海参肠对吲哚美辛诱导的大鼠胃黏膜损伤的保护作用及机制探讨-内科学(消化系病)专业论文.docxVIP

万方数据 万方数据 Abstract AIM: Our study aimed to investigate the protective effects and mechanism of Holothurian intestines(HI) on NSAIDs-induced gastric mucosal damage METHODS: 60 male Wistar rats were randomly divided into 6 groups: the blank control group, the model group, the sucralfate group and the HI groups (low-dose 、 medium-dose 、 high-dose) , 10 rats in each group. The rats were pretreated for 15 consecutive days with saline, sucralfate, or HI prior to IDM treatment. 6 hours later of IDM-indeced gastric mucosal injury, we observed the gastric macroscopic damage, microscopic features and measured the ulcer index. The interleukin-1β (IL-1β), IL-17, tumer neurosis factor-β (TNF-β), TGF-β and prostaglandin E2 (PGE2) in serum were studied. Then total superoxide dismutase (T-SOD), glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), PGE2 and total hexosamine in tissue were measured. The expression of cyclooxygenase (COX) mRNA in the gastric tissue were determined by quantitative polymerase chain reaction (qPCR) RESULTS: The gastric tissues were damaged serious in model group compared with blank group, gastric ulcer indexes, levels of serum pro-inflammatory cytokines (IL-1β, IL-17, TNF-α) and tissue MDA were significantly increased (P0.05). The gastric damage in sucralfate group and HI-treated groups were better, and the above-mentioned indicators were lower than that of rats in the model group (P0.05). Compared with the blank group, the levels of protective factors (TGF-β, SOD activity, GSH, NO, PGE2 and total hexosamine) in gastric tissue in the model group were decreased obviously (P0.05), the obove indicators of rats in sucralfate group and HI-treated groups were all significantly elevated (P0.05, 0.01). The expression of COX-2 mRNA in gastric tissue was increased significantly in model group (P0.05), and decreased significantly in HI groups (P0.05), however, the sucralfate had no obvious influence on it (P0.05); Compared with the blank group, COX-1 mRN