褪黑素对枪击噪音应激大鼠胃黏膜损伤的影响及机制

Effect of melatonin on gunfire noise stress-induced gastric mucosal lesions in rats and its mechanism

目的:研究褪黑素(MT)对噪音应激大鼠胃黏膜损伤的影响及其可能机制.方法:将14只SD大鼠随机分为两组:实验组(模型+MT腹腔注射)和对照组(模型+生理盐水腹腔注射).以56式冲锋枪射击时产生的噪音为心理应激源,建立心理应激模型.于应激前30min两组分别腹腔注射MT(15mg/kg)和等体积生理盐水.120dB枪击噪音应激8h后,利用放射免疫分析及组织化学的方法,测定各组血浆降钙素基因相关肽(CGRP),胃动素(MTL),丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的活性;观察胃黏膜损伤情况,测定胃黏膜损伤指数并观察胃黏膜的组织学改变.结果:实验组与对照组比较,胃黏膜损伤明显减轻,胃黏膜损伤指数显著降低(P<0.01),血浆CGRP含量、SOD活性显著升高(分别为P<0.05和P<0.01),血浆MTL,MDA含量显著降低(P<0.05).结论:MT对噪音应激性胃黏膜损伤有保护作用,其机制可能与MT改善胃黏膜血流、清除胃黏膜自由基、抑制胃蠕动和胃酸分泌有关.

AIM： To explore the effect of melatonin （MT） on gunfire noise stress-induced gastric mucosal lesions in rats and its mechanism. METHODS： Fourteen SD rats were divided into 2 groups： experimental group （gunfire noise stress ＋ MT ）, control group （gunfire noise stress ＋ sodium chloride ）. The 120 dB gunfire noise was applied to establish psychological stress model in rats. Experimental group and control group were given intraperitoheal injection of MT （ 15 mg/kg） and equal volume sodium chloride , respectively, 30 min before stress. Eight hours after stress, plasma levels of calcitonin gene-related peptide（ CGRP）, motilin （ MTL ）, malondialdehyde （ MDA ） and superoxide dismutase （SOD） were measured by the radioimmunoassay and histochemical method. The gastric mucosal changes in each group were observed, and the mucosal lesion index, histological changes were evaluated. RESULTS： The mucosal damage 8 h after stress was slighter in the experimental group than that in the control group. The mucosal lesion index decreased significantly （P 〈0.01 ）, the plasma levels of CGRP and SOD both increased significantly （P 〈 0.05 and P 〈 0. 01 respectively）, the plasma levels of MTL and MDA both decreased significantly （P 〈 0.05 ） in the experimental group as compared with those in the control group. CONCLUSION： MT is effective in preventing noise stressinduced gastric mucosal lesion. The mechanism may be related with the increase of gastric mucosal blood flow, the elimination of gastric mucosal free radical and the depression of gastric motor and the secretion of gastric acid by MT.