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为研究N-乙酰-L-半胱氨酸(N-acetylcysteine,NAC)减轻大鼠胃缺血/再灌注(gastric ischemia/reperfusion,GI/R)损伤的机制,在大鼠股静脉注射NAC(150mg/kg),夹闭大鼠腹腔动脉30min,再灌注1h制备GI/R模型。取胃后计数胃黏膜损伤指数(gastric mucosal damage index,GMDI),用原位检测(TUNEL)法观察胃黏膜细胞的凋亡,用免疫印迹法测定胃黏膜组织中p-ERK,p-JNK和NF-κB的表达,用RT-PCR法检测TNF-α,Caspase-3的mRNA表达。结果显示,NAC可以减轻GI/R损伤大鼠胃黏膜细胞的凋亡;促进大鼠I/R损伤的胃黏膜组织中p-ERK蛋白的表达,抑制p-JNK和NF-κB的蛋白表达,同时也抑制TNF-α mRNA和Caspase-3 mRNA的表达。股静脉给予辣椒素受体(vanilloid receptor subtype1,VR1)拮抗剂(capsaizepin,CPZ)400mg/kg,能逆转NAC对大鼠GI/R损伤的保护作用。以上结果提示:NAC对大鼠GI/R损伤具有减轻作用,其保护机制可能是通过上调胃黏膜组织中p-ERK,下调p-JNK和NF-κB实现的,且这种保护作用可能与VR1有关。
In order to study the mechanism of N-acetylcysteine (NAC) attenuating gastric ischemia / reperfusion (GI / R) injury in rats, 150mg / kg). The GI / R model was prepared by clamping the celiac artery of rats for 30min and reperfused for 1h. Gastric mucosal damage index (GMDI) was taken after the stomach was taken. The apoptosis of gastric mucosal cells was observed by TUNEL method. The expressions of p-ERK and p-JNK in gastric mucosa were detected by Western blotting The expression of NF-κB and the mRNA expression of TNF-α and Caspase-3 were detected by RT-PCR. The results showed that NAC could alleviate gastric mucosal cell apoptosis induced by GI / R injury, promote the expression of p-ERK protein, and inhibit the expression of p-JNK and NF-κB in I / R injury gastric mucosa, It also inhibited the expression of TNF-α mRNA and Caspase-3 mRNA. The femoral vein administration of capsaizepin (400 mg / kg) to vanilloid receptor subtype 1 (VR1) reversed the protective effect of NAC on GI / R injury in rats. The above results suggest that NAC can reduce the damage of GI / R in rats, and its protective mechanism may be through the upregulation of p-ERK, downregulation of p-JNK and NF-κB in gastric mucosa, and this protective effect may be related to VR1 related.