溃结康调控PERK-elF2α-ATF4-CHOP信号通路干预内质网应激治疗溃疡性结肠炎的机制研究  

Mechanisms of Kuijie Kang Decoction Regulating PERK-elF2α-ATF4-CHOP Signaling Pathway of Endoplasmic Reticulum Stress to Treat Ulcerative Colitis

作　　者：李小丝 马建国 徐荣漪 祁燕 LI Xiaosi;MA Jianguo;XU Rongyi;Qi Yan(Central Laboratory of the First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine,Kunming 650000,China;Anorectal Branch,the First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine,Kunming 650021,China)

机构地区：[1]云南中医药大学第一附属医院中心实验室,云南昆明650000 [2]云南中医药大学第一附属医院肛肠科,云南昆明650021

出　　处：《中国民族民间医药》2024年第2期8-13,共6页Chinese Journal of Ethnomedicine and Ethnopharmacy

基　　金：国家自然科学基金资助项目(编号:81960868);云南省科技厅-云南中医药大学联合专项基金资助项目(编号:202001AZ070001-051)。

摘　　要：目的:探讨溃结康(KJK)调控PERK-elF2α-ATF4-CHOP通路改善溃疡性结肠炎(UC)的作用机制。方法:C57BL/6小鼠分为空白组、模型组、阳性对照组、KJK(6.4 g/kg、12.8 g/kg)组,制备DSS诱导的UC小鼠模型,造模同时给予对应药物治疗7 d后处死小鼠,测量结肠长度;HE染色观察结肠病理损伤;western blot法检测PERK-elF2α-ATF4-CHOP信号通路蛋白表达。结果:与空白组比较,模型组小鼠DAI评分、Geboes评分明显升高(P<0.001);结肠长度明显缩短(P<0.01);结肠组织中GRP78、CHOP、ATF4、p-PERK、p-elF2α蛋白表达明显升高(P<0.01);与模型组比较,KJK 6.4 g/kg及12.8 g/kg组小鼠DAI评分及Geboes评分明显降低,结肠长度明显缩短(P<0.05,P<0.01);结肠组织中GRP78、CHOP、ATF4、p-PERK蛋白表达明显降低(P<0.05,P<0.01)。结论:KJK可抑制PERK-elF2α-ATF4-CHOP通路信号转导,改善UC小鼠症状。Objective To investigate the mechanism by which Kuijie Kang(KJK)regulates the PERK-elF2α-ATF4-CHOP pathway to improve ulcerative colitis(UC).Method C57BL/6 mice were divided into normal,model,positive control,and KJK(6.4 g/kg,12.8 g/kg)groups.A DSS-induced UC mouse model was established,and corresponding drugs were administered for 7 days before sacrificing the mice.Colon length was measured and HE staining was performed to observe colon pathological changes.Western blotting was used to detect the expression of proteins in the PERK-elF2α-ATF4-CHOP signaling pathway.Results Compared with the normal group,the DAI score and Geboes score of the model group mice were significantly increased(P<0.001);colon length was significantly shortened(P<0.01);the expression of GRP78,CHOP,ATF4,p-PERK,and p-elF2αproteins in colon tissue was significantly elevated(P<0.01).Compared with the model group,the DAI score,Geboes score,and colon length of the KJK 6.4 g/kg and 12.8 g/kg groups were significantly reduced(P<0.05,P<0.01);the expression of GRP78,CHOP,ATF4,and p-PERK proteins in colon tissue was significantly decreased(P<0.05,P<0.01).Conclusion KJK can inhibit the PERK-elF2α-ATF4-CHOP pathway and improve symptoms of UC in mice.

关 键 词：溃疡性结肠炎 内质网应激 溃结康 PERK-elF2α-ATF4-CHOP信号通路 

分 类 号：R285.5[医药卫生—中药学]