白及多糖通过Keap1/Nrf2/HO-1信号通路治疗大鼠胃溃疡的作用机制研究OA
Mechanism of Bletilla striata Polysaccharide in Treating Gastric Ulcer in Rats through Keap1/Nrf2/HO-1 Signaling Pathway
目的 基于Keap1/Nrf2/HO-1信号通路探究白及多糖(BSP)对乙醇诱导大鼠胃溃疡胃黏膜的保护作用.方法 36只SD雄性大鼠随机分为正常组(Control组)、模型组(Model组)、雷尼替丁组(Ranitidine组)、白及多糖低剂量组(BSP-L组)、白及多糖中剂量组(BSP-M组)和白及多糖高剂量组(BSP-H组),每组6只.Ranitidine组灌胃给予0.1 g/kg雷尼替丁,BSP-L、BSP-M、BSP-H组灌胃0.125、0.25、0.5 g/kg白及多糖,持续给药7 d.末次给药后1 h,除Control组外,其余组大鼠灌服无水乙醇0.75 mL/100 g,1 h后腹腔注射麻醉,处死.采用改良Guth法计算大鼠表观评分,HE染色观察胃组织病理变化,ELISA检测氧化应激(SOD、NO)及炎症因子(TNF-α、IL-6)水平,Western blot检测Keap1/Nrf2/HO-1通路关键蛋白表达.结果 与Model组比较,BSP各剂量组胃黏膜损伤明显减轻,表观评分极显著降低(P<0.01);病理损伤明显改善,BSP-L组见少量胃腺细胞异常及轻微充血出血,BSP-M和BSP-H组仅见少量炎症细胞浸润;BSP-M组和BSP-H组可显著降低TNF-α、IL-6、NO水平(P<0.05,P<0.01),升高SOD活性(P<0.01),并显著上调Nrf2、HO-1蛋白表达,下调Keap1蛋白表达(P<0.01).结论 BSP可通过抑制氧化应激和炎症反应,调控Keap1/Nrf2/HO-1信号通路发挥对乙醇诱导大鼠胃溃疡的胃黏膜保护作用.
Objective To investigate the protective effect of Bletilla striata polysaccharide(BSP)on gastric mucosa against ethanol-induced gastric ulcer in rats via Keap1/Nrf2/HO-1 signaling pathway.Methods Thirty-six male Sprague-Dawley(SD)rats were randomly divided into six groups:control group,model group,ranitidine group,low-dose BSP(BSP-L)group,medium-dose BSP(BSP-M)group,and high-dose BSP(BSP-H)group,with six rats in each group.Ranitidine group received ranitidine at a dose of 0.1 g/kg by gavage,while BSP-L,BSP-M,and BSP-H groups received BSP at doses of 0.125,0.25,and 0.5 g/kg by gavage,respectively.All treatments were administered once daily for 7 consecutive days.One hour after the final administration,all groups except those the control group received absolute ethanol at a dose of 0.75 mL/100 g by gavage.One hour later,all groups were anesthetized via intraperitoneal injection and subsequently euthanized.The macroscopic score was calculated using the modified Guth method.Pathological changes of gastric tissue were observed by hematoxylin-eosin(HE)staining.The levels of oxidative stress markers(SOD and NO)and inflammatory cytokines(TNF-α and IL-6)were detected by ELISA.The expression of key proteins in the Keap1/Nrf2/HO-1 pathway were determined by Western blot.Results Compared with the model group,gastric mucosal injury was significantly alleviated in all BSP-treated groups,with a significant decrease in the macroscopic score(P<0.01).Pathological damage was obviously improved:the BSP-L group only showed a small number of abnormal gastric gland cells and slight hyperemia and hemorrhage,while the BSP-M and BSP-H groups only exhibited mild inflammatory cell infiltration.In addition,BSP-M and BSP-H groups showed significantly reduced the levels of TNF-α,IL-6 and NO(P<0.05,P<0.01),increased SOD activity(P<0.01),significantly up-regulated the protein expressions of Nrf2 and HO-1,and down-regulated Keap1 expression(P<0.01).Conclusion BSP exerts a protective effect on gastric mucosa against ethanol-induced gastric ulcer in rats by inhibiting oxidative stress and inflammatory response and regulating the Keap1/Nrf2/HO-1 signaling pathway.
唐秀胜;王宗明;黄华进;杨孝斌;方镕泽
遵义市中医院,贵州 遵义 563000遵义市中医院,贵州 遵义 563000遵义市中医院,贵州 遵义 563000遵义市中医院,贵州 遵义 563000贵州中医药大学,贵州 贵阳 550025
胃溃疡白及多糖Keap1/Nrf2/HO-1氧化应激炎症
Gastric ulcerBletilla striata polysaccharideKeap1/Nrf2/HO-1Oxidative stressInflammation
《中医药信息》 2026 (10)
13-18,6
贵州省科技计划项目(黔科合支撑[2020]4Y075号)2026年度贵州省卫生健康委科学技术基金项目(gzwkj2026-504)遵义市科技计划项目(遵市科合HZ字[2022]433号)贵州中医药大学科研项目(贵中医科余[2026]05号)
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