摘要
探究银杏内酯B对三硝基苯磺酸(trinitrobenzenesulfonic acid,TNBS)诱导的小鼠溃疡性结肠炎(ulcerative colitis,UC)的保护作用及其机制。将60只无特定病原体级雄性C57BL/6小鼠随机分为6组:对照组、模型组、银杏内酯B低剂量组(2.5 mg/kg)、银杏内酯B中剂量组(5 mg/kg)、银杏内酯B高剂量组(10 mg/kg)、柳氮磺吡啶组(100 mg/kg)。将TNBS溶液通过软导管缓慢注入小鼠结肠建立UC模型。通过体重、结肠长度和疾病活动指数(disease activity index,DAI)评估UC严重程度;H-E染色观察组织学变化;ELISA检测炎性因子的表达;试剂盒检测超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)水平;Western blotting检测TLR4/NF-κB通路蛋白的表达。与模型组相比,银杏内酯B中、高剂量组小鼠的体重下降较少,结肠长度较长,DAI评分降低,结肠炎病理损伤明显改善,TNF-α、IL-1β、IL-6、IL-2、IL-12的表达明显降低,而IL-10的表达显著升高,SOD和GSH-Px水平升高,MDA水平降低。此外,TLR4/NF-κB通路蛋白的活化受到抑制。综上所述,银杏内酯B对UC有明显的保护作用,其机制可能与抑制TLR4/NF-κB信号通路的激活有关。
To investigate the protective effect and underlying mechanism of ginkgolide B against trinitrobenzenesulfonic acid(TNBS)-induced ulcerative colitis(UC)in mice,this study used 60 specific pathogen free grade male C57BL/6 mice randomly divided into 6 groups:the control group,the UC model group,the ginkgolide B low-dose group(2.5 mg/kg),the ginkgolide B medium-dose group(5 mg/kg),the ginkgolide B high-dose group(10 mg/kg),and the sulfasalazine group(100 mg/kg).The UC model was established by slowly injecting TNBS solution into the mouse colon through a flexible catheter.The severity of UC was assessed by body weight,colon length,and disease activity index(DAI).Histological changes were observed by H-E staining and the expressions of inflammatory factors were detected by ELISA.The levels of superoxide dismutase(SOD),malondialdehyde(MDA),and glutathione peroxidase(GSH-Px)were detected by corresponding activity measuring kits.The protein expressions of the TLR4/NF-κB pathway were detected by Western blotting.The results showed that,compared to the model group,mice in both the ginkgolide B medium-and high-dose groups showed less weight loss,longer colon length,lower DAI scores,significantly improved pathological damage of colitis,significantly lower expressions of TNF-α,IL-1β,IL-6,IL-2,and IL-12,significantly higher expression of IL-10,higher levels of SOD and GSH-Px,and lower levels of MDA.In addition,the activation of proteins in the TLR4/NF-κB pathway were inhibited.In summary,ginkgolide B has a significant protective effect on UC,and the mechanism may be related to the inhibition of the activation of TLR4/NF-κB signaling pathway.
作者
梁建云
许金松
金爱莲
赵瑞
LIANG Jianyun;XU Jinsong;JIN Ailian;ZHAO Rui(Department of Pharmacology,Henan Nursing Vocational College,Anyang 455000,China;Department of Clinical Pharmacy,Department of Pharmacy,Anyang Regional Hospital,Anyang 455000,China;Department of Orthopedics,Anyang Regional Hospital,Anyang 455000,China;Department of Cardiology,The First People's Hospital of Shangqiu,Shangqiu 476100,China)
出处
《现代免疫学》
2025年第3期278-283,310,共7页
Current Immunology
基金
河南省医学科技攻关计划项目(LHGJ20209002)。
