目的:观察舒芬太尼对浸水束缚应激(WIRS)导致的大鼠急性胃黏膜病变(AGML)的保护作用以及对下丘脑、胃黏膜TRPV1 mRNA的影响。方法:选取雄性SPF级Wistar大鼠30只,随机分为3组,正常组(NC组,n=10)、浸水束缚应激模型组(WIRS组,n=10)和舒芬太尼预先给药组(SF组,n=10)。采用WIRS法复制AGML模型,于应激6 h后取胃观察胃黏膜大体损伤情况,计数胃黏膜损伤溃疡指数(UI)、胃液 pH,并采用实时荧光定量PCR法对各组下丘脑及胃黏膜内TRPV1 mRNA进行实时定量检测;检测各组血清中超氧化物歧化酶(SOD)、丙二醛(MDA)的水平。结果:与正常组比较,WIRS 组胃黏膜损伤明显,UI、MDA含量显著升高(P<0.05),SOD活力变化不明显;TRPV1 mRNA在胃黏膜内的表达显著降低(P<0.05)。 SF 由WIRS导致的AGML 明显减轻,UI 和血清MDA含量降低,下丘脑、胃黏膜TRPV1 mRNA的表达(P<0.05)。结论:舒芬太尼预先给药可有效减轻WIRS诱导的急性胃黏膜损伤,其机制可能与控制机体氧化应激反应、减少胃酸分泌以及调控中枢和外周TRPV1的表达有关。%Objective To observe the protective effect of sufentanil pretreatment on the rats with acute gastric mucosa lesion (AGML) induced by water immersion and restrain stress (WIRS) and its effect on TRPV1 mRNA expression in the hypothalamus and gastric mucosa. Methods Thirty male Wistar rats were randomly designed into 3 groups, including the normal control group (Group NC, n = 10), the group treated with WRIS for 6 h (Group WIRS, n = 10) and the group pretreated with sufentanil (Group SF, n = 10). The model of AGML was established by the classic WIRS method , and observed for the general extent of gastric mucosal injury at WIRS for 6 hr, and calculated gastric mucosal injury ulcer index (UI) and the PH value of gastric juice; The quantification of TRPV1 mRNA expression in hypothalamus and gastric mucosa was performed using quantitative real-time PCR; In addition, the activity of super oxide dismutase (SOD) and the level of malondialdehyde (MDA) in serum were detected. Results Compared with group NC, gastric mucosal in Group WIRS was injured more seriously , and the UI and the activity of MDA were also obviously increased , but the change of SOD activity was not apparent; The TRPV1 expression in gastric mucosal decreased apparently. Sufentanil pretreatment could effectively relieve gastric mucosal injury induced by WIRS , and make the UI and the activity of MDA decreased , and up-regulate TRPV1 mRNA expression in the hypothalamus and gastric mucosa. Conclusions Sufentanil pretreatment can effectively relieve AGML induced by WIRS , which may be related to the control of oxidative stress response , the reduced gastric acid secretion , and the upregulation of the TRPV1 mRNA expression in the central and periphera nerve.
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