牛珀至宝微丸对内毒素休克大鼠肺组织高迁移率族蛋白B1表达的影响

目的：观察牛珀至宝微丸对内毒素休克大鼠肺组织高迁移率族蛋白B1（high-mobility group box-1 protein,HMGB1）表达的影响。 方法：30只SPF级Sprague-Dawley大鼠随机分为正常组、内毒素组和牛珀至宝微丸组。牛珀至宝微丸组大鼠每天以含生药量3mg的牛珀至宝微丸生理盐水悬液3mL灌胃,连续7d,正常组予生理盐水。模型组和牛珀至宝微丸组大鼠用静脉注射内毒素（1.5mg/kg）联合腹腔注射D-氨基半乳糖（100mg/kg）方法建立内毒素休克模型。采用二氨基联苯胺（diaminobenzidine,DAB）显色和异硫氰酸荧光素（fluorescein isothiocyanate,FITC）荧光标记的免疫组织化学染色以及蛋白印迹等方法检测大鼠肺组织内HMGB1的表达。 结果：正常组HMGB1表达较弱,仅有少量细胞呈阳性,阳性部位多在细胞核;内毒素组HMGB1表达增加,阳性部位主要在细胞质;牛珀至宝微丸组HMGB1表达更高,阳性部位主要在细胞核。 结论：牛珀至宝微丸能使HMGB1定位于细胞核内,从而可能避免被分泌出胞,产生毒性,这可能是其治疗感染性休克的作用机制之一。

Effects of Niupo Zhibao Pellet on high-mobility group box-1 protein expression in lung tissues of endotoxin shock rats

Objective： To observe the effects of Niupo Zhibao Pellet, a compound traditional Chinese herbal medicine, on high-mobility group box-1 protein （HMGB1） expression in lung tissues of rats with endotoxin shock.
Methods： Thirty SPF Sprague-Dawley rats were randomly divided into control group, lipopolysaccharide （LPS） group and Niupo Zhibao Pellet group. Rats in Niupo Zhibao Pellet group were consecutively administered 7 days with 3 mL （1 g/L） Niupo Zhibao Pellet saline suspension every day by intragastric administration. Endotoxin shock was induced in rats of theLPSand Niupo Zhibao Pellet groups by intravenous injection of LPS （1.5 mg/kg） and intraperitoneal injection of D-galactosamine （100 mg/kg）. Expression of HMGB1 in lung tissues was measured by immunohistochemical method with diaminobenzidine （DAB） coloration, fluorescein isothiocyanate （FITC） labeling, and by Western blotting. Results： Expression of HMGB1 in lung tissues in the LPS group was increased and that in Niupo Zhibao Pellet group was higher than that in the LPS group and the control group. HMGB1 was presented in the cytoplasm of positive cells in the LPS group, but in the nucleus of positive cells in the Niupo Zhibao Pellet group. However, HMGB1 was little expressed in the lung tissues of normal rats. Conclusion： Niupo Zhibao Pellet can increase HMGB1 expression and locate HMGB1 in the nucleus but not the cytoplasm, which may be one of its mechanisms in reducing endotoxin shock.