论文部分内容阅读
目的探讨酒精对大鼠胃缺血再灌注损伤的影响机制。方法制备胃缺血再灌注及慢性饮酒大鼠模型,实验分为6组:假手术、饮酒假手术、胃缺血再灌注1、2 h组、饮酒胃缺血再灌注1、2 h组,每组6只;记录各组胃黏膜损伤指数并检测胃黏膜丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性;缺口末端标记法(TUNEL)检测胃黏膜细胞凋亡情况。结果缺血再灌注1、2 h后胃黏膜损伤指数分别为(106.0±12.0)和(74.4±11.0),黏膜细胞凋亡率分别为(73.2±6.5)%和(54.0±7.4)%,明显高于假手术组(P<0.05);与假手术组比较,缺血再灌注1 h后胃黏膜MDA含量[(7.98±2.1)nmol/mgprot]明显增加,SOD活性[(141±16.1)U/mgprot]明显降低;饮酒可引起胃黏膜轻微损伤(损伤指数为9.2±0.7),但饮酒并未加剧缺血再灌注带来的胃黏膜损伤,仅使机体自身修复能力降低。结论饮酒可导致SOD活性下降,加剧机体内氧化和抗氧化平衡失调,使胃黏膜自身修复损伤能力降低。
Objective To investigate the mechanism of alcohol on gastric ischemia-reperfusion injury in rats. Methods The model of gastric ischemia-reperfusion and chronic alcohol drinking rats were divided into 6 groups: sham operation, alcohol-drinking sham operation, gastric ischemia-reperfusion 1 and 2 h group, gastric alcohol reperfusion 1 and 2 h group, (N = 6). Gastric mucosal lesion index and gastric mucosal malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured and the apoptosis of gastric mucosal cells was detected by nick end labeling (TUNEL). Results The gastric mucosal lesion indexes were (106.0 ± 12.0) and (74.4 ± 11.0) h after ischemia and reperfusion, respectively. The rates of mucosal apoptosis were (73.2 ± 6.5)% and (54.0 ± 7.4)% (P <0.05). Compared with the sham group, the content of MDA in gastric mucosa increased significantly ([(7.98 ± 2.1) nmol / mgprot] 1 h after ischemia reperfusion and the activity of SOD [(141 ± 16.1) U / mgprot] was significantly lower; alcohol consumption could cause mild gastric mucosal injury (injury index 9.2 ± 0.7), but alcohol consumption did not exacerbate the gastric mucosal injury caused by ischemia-reperfusion, leaving only the body’s ability to repair itself reduced. Conclusion Alcohol consumption can lead to the decrease of SOD activity, exacerbate the imbalance of oxidation and anti-oxidation in the body, and reduce the ability of gastric mucosa to repair itself.