Article(id=1291706998266028045, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.24.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1763308800000, receivedDateStr=2025-11-17, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896547142, onlineDateStr=2026-08-05, pubDate=1766851200000, pubDateStr=2025-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896547142, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896547142, creator=13701087609, updateTime=1785896547142, updator=13701087609, issue=Issue{id=1291706966187991876, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='24', pageStart='3451', pageEnd='3600', issueExtLink='null', onlineDate='null', pubDate='1766851200000', pubDateStr='2025-12-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896539494, creator='13701087609', updateTime=1785998798662, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292135872292479273, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292135872296673578, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3512, endPage=3517, ext={EN=ArticleExt(id=1291706998542852110, articleId=1291706998266028045, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research on the therapeutic targets of HSK31679 for metabolic dysfunction related steatohepatitis, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective This article aimed to explore the targets of the innovative drug HSK31679 in treating metabolic dysfunction-associated steatohepatitis (MASH), and to validate the changes in drug efficacy before and after target knockout through in vivo experiments.
Methods Using the drug and disease databases, HSK31679 and MASH related targets were identified. The core targets were further determined by Cytoscape software. Auto Dock predicted the binding affinity of corresponding proteins to HSK31679. MASH mouse models of wild-type and liver caspase 8 (CASP8) knockout were constructed. Mice were divided into control group (normal feeding of mice + 0.5 mL saline administration), model group (modeling of mice + 0.5 mL saline administration), experimental group (modeling of mice + 3 mg·kg-1 HSK31679 administration), ΔCASP8 model group (modeling of CASP8 knockout mice + 0.5 mL saline administration) and ΔCASP8 experimental group (modeling of CASP8 knockout mice + 3 mg·kg-1 HSK31679 administration), with 8 mice in each group. Serum biochemical indicators were measured using an enzyme-linked immunosorbent assay (ELISA) after treatment, and liver sections were stained with HE to velidate the role of core targets of HSK31679′s treatment of MASH.
Results HE staining revealed significant and typical MASH-associated cellular damage in hepatocytes of the model group, indicating successful model establishment. Five major core targets associated with both HSK31679 and MASH were identified, and HSK31679 exhibited favorable binding activity with the CASP8 protein among them. In animal experiments, the serum triglyceride (TG) levels in the blank group, model group, experimental group, ΔCASP8 model group, and ΔCASP8 experimental group were (0.61±0.05), (1.01±0.15), (0.66±0.13), (0.62±0.09), and (0.63±0.12) mmol·L-1, respectively; the total cholesterol (TC) levels were (1.24±0.13), (2.88±0.32), (1.60±0.29), (1.30±0.35), and (1.32±0.10) mmol·L-1, respectively; the alanine aminotransferase (ALT) levels were (74.64±9.31), (140.20±23.74), (88.67±13.67), (78.18±17.66), and (73.58±16.15) IU·L-1, respectively; the aspartate aminotransferase (AST) levels were (106.33±26.77), (227.32±20.51), (124.58±13.63), (138.37±18.08), and (115.54±27.14) IU·L-1, respectively. Compared with the model group, the differences of above indicators in the experimental group were all statistically significant (all P<0.01). In HE staining, hepatocytes were arranged in a relatively orderly and dense manner, with a significant reduction in cytoplasmic vacuoles. The aforementioned indicators in the ΔCASP8 experimental group showed no statistically significant differences compared to the ΔCASP8 model group (all P>0.05). There was also no significant difference in the degree of hepatocyte degeneration between the two groups.
Conclusion CASP8 protein is the key target of HSK31679 in the treatment of MASH. HSK31679 alleviated MASH-related hepatic inflammatory symptoms by binding to CASP8 protein and reducing its activity.
, authors=Chen-shu DAI
1, 2, Tian-tian QI
2, 3, Yu-hang ZHANG
2, Yi-min CUI
1, 2, authorsList=Chen-shu DAI, Tian-tian QI, Yu-hang ZHANG, Yi-min CUI, authorCompany=null, correspAuthors=Yi-min CUI, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291706998823870479, articleId=1291706998266028045, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=HSK31679治疗代谢功能障碍相关脂肪性肝炎靶点的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 本文旨在探索创新药HSK31679治疗代谢功能障碍相关脂肪性肝炎（MASH）的作用靶点，并以体内实验验证靶点敲除前后药物疗效变化。
方法 借助药物与疾病数据库，获得HSK31679和MASH相关靶点，分别用Cytoscape和Auto Dock软件进一步确定治疗核心靶点并预测相应蛋白与HSK31679分子的结合能力。构建野生型和肝胱天蛋白酶8（CASP8）敲除型MASH小鼠模型，将小鼠分为空白组（普通小鼠正常喂养+0.5 mL生理盐水灌胃）、模型组（普通小鼠造模+0.5 mL生理盐水灌胃）、实验组（普通小鼠造模+ 3 mg·kg-1 HSK31679灌胃）、ΔCASP8模型组（CASP8敲除型小鼠正常喂养+0.5 mL生理盐水灌胃）和ΔCASP8实验组（CASP8敲除型小鼠正常喂养+3 mg·kg-1 HSK31679灌胃），每组8只。分组治疗后，用酶标仪测定血清生化指标，对肝切片进行苏木精-伊红（HE）染色，以验证核心靶点在HSK31679治疗MASH过程中的作用。
结果 HE染色显示，模型组小鼠肝细胞存在显著典型的与MASH相关的细胞损伤迹象，提示造模成功。发现5个HSK31679-MASH相关的主要核心靶点，HSK31679分子与其中的CASP8蛋白具有良好结合活性。在动物实验中，空白组、模型组、实验组、ΔCASP8模型组和ΔCASP8实验组小鼠的血清甘油三酯（TG）水平分别为（0.61±0.05）、（1.01±0.15）、（0.66±0.13）、（0.62±0.09）和（0.63±0.12）mmol·L-1；总胆固醇（TC）水平分别为（1.24±0.13）、（2.88±0.32）、（1.60±0.29）、（1.30±0.35）和（1.32±0.10）mmol·L-1；谷丙转氨酶（ALT）水平分别为（74.64±9.31）、（140.20±23.74）、（88.67±13.67）、（78.18±17.66）和（73.58±16.15）IU·L-1；谷草转氨酶（AST）水平分别为（106.33±26.77）、（227.32±20.51）、（124.58±13.63）、（138.37±18.08）和（115.54±27.14）IU·L-1，实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.01）；HE染色中，肝细胞排列均较为有序、紧密，胞浆空泡明显减少。ΔCASP8实验组的上述指标与ΔCASP8模型组比较，在统计学上差异均无统计学意义（均P>0.05）；两组的肝细胞变性程度也无明显差异。
结论 CASP8蛋白是HSK31679治疗MASH的关键靶点，HSK31679通过结合CASP8蛋白、降低其活性，从而达到缓解MASH肝脏炎症症状的效果，为HSK31679治疗MASH的后续实验研究提供一定理论依据。
, authors=戴晨曙
1, 2, 齐田田
2, 3, 张宇航
2, 崔一民
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戴晨曙（2000-），女，硕士研究生，主要从事药学的相关研究
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1.温州医科大学 药学院，浙江 温州 325035
2.北京大学 第一医院，临床药理研究所，北京 100034, bio={"content":"
戴晨曙（2000-），女，硕士研究生，主要从事药学的相关研究
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2.a. Institute of Clinical Pharmacology, b. Department of Pharmacy, Peking University First Hospital, Beijing 100034, China
3.School of Pharmacy, Xuzhou Medical University, Xuzhou 221004, Jiangsu Province, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1291707001621471268, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1291706998266028045, authorId=1291707001378201632, language=CN, stringName=齐田田, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=
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2.北京大学 第一医院，临床药理研究所，北京 100034
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1.School of Pharmacy, Wenzhou Medical University, Wenzhou 221004, Zhejiang Province, China
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1.温州医科大学 药学院，浙江 温州 325035
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