshinone II A, Astragalus polysaccharides, Salvianolate, Salvianolic acids A and B, and Ginkgolide A and B, on improving heart injury. These TCM monomers are potential therapeutic agents for CICC, each with specific mechanisms that could potentially reverse the pathological processes associated with CICC. Advanced drug delivery strategies, such as nano-delivery systems and exosome-delivery systems, are discussed as targeted administration options for the therapy of CICC.KEY MESSAGEThis review summarizes the pathological mechanisms of CICC and explores the pharmacological treatment of TCM monomers that promote anti-inflammation, antioxidation, and pro-survival. It also considers pharmaceutical strategies for administering TCM monomers, highlighting their potential as therapies for CICC.","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":"53 1","pages":"1-13"},"PeriodicalIF":3.1,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142180028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent Advances in the Therapeutic Potential of Sinomenine for Cancer Treatment.","authors":"PanZhen Jiang, Aqeela Zahra, Xi Guo, Jianping Wu","doi":"10.1159/000536133","DOIUrl":"10.1159/000536133","url":null,"abstract":"<p><strong>Background: </strong>Cancer is a major cause of death worldwide. Although modern medicine has made strides in treatment, a complete cure for cancer remains elusive.</p><p><strong>Summary: </strong>Utilization of medicinal plants in traditional medicine for the treatment of multiple diseases, including cancer, is a well-established practice. Sinomenine is an alkaloid extracted from a medicinal plant and has a diverse range of biological properties, including anti-oxidative, anti-inflammatory, and antibacterial effects. Sinomenine exhibits inhibitory effects on various types of tumor cells, including breast, lung, and liver cancers. The anticancer properties of sinomenine are believed to involve stimulation of apoptosis and autophagy as well as suppression of cell proliferation, invasion, and metastasis.</p><p><strong>Key message: </strong>This review summarizes the current research on sinomenine's potential as an anticancer agent, which may contribute to the discovery of more effective cancer treatments.</p>","PeriodicalId":20209,"journal":{"name":"Pharmacology","volume":" ","pages":"76-85"},"PeriodicalIF":3.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}