黄芪对失血性休克再灌注肠黏膜肥大细胞活性及肠黏膜炎症反应的影响

目的：探讨黄芪对失血性休克再灌注后肠黏膜肥大细胞活性及肠黏膜炎症反应的影响。方法：Wistar大鼠32只,随机分成正常组、模型组、黄芪高,低剂量组(20,10 g·kg_-1)。复制重度失血性休克及复苏动物模型,观察各组动物肠黏膜病理学变化,测定小肠组织丙二醛(MDA)、肿瘤坏死因子(TNF-α)及组胺浓度和超氧化物歧化酶(SOD)活性,观察肠黏膜肥大细胞(intestinal mucosal mast cells,IMMC)数量及超微结构变化。结果：模型组Chiu’s评分,类胰蛋白酶表达,IMMC数目,MDA,TNF-α明显升高及SOD活性、组胺明显降低且出现明显脱颗粒现象；黄芪能减轻上述变化(P<0.05)。相关分析显示Chiu’s评分与小肠组胺浓度呈负相关,与TNF-α浓度呈正相关,SOD活性与组胺浓度呈正相关(P<0.05)。结论：黄芪注射液能减轻大鼠失血性休克再灌注肠黏膜损害,可能与抑制肥大细胞活化有关。

Effect of astragalus membranacaus injection on activity of intestinal mucosal mastcells and inflammatory response after hemorrahagic shock-reperfusion in rats

OBJECTIVE: To observe the effects of astragalus membranacaus injection on the activity of the intestinal mucosal mast cells (IMMC) and inflammatory response after hemorrahagic shock-reperfusion in rats. METHOD: Thirty-two Wistar rats were randomly divided into four groups: normal group, model group, low dosage group, (treated with astragalus membranacaus 10 g kg(-1)) and high dosage group (treated with astragalus membranacaus 20 g kg(-1)). Models of hemorrhage shock for 60 minutes and reperfusion for 90 minutes were created. The animals were administrated 3 mL therapeutic solution before reperfusion. At the end of study, intestinal pathology, ultrastructure of IMMC, and expression of tryptase were observed. The levels of MDA, TNF-a, histamine, and SOD activity of intestinal were detected, and the number of IMMC was counted. RESULT: The degranulation of IMMC was seen in model group and was attenuated by astragalus membranacaus treatment. Chiu's score of model group was higher than that of the other groups. Astragalus membranacaus could attenuate the up-regulation of the Chiu' s score, the levels of MDA and TNF-alpha, expression of tryptase, and the down-regulation of SOD activity and histamine concentration. The Chiu's score and MDA content were negatively, while SOD activity was positively correlated to the histamine concentration respectively in the four groups. CONCLUSION: Astragalus membranacaus can reduce small intestine mucosal damage by inhibiting the activity of IMMC after hemorrhage shock reperfusion.