中国药房2025，Vol.36Issue(4)：427-433,7.DOI:10.6039/j.issn.1001-0408.2025.04.07
芍药苷对溃疡性结肠炎小鼠氧化应激的影响及机制
Effects and mechanism of paeoniflorin on oxidative stress of ulcerative colitis mice
摘要
Abstract
OBJECTIVE To investigate the effects and potential mechanism of paeoniflorin on oxidative stress of ulcerative colitis(UC)mice based on adenosine monophosphate-activated protein kinase(AMPK)/nuclear factor-erythroid 2-related factor 2(Nrf2)pathway.METHODS Male BALB/c mice were randomly divided into control group,model group,inhibitor group(AMPK inhibitor Compound C 20 mg/kg),paeoniflorin low-,medium-and high-dose groups(paeoniflorin 12.5,25,50 mg/kg),high-dose of paeoniflorin+inhibitor group(paeoniflorin 50 mg/kg+Compound C 20 mg/kg),with 8 mice in each group.Except for the control group,mice in all other groups were given 4%dextran sulfate sodium solution for 5 days to establish the UC model.Subsequently,mice in each drug group were given the corresponding drug solution intragastrically or intraperitoneally,once a day,for 7 consecutive days.The changes in body weight of mice were recorded during the experiment.Twenty-four hours after the last administration,colon length,malondialdehyde(MDA)content,and activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)in colon tissues were measured;histopathological morphology of colon tissues,tight junctions between intestinal epithelial cells,and histopathological scoring were all observed and evaluated;the mRNA expressions of AMPK and Nrf2,as well as the protein expressions of heme oxygenase-1(HO-1),occludin and claudin-1,were all determined in colon tissue.RESULTS Compared with model group,paeoniflorin groups exhibited recovery from pathological changes such as inflammatory cell infiltration and crypt damage in the colon tissue,as well as improved tight junction damage between intestinal epithelial cells.Additionally,significant increases or upregulations were observed in body weight,colon length,activities of SOD and GSH-Px,phosphorylation level of AMPK,and protein expression of Nrf2,HO-1,occludin,claudin-1,and mRNA expressions of AMPK and Nrf2;concurrently,MDA content and histopathological scores were significantly reduced(P＜0.05 or P＜0.01).In contrast,the inhibitor group showed comparable(P＞0.05)or worse(P＜0.05 or P＜0.01)indicators compared to the model group.Conversely,the addition of AMPK inhibitor could significantly reverse the improvement of high-dose paconiflorin(P＜0.01).CONCLUSIONS Paeoniflorin can repair intestinal epithelial cell damage in mice,improve tight junctions between epithelial cells,upregulate the expression of related proteins,and promote the expression and secretion of antioxidant-promoting molecules,thereby ameliorating UC;its mechanism may be associated with activating AMPK/Nrf2 antioxidant pathway.关键词
芍药苷/溃疡性结肠炎/氧化应激/AMPK/Nrf2通路Key words
paeoniflorin/ulcerative colitis/oxidative stress/AMPK/Nrf2 pathway分类
医药卫生引用本文复制引用
代鑫,王莹,任鑫悦,范丁兴,李贤哲,冯嘉轩,娄石磊,阎慧,孙聪..芍药苷对溃疡性结肠炎小鼠氧化应激的影响及机制[J].中国药房,2025,36(4):427-433,7.基金项目
吉林省自然科学基金项目(No.YDZJ202401060 ZYTS) （No.YDZJ202401060 ZYTS）
吉林省教育厅科学技术研究项目(No.JJKH20230949KJ) （No.JJKH20230949KJ）
长春中医药大学国家级大学生创新创业训练计划项目(No.202210199023) （No.202210199023）
