艾灸预处理对应激性溃疡大鼠胃黏膜增殖修复的影响

Effect of pre-moxibustion on proliferation and restoring of gastric mucosa in rats with acute gastric ulcer

目的:观察艾灸预处理对应激性溃疡大鼠胃黏膜损伤后细胞增殖的影响,分析其与胃黏膜血流量(GMBF)、胃黏膜前列腺素E2(PGE2)和转化生长因子α(TGF-α)含量的关系,揭示艾灸足三里、梁门穴促进胃黏膜修复,保护胃黏膜的机制。方法:60只健康SD大鼠随机分为4组,即束缚对照组,模型组,艾灸足三里、梁门穴组,艾灸非穴对照点组。束缚水浸应激法制备胃溃疡模型,采用生物信号分析仪检测MBFG-MBF,放射免疫方法测定PGE2和TGF-α的含量,免疫组织化学方法检测胃黏膜增殖细胞核抗原(PCNA)表达。结果:预先艾灸足三里、梁门穴可显著降低随后的应激性胃黏膜损伤指数,增加MBF、PGE2和TGF-α的含量,增加胃黏膜增殖指数(P<0.05或P<0.01)。结论:艾灸足三里、梁门穴预处理可促进束缚水浸应激所造成大鼠胃黏膜损伤的修复,这一作用可能是通过增加PGE2和TGF-α的含量,改善MBF、促进细胞增殖而实现的。

Objective. Observation the effects on proliferation and restoring of gastric mucosa in rats with acute gastric ulcer by pre-moxibustion, analyze whether this effect is associated to Gastric Mucosa Blood Flow （GMBF）, the content of Prostaglandin E2 （PGE2） and Transforming Growth Factor α（TGF-α）, reveal the mechanism of moxibution at ＂Zusanli＂ and ＂Liangmen＂ to accelerate the repair of gastric mucosal lesion and protecting gastric mucosa. Methods： Sixty healthy SD rats were randomly assigned into 4 groups, named as binding controlgroup（A）, modelgroup （B）. moxibustion at ＂Zusanli＂ and ＂Liangmen＂ （B） and moxibustion at non-acupoints control groups（D）, the animal model of acute gastric ulcer was established by water immersion and restraint stress, the rats in groupA, B, and D served as the restraint, model, and non-accupoint controls, while those in group C received moxibustion at Zusanli and Liangmen. Biological signal analyzer was applied to measure GMBF. The level of PGE2 and TGF-α was detected by radioimmu- noassay. Immunohistochemical method was used to detect the Proliferating Cell Nuclear anti-gen （PCNA） in all the groups. Results： Pre-moxibustion at Zusanli and Liangmen point significantly decreased the gastric mucosal injury index （UI）, increased the GMBF ,the content of PGE2 and TGF-αin gastric mucosa; enhanced expression of PCNA （P〈0.05 or P〈0.01）. Conclusion. Pre-moxibustion at ＂Zusanli＂ and ＂Liangmen＂ could accelerate to restore the gastric mucosa injury by water immersion restraint, the mechanism maybe concern with the increase of content of PGE2 and TGF-αin gastric mucosa , improving GMBF and accelerate gastric mucosal cell proliferation.