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20只Wistar雄性大鼠随机分为4组:对照组(生理盐水)、精氨酸组(L-Arg)、NG-硝基-L-精氨酸甲酯组(L-NAME)、L-NAME+L-Arg组。实验结果发现L-Arg作为一氧化氮(NO)的前体物质可以减轻乙醇所致的胃粘膜损伤,L-NAME作为NO合成酶抑制剂可加重乙醇所致的粘膜损伤,而L-NAME+L-Arg组胃粘膜损伤与对照组无显著性差异。证明外源性给予L-Arg可起到保护胃粘膜的作用,而抑制内源性NO合成则加重胃粘膜损害。
Twenty male Wistar rats were randomly divided into 4 groups: control group (saline), arginine group (L-Arg), NG-nitro-L-arginine methyl ester group NAME + L-Arg group. The experimental results showed that L-Arg as a nitric oxide (NO) precursors can reduce ethanol-induced gastric mucosal injury, L-NAME as an NO synthase inhibitor can aggravate ethanol-induced mucosal injury, and L-NAME + There was no significant difference between the L-Arg group and the control group in gastric mucosal injury. Proved that exogenous administration of L-Arg can play a protective role of the gastric mucosa, while inhibiting the endogenous synthesis of NO exacerbate gastric mucosal damage.