Article(id=1317115293860745608, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.05.025, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791954356875, onlineDateStr=2026-10-14, pubDate=1778342400000, pubDateStr=2026-05-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791954356875, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791954356875, creator=13701087609, updateTime=1791954356875, updator=13701087609, issue=Issue{id=1317115025307845060, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='5', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1778342400000', pubDateStr='2026-05-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791954292847, creator='13701087609', updateTime=1791958713604, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133567340171275, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133567340171276, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115025307845060, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=132, endPage=137, ext={EN=ArticleExt(id=1317115294057877897, articleId=1317115293860745608, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Mechanism of Anchang Decoction (安肠汤) on Improving Mitophagy in Intestinal Epithelial Cells of Rats with Ulcerative Colitis Based on PHB2/PGAM5/PINK1/Parkin Signaling Axis, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To observe the effect of Anchang Decoction (安肠汤, ACD) on mitophagy in intestinal epithelial cells of the rats with ulcerative colitis (UC) through PTEN inducing putative kinase 1 (PINK1) /Parkinson's disease protein (Parkin) /antiproliferative protein 2 (PHB2) /phosphoglycinate mutase 5 (PGAM5) signaling axis.
Methods Forty-eight Wistar rats were randomly divided into Control group, Model group, Mesalazine group (0.42 g·kg-1) and ACD low, medium and high groups (ACD-L, ACD-M, ACD-H; 11.55, 23.1, 46.2 g·kg-1), 8 rats in each group. Except for the Control group, the UC model was established by 2, 4, 6-trinitrobenzenesulfonic acid (TNBS) . After the model was successfully established, the blank group and the model group were given the normal saline by gavage, and the other groups were given the corresponding drugs by gavage for 14 days. After the intervention, the general condition of the rats in each group was observed and the body weight was recorded, the disease activity index (DAI) score was calculated, the pathological changes of intestinal tract were observed by hematoxylin-eosin staining, and the levels of interleukin-6 (IL-6) and interleukin-18 (IL-18) were detected by enzyme-linked immunosorbent assay. The mitochondrial ultrastructure of colonic epithelial cells (IECs) was observed by transmission electron microscopy. The expressions of mitochondrial microtubule-associated protein 1 light chain 3 (LC3) and selective autophagy receptor (p62) were detected by immunofluorescence. The protein expression levels of PHB2, PGAM5, PINK1, Parkin, LC3 and p62 in colon tissues were detected by Western Blot. The mRNA expression levels of PHB2, PGAM5, PINK1 and Parkin in colon tissues were detected by Real-time fluorescent quantitative polymerase chain reaction.
Results Compared with those of the Control group, the general condition of the Model group was worse, the body weight was significantly decreased, the DAI score was significantly increased (P<0.01), the pathological changes of colon tissue were obvious, the serum levels of IL-6 and IL-18 were increased (P<0.01), the mitochondrial structure of IECs was obviously missing, the number of Iecs was decreased, and the mitochondrial cristae was broken. The mitochondrial morphology was swollen and vacuolated, the protein and mRNA expression levels of LC3, PHB2, PGAM5, PINK1 and Parkin were decreased, and the protein expression level of p62 was increased in the treatment group (P<0.05, P<0.01) . Compared with those in the Model group, the rats in the Mesalazine group and each dose group of ACD were significantly improved, the body weight increased, the DAI score increased significantly (P<0.05, P<0.01), the colonic mucosal structure recovered to varying degrees, and the serum levels of IL-6 and IL-18 decreased (P<0.05, P<0.01) . The mitochondrial membrane of IECs was more complete, the number was increased, the swelling degree was decreased, and the structure of mitochondrial cristae was improved. ACD-Mand ACD-H showed more obvious autophagosomes or autolysosomes. The expression levels of LC3 protein, PHB2, PGAM5, PINK1 and Parkin protein and mRNA were increased in varying degrees. The p62 protein levels were decreased in different degrees (P<0.05, P<0.01) .
Conclusions ACD reduces inflammatory response and promotes intestinal mucosal recovery to improve UC symptoms possibly by regulating the PHB2/PGAM5/PINK1/Parkin axis to promote mitophagy in IECs.
, authors=Xiaoxin DUAN, Jiaqi LIU, Hudan SONG, Jie DONG, Nating PAN, Peiyuan ZHANG, Yilei WEN, Pingliang SUN, authorsList=Xiaoxin DUAN, Jiaqi LIU, Hudan SONG, Jie DONG, Nating PAN, Peiyuan ZHANG, Yilei WEN, Pingliang SUN, authorCompany=null, correspAuthors=Pingliang SUN, 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=1317115294284370314, articleId=1317115293860745608, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=基于PHB2/PGAM5/PINK1/Parkin信号轴探讨安肠汤改善溃疡性结肠炎大鼠肠上皮细胞线粒体自噬的作用机制, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 观察安肠汤（Anchang decoction，ACD）通过PTEN诱导假定激酶1（PTEN-induced putative kinase 1，PINK1）/帕金森病蛋白（Parkin）/抗增殖蛋白2（Prohibitin2，PHB2）/磷酸甘油酸变位酶5（Phosphoglycerate mutase family member 5，PGAM5）信号轴改善溃疡性结肠炎（Ulcerative colitis，UC）大鼠肠上皮细胞线粒体自噬的作用机制。
方法 将48只Wistar大鼠随机分为空白组（Control）、模型组（Model）、美沙拉嗪组（Mesalazine，0.42 g·kg-1）以及安肠汤低、中、高剂量组（ACD-L、ACD-M、ACD-H，11.55、23.1、46.2 g·kg-1），每组各8只。除空白组外，其余各组大鼠采用2，4，6-三硝基苯磺酸（2，4，6-Trinitrobenzene sulfonic acid，TNBS）建立UC模型，模型构建成功后，Control组、Model组予以生理盐水灌胃，其余各组分别进行相应药物灌胃，灌胃14 d。干预结束后，观察各组大鼠一般情况并记录体质量，计算疾病活动指数（Disease activity index，DAI）评分，通过苏木素-伊红（Hematoxylin-eosin staining，HE）染色观察大鼠肠道病理变化，酶联免疫吸附测定法（Enzyme-linked immunosorbent assay，ELISA）检测白细胞介素（Interleukin，IL）-6、IL-18水平，透射电镜观察结肠上皮细胞（Intestinal epithelial cells，IECs）线粒体超微结构，免疫荧光（Immunofluorescence，IF）检测线粒体微管相关蛋白1轻链3（Microtubule-associated protein 1 light chain 3，LC3）、选择性自噬接头蛋白62（Selective autophagy adaptor protein 62，p62）表达，蛋白质印迹检测结肠组织PHB2、PGAM5、PINK1、Parkin、LC3、p62蛋白表达水平，实时荧光定量聚合酶链式反应（Real-time PCR，RT-PCR）检测结肠组织PHB2、PGAM5、PINK1、Parkin mRNA表达量。
结果 与Control组相比，Model组一般情况变差，体质量明显降低，DAI评分明显升高（P<0.01），结肠组织病理损伤变化明显，血清中IL-6、IL-18含量升高（P<0.01），IECs线粒体结构缺失明显，数量减少，线粒体嵴出现断裂，线粒体形态肿胀和空泡化，LC3蛋白以及PHB2、PGAM5、PINK1、Parkin蛋白和mRNA表达水平明显下降，p62蛋白表达明显升高（P<0.05，P<0.01）。与Model组相比，Mesalazine组及ACD各剂量组大鼠状态明显好转体质量增加，DAI评分明显降低（P<0.05，P<0.01），结肠黏膜结构均有不同程度的恢复，血清中IL-6、IL-18含量降低（P<0.05，P<0.01），IECs线粒体膜较完整，数量增加，肿胀程度降低，线粒体嵴结构改善，ACD-M、ACD-H更为明显出现自噬小体或自噬溶酶体，LC3蛋白以及PHB2、PGAM5、PINK1、Parkin蛋白和mRNA表达水平均有不同程度上升，p62蛋白水平不同程度降低（P<0.05，P<0.01）。
结论 安肠汤降低UC炎症反应、促进肠黏膜恢复以改善UC症状的作用机制，可能通过调控PHB2/PGAM5/PINK1/Parkin轴促进IECs线粒体自噬有关。
, authors=段晓鑫, 刘嘉琪, 宋胡丹, 董杰, 潘娜婷, 张培源, 文亦磊, 孙平良, authorsList=段晓鑫, 刘嘉琪, 宋胡丹, 董杰, 潘娜婷, 张培源, 文亦磊, 孙平良, authorCompany=null, correspAuthors=孙平良, authorNote=
段晓鑫（1997-），女，安徽阜阳人，博士，研究方向：中医药防治肛肠疾病。
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段晓鑫（1997-），女，安徽阜阳人，博士，研究方向：中医药防治肛肠疾病。
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段晓鑫（1997-），女，安徽阜阳人，博士，研究方向：中医药防治肛肠疾病。
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