摘要
目的 探讨茯苓酸(PA)对大鼠幽门螺旋杆菌(Hp)相关性胃炎的治疗效果及作用机制。方法 建立Hp相关性胃炎大鼠模型;所有大鼠分为对照组(CT组)、模型组(M组)、PA低剂量组(PA L组)和PA高剂量组(PA H组)、PA H+磷脂酰肌醇3-激酶(PI3K)激活剂(740 Y-P)组;评估各组大鼠胃黏膜损伤指数(UI),透射电子显微镜观察胃黏膜细胞形态学,HE染色评价胃黏膜病理学特征,ELISA检测胃组织白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、IL-10、诱导型一氧化氮合酶(iNOS)、超氧化物歧化酶(SOD)的水平,Western blot法检测PI3K、磷酸化-PI3K(p-PI3K)、蛋白激酶B(AKT)、p-AKT、核因子(NF)-κB p65、p-NF-κB p65蛋白表达。结果 与CT组比较,M组大鼠胃黏膜糜烂,上皮水肿、充血、溃疡严重,上皮细胞固缩,炎性细胞浸润,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平升高,IL-10和SOD水平降低(P<0.05);与M组比较,PA L组、PA H组大鼠胃黏膜损伤改善,炎性细胞浸润减少,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平降低,IL-10和SOD水平升高(P<0.05);与PA H组比较,PA H+740 Y-P组大鼠胃黏膜病理损伤加重,上皮细胞固缩,UI、IL-6、TNF-α、iNOS以及p-PI3K/PI3K、p-AKT/AKT、p-NF-κB p65/NF-κB p65蛋白表达水平升高,IL-10和SOD水平降低(P<0.05)。结论 PA可能通过抑制PI3K/AKT/NF-κB信号通路发挥对大鼠Hp相关性胃炎的治疗作用。
Objective To explore the therapeutic effect and mechanism of pachymic acid(PA)on Helicobacter pylori(Hp)-associated gastritis in rats.Methods A rat model of Hp-associated gastritis was established;all rats were separated into control group(CT group),model group(group M),PA low-dose group(PA L group),PA high-dose group(PA H group),and PA H+phosphatidylinositol 3-kinase(PI3K)activator(740 Y-P)group;the gastric mucosal injury index(UI)of rats in each group was evaluated,transmission electron microscopy was applied to observe the morphology of gastric mucosal cells.HE staining was applied to evaluate the pathological characteristics of gastric mucosa.ELISA was applied to detect the levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),IL-10,inducible nitric oxide synthase(iNOS),and superoxide dismutase(SOD)in gastric tissue.Western blot method was applied to detect the expression of PI3K,phosphorylated PI3K(p-PI3K),protein kinase B(AKT),p-AKT,nuclear factor(NF)-κB p65,and p-NF-κB p65 proteins.Results Compared with the CT group,the gastric mucosa erosion,epithelial edema,congestion,and severe ulcers were observed in the group M,with epithelial cell pyknosis and inflammatory cell infiltration,the UI,IL-6,TNF-α,iNOS,and the expression levels of p-PI3K/PI3K,p-AKT/AKT,p-NF-κB p65/NF-κB p65 proteins increased,the levels of IL-10 and SOD decreased(P<0.05);compared with group M,the gastric mucosal damage and inflammatory cell infiltration in the PA L and PA H groups were improved,the UI,IL-6,TNF-α,iNOS by the host animal and the expression of p-PI3K/PI3K,p-AKT/AKT,p-NF-κB p65/NF-κB p65 proteins all decreased,the level of IL-10 and SOD was increased(P<0.05);compared with the PA H group,the pathological damage of the gastric mucosa in the PA H+740 Y-P group was aggravated,with epithelial cell pyknosis.The UI,IL-6,TNF-α,iNOS,and the expression of p-PI3K/PI3K,p-AKT/AKT,p-NF-κB p65/NF-κB p65 proteins increased,the levels of IL-10 and SOD decreased(P<0.05).Conclusions PA might facilitate the treatment of Hp-associated gastritis in rats by inhibiting the PI3K/AKT/NF-κB signaling pathway.
作者
徐璐
张冬雨
王瑞锋
XU Lu;ZHANG Dongyu;WANG Ruifeng(Department of Clinical Laboratory,Zhengzhou Key Laboratory of Child Infection and Immunity,Children′s Hospital Affiliated to Zhengzhou University/Henan Children′s Hospital Zhengzhou Children′s Hospital,Zhengzhou 450000,China;Department of Gastroenterology,Children′s Hospital Affiliated to Zhengzhou University/Henan Children′s Hospital Zhengzhou Children′s Hospital,Zhengzhou 450000,China)
出处
《基础医学与临床》
CAS
2024年第4期489-495,共7页
Basic and Clinical Medicine
基金
河南省医学科技攻关计划项目(LHGJ20220763)。
关键词
茯苓酸
幽门螺旋杆菌相关性胃炎
磷脂酰肌醇3-激酶/蛋白激酶B/核因子-κB信号通路
pachymic acid
Helicobacter pylori-associated gastritis
phosphatidylinositol 3-kinase/protein kinase B/nuclear factor-κB signaling pathway(PI3K/AKT/NF-κB)
