摘要
目的:采用幽门螺旋杆菌脂多糖诱导的胃炎动物模型考察黄连总生物碱(TA)对黏膜炎症反应的作用及可能机制。方法:幽门螺旋杆菌脂多糖(Helicobacter pyloriLPS)灌胃,连续4 d即可引起急性胃炎的黏膜反应症状,分组给予50,100,200 mg.kg-1TA后,组织学观察病变及用药后的改善情况;一氧化氮合酶检测试剂盒检测TA对组成型(cNOS)和诱导型(NOS-2)一氧化氮合酶的影响;肿瘤坏死因子(TNF-α)检测试剂盒测定TA对胃黏膜TNF-α生成的影响。结果:H.pyloriLPS可显著刺激胃黏膜上皮细胞凋亡,增强黏膜组织NOS-2的表达,并降低cNOS的表达,同时增加血清中TNF-α含量。高、中、低剂量TA可显著降低H.pyloriLPS诱导的胃黏膜上皮细胞凋亡发生,同时抑制NOS-2的表达,增强cNOS的表达,并抑制血清中TNF-α的含量。结论:TA对H.pyloriLPS引起的大鼠胃部炎症有保护作用,其机制可能是由于TA抑制胃炎时黏膜细胞的凋亡有关,同时TA可通过影响cNOS和NOS-2的表达调节NO的生成,并抑制TNF-α生成,从而减轻胃部炎症反应的发生。
Objective： To study the effects and its possible mechanisms of total alkaloids （TA） from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats. Method： H. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100,200 mg·kg^-1 TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-α and the gastric mucus epithelial cell apoptosis. Result： H. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-α in serum. Treatment with 50, 100, 200 mg·kg^-1 TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-α in serum, decline in NOS-2, and increase in cNOS. Conclusion： The findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammarion. The concerned mechanisms may be relaled to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregnlating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-α.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2007年第13期1333-1336,共4页
China Journal of Chinese Materia Medica
