Article(id=1307269638182687312, tenantId=1146029695717560320, journalId=1302318977290174537, issueId=1307269637637427792, articleNumber=null, orderNo=null, doi=10.19664/j.cnki.1002-2392.260071, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1733673600000, receivedDateStr=2024-12-09, revisedDate=1761321600000, revisedDateStr=2025-10-25, acceptedDate=null, acceptedDateStr=null, onlineDate=1789606969638, onlineDateStr=2026-09-17, pubDate=1776614400000, pubDateStr=2026-04-20, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1789606969638, onlineIssueDateStr=2026-09-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1789606969638, creator=13701087609, updateTime=1789606969638, updator=13701087609, issue=Issue{id=1307269637637427792, tenantId=1146029695717560320, journalId=1302318977290174537, year='2026', volume='54', issue='4', pageStart='1', pageEnd='127', issueExtLink='null', onlineDate='null', pubDate='1776614400000', pubDateStr='2026-04-20', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1789606969508, creator='13701087609', updateTime=1789606969508, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=24, endPage=30, ext={EN=ArticleExt(id=1307269638367236689, articleId=1307269638182687312, tenantId=1146029695717560320, journalId=1302318977290174537, language=EN, title=Mechanism Study on Rhubarb Improving Systemic Inflammatory Response and Protecting Intestinal Structure in Sepsis through Regulating Mitophagy by Intervening in Inflammasome Activation, columnId=null, journalTitle=Acta Chinese Medicine and Pharmacology, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: To investigate the mechanism of rhubarb by activating the PINK1/Parkin pathway to regulate mitophagy and intervene in inflammasome activation to inhibit systemic inflammatory response and protect intestinal structure in sepsis mice.
Method: A total of 40 6-8-week-old C57BL/6J male mice were randomly divided into high-dose rhubarb group, medium-dose rhubarb group, low-dose rhubarb group, sepsis model group and blank group. The high-dose rhubarb group, the medium-dose group, the low-dose group, and the sepsis model group were all modeled by cecal ligation and perforation to establish a mouse model of sepsis, After successful modeling, each dose group of rhubarb was given 0.52 mL/day of rhubarb liquid by gavage every day for 7 days, and on the 8th day, the eyeball blood of mice in each group was collected after successful modeling, serum was prepared, and intestinal tissue was retained; HE staining was used to observe the histopathological changes of intestinal tissue, and the levels of TNF-α, IL-1β and IL-6 in serum were detected by ELISA, Western blot was used to detect the expression levels of NLRP3, PINK1, Parkin, LC3I, LC3II in ileal tissues of mice in each group.
Results: HE staining showed that the intestinal mucosal epithelial cell injury was the most serious in the sepsis model group, with multiple ulcers formed, obvious intestinal villi with a large amount of necrosis and large sloughing, accompanied by mucosal bleeding and edema, inflammatory cell infiltration reached the muscularis mucosa, goblet cells were significantly reduced, paneth cells were significantly increased, and inflammatory cells infiltrated into the muscularis mucosa; Compared with the model group, the intestinal mucosal epithelial cell damage, microvilli destruction and inflammatory cell infiltration in the rhubarb group were improved, and the number of goblet cells increased, while the number of paneth cells decreased, and the inflammatory cell infiltration was basically limited to the lamina propria. The serum TNF-α, IL-1β, IL-6 level in the sepsis model group was significantly increased(P < 0.01), and the serum TNF-α, IL-1β, IL-6 level in the rhubarb group decreased after treatment(P < 0.05, P < 0.01). The expression levels of NLRP3, PINK1, Parkin, LC3I, LC3II were significantly increased in the intestinal tissues of mice in the sepsis model group(P < 0.01). After treatment, the level of NLRP3 in each dose group of rhubarb decreased(P < 0.01), which was negatively correlated with the dose, and the expression level of PINK1, Parkin, LC3I, LC3II increased to varying degrees(P < 0.05, P <0.01), which was positively correlated with the dose.
Conclusion: By inhibiting the activation of intestinal NLRP3 inflammasomes, rhubarb activates the PINK1/Parkin pathway and increases the degree of mitophagy, thereby reducing the production of systemic inflammatory factors and protecting the intestinal structure.
, authors=Ting WANG, Lv LI, Shaojin XU, Hanhong ZHANG, Quan LI
*, authorsList=Ting WANG, Lv LI, Shaojin XU, Hanhong ZHANG, Quan LI, authorCompany=null, correspAuthors=Quan LI, 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=1307269638686003794, articleId=1307269638182687312, tenantId=1146029695717560320, journalId=1302318977290174537, language=CN, title=大黄干预炎症小体活化调控线粒体自噬改善脓毒症全身炎症反应及保护肠道结构机制研究, columnId=1303760926633652690, journalTitle=中医药学报, columnName=实验研究, runingTitle=null, highlight=null, articleAbstract=
目的： 探讨大黄通过干预炎症小体NLRP3活化、激活PINK1/Parkin途径调控线粒体自噬，从而对脓毒症小鼠全身炎症反应的抑制及肠道结构的保护机制。
方法： 将40只6~8周龄C57BL/6J雄性小鼠采用随机数字表法分为大黄高剂量组、大黄中剂量组、大黄低剂量组，模型组，空白组；大黄高剂量组、大黄中剂量组、大黄低剂量组以及模型组均运用盲肠结扎与穿孔术建立脓毒症小鼠模型，造模成功后大黄各剂量组每天灌胃相应浓度的大黄液0.52 mL/d，持续给药7 d，第8天采集血液，制备血清，留取肠道组织；采用HE染色观察各组小鼠肠组织病理学改变，采用ELISA法检测血清中TNF-α、IL-1β、IL-6的水平，应用Western Blot法检测各组小鼠回肠组织NLRP3、PINK1、Parkin、LC3I、LC3II的蛋白表达水平。
结果： HE染色可见模型组小鼠肠黏膜上皮细胞损伤最严重，见多个溃疡形成，明显的肠绒毛大量坏死及大片脱落，并伴有黏膜出血和水肿，炎性细胞浸润达黏膜肌层，杯状细胞明显减少，潘氏细胞明显增多；与模型组相比，大黄各剂量组小鼠肠黏膜上皮细胞损伤、微绒毛破坏及炎症细胞浸润均改善、杯状细胞数量增加，而潘氏细胞数量减少，炎性细胞浸润基本局限于固有层，其中大黄高剂量组小鼠肠黏膜上皮细胞损伤、肠绒毛破坏程度最轻，黏膜腺体排列形态趋于正常形态，黏膜无明显出血及水肿。模型组小鼠血清中TNF-α、IL-1β、IL-6水平明显升高（P < 0.01），大黄各剂量组给药后血清中TNF-α、IL-1β、IL-6水平均降低（P < 0.05, P < 0.01）。模型组小鼠肠道组织中NLRP3表达水平明显升高（P < 0.01），PINK1、Parkin的表达水平升高（P < 0.01），自噬相关蛋白LC3I、LC3II表达水平明显升高（P < 0.01），大黄各剂量组给药后NLRP3水平均不同程度降低（P < 0.01），且与大黄剂量呈负相关，PINK1、Parkin、自噬相关蛋白LC3I、LC3II表达水平不同程度升高（P < 0.05，P < 0.01），与大黄剂量呈正相关。
结论： 大黄通过对肠道NLRP3炎症小体活化的抑制，激活PINK1/Parkin途径增加线粒体自噬程度，从而达到减少全身炎症因子产生及肠道结构保护作用。
, authors=王婷, 李绿, 许少金, 张汉洪, 李泉
*, authorsList=王婷, 李绿, 许少金, 张汉洪, 李泉, authorCompany=null, correspAuthors=李泉, authorNote=
王婷（1990-），女，硕士，主治医师，从事中医急危重症治疗相关研究。
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* 李泉（1980-），男，副主任医师，从事中医急危重症治疗相关研究。
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