安胃汤对慢性萎缩性胃炎大鼠模型Bcl-2及NF-κB表达的影响

Effect of Anwei Decoction on expression of Bcl-2 and NF-κB in Rats with Chronicatrophic Gastritis

目的:探讨安胃汤治疗CAG的机制。方法:将84大鼠随机分为空白组、模型组、治疗组(大、中、小剂量组)、对照组(维酶素、胃复春),每组各12只。采用MNNG慢性萎缩性胃炎大鼠模型,用RT-PCR法测定大鼠胃粘膜组织及血液中Bcl-2及NF-κB含量的表达。结果:安胃汤治疗各组和胃复春组与病理组相比,胃粘膜Bcl-2基因的表达量均明显升高,有极显著性差异(P<0.01),安胃汤中剂量组Bcl-2基因的表达量与维酶素组相比差异有显著性(P<0.05);安胃汤中、大剂量组大鼠外周血淋巴细胞中Bcl-2基因的表达量与病理组相比显著升高,差异有显著性(P<0.05);安胃汤中、大剂量组大鼠外周血淋巴细胞中NF-κB基因的表达量与病理组相比显著升高,差异有显著性(P<0.01或P<0.05)。结论:安胃汤能明显降低Bcl-2mRNA及NF-kBmRNA在大鼠胃黏膜及血液中的表达,调节促进细胞凋亡,增强黏膜屏障的防御和修复的功能,可能是治疗CAG的机制之一。

Objective： To investigate the mechanism of Anwei Decoction in the treatment of chronic atrophic gastritis （CAG）. Methods ： Eighty four rats were randomly divided into blank group, model group, treatment group （ high, medium, low dose group） , controlled group （Weimeisu, Weifuchun） , with 12 rats in each group. CAG was inducedin rats with N-methy-N-nitro-N-nitroguanidine （MNNG）. The expression of Bcl-2, NF-κBmRNAs in rat gastric mucosa and blood were determined by reahimepolymerase chain reaction （PCR）. Results： Anwei Decoction treatment group and Weifuchun group compared with the pathologic group, the expression of Bel-2gene in gastric mncosa were significantly increased, with a significant difference （P 〈0. 01 ）, compared with the Weimeisu group, the expression of Bcl-2 gene of Anwei Decoction medium dose group was a significant difference （ P 〈0. 05 ） ; Bcl-2 gene in the high dose group of rat peripheral blood lymphocytes of expression were significantly increased compared with the pathological group, there was significant difference （P 〈0. 05）; NF-κB gene of Anwei Decoction, high dose group of rat peripheral blood lymphoeytes of expression were significantly increased compared with the pathological group, there was significant difference （P 〈0. 01 or P 〈0. 05 ）. Conclusion： Anwei Decoction can obviously reduce the expression of Bcl-2mRNA and NF-κBmRNA in gastric mucosa and blood of rats, regulate apoptosis, enhance defense and repair mucosal barrier function, may be one of the mechanisms in the treatment of CAG.