蒙古族药阿给炭对胃溃疡大鼠溃疡组织VEGF,bFGF及其受体mRNA表达的影响

Effect of Mongolian Drug Charred Arteisia frigida on mRNA and Protein Expression of VEGF / VEGF Receptor and b FGF / b FGF Receptor of Peptic Ulcer in Rats

目的:研究蒙古族药阿给炭对应激型胃溃疡模型大鼠溃疡组织血管内皮生长因子(VEGF),碱性成纤维细胞生长因子(b FGF)及其受体mRNA表达的变化,探讨阿给炭促进胃溃疡愈合的分子机制。方法:84只SD大鼠分为7组,即正常组,模型组,阳性药云南白药组(0.18 g·kg-1),阿给生药组(1.35 g·kg-1),阿给炭药低、中、高剂量组(0.9,1.35,1.8 g·kg-1),除正常组外,其余各组采用水浸束缚应激方法复制急性胃溃疡大鼠模型。连续给药1周后,常规处死动物,剪取胃部溃疡组织,采用Western blot及RT-PCR技术检测VEGF及VEGF受体(VEGFR),b FGF及b FGF受体(b FGFR)mRNA及蛋白表达水平。结果:与正常组比较,急性应激性溃疡导致大鼠溃疡组织b FGF(P<0.01)和b FGFR(P<0.05)蛋白表达水平显著降低。与模型组比较阿给炭低剂量组明显升高了大鼠溃疡组织VEGF mRNA(P<0.05)以及VEGF和VEGFR蛋白表达(P<0.05),但无剂量相关性;其他各组与模型组无差异;中剂量、高剂量阿给炭和云南白药显著升高b FGF的蛋白表达(P<0.01),高剂量阿给炭同时也升高了b FGF和b FGFR mRNA(P<0.01)和b FGFR蛋白表达(P<0.05)。结论:阿给炭促进胃溃疡愈合的分子机制可能与上调VEGF及其受体蛋白,b FGF及其受体蛋白有关,对VEGF,b FGF和b FGFR的调控是在转录水平,对VEGFR的调控是在后转录水平。

Objective： To study the effect of charred Arteisia frigida on the change of mRNA expressions of vascular endothelial growth factors（ VEGF）,basic fibroblast growth factors（ b FGF） and their receptors in ulcer tissues of stress gastric ulcer model rats,and investigate the molecular mechanism for charred A. frigida to promote the healing of gastric ulcers. Method： 84 SD rats were randomly divided into 7 groups,named control group,model group,Yunnanbaiyao group（ Positive drug,0. 18 g · kg^-1）,A. frigida crude drug group（ 1. 35 g ·kg^-1）,low dose charred A. frigida group,middle dose charred A. frigida group and high dose charred A. frigida group（ 0. 9,1. 35,1. 8 g · kg^-1）. Water-immersion stress method was used in all other groups except normal group to establish rat models of cute gastric ulcer. After intragastric administration for one continuous week,stomach ulcer tissues were scissored from the conventionally sacrificed animals. Western blot and RT-PCR technique were used to detect mRNA and protein expressions of VEGF and its receptor VEGFR,b FGF and its receptor b FGFR. Result： Compared with the normal group,ulcer tissues in rats with acute stress ulcer had significantly decreased b FGF（ P〈0. 01） and b FGFR（ P〈0. 05） protein expressions. Compared with the model group,charred A. frigida low dose group significantly increased VEGF mRNA expression（ P〈0. 05）,VEGF protein expression VEGFR protein expression（ P〈0. 05）,but without dose dependence; no difference was found between the other groups and the model group. charred A. frigida middle dose group,high dose group and Yunnanbaiyao group significantly increased b FGF protein expression（ P〈0. 01）,and charred A. frigida high dose group also increased b FGF mRNA expression, b FGFR mRNA expression（ P〈0. 01） and b FGFR protein expression（ P〈0. 05）. Conclusion： The molecular mechanism for charred A. frigida to promote the healing of gastric ulcers may be associated with up-regulation of VEGF and VEGFR protein expressions,b FGF and b FGFR protein expressions. The regulation of VEGF,b FGF,and b FGFR is at the level of transcription,and the regulation of VEGFR is at the post-transcriptional levels.