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目的研究急性炎症状态下大鼠肝P-糖蛋白翻译后修饰的机制。方法 20只大鼠随机分成2组,模型组10只,对照组10只。模型组予以腹腔单次注射5 mg·kg-1脂多糖,对照组予以腹腔单次注射等体积0.9%氯化钠。24 h后,取肝组织,制备匀浆,分别用Western blot、免疫沉淀法和荧光法检测模型组和对照组的肝P-糖蛋白表达水平、P-糖蛋白泛素化水平和26S蛋白体活性的变化。结果与对照组相比,模型组肝P-糖蛋白蛋白表达水平显著降低(P<0.01),肝P-糖蛋白泛素化水平显著升高(P<0.01),26S蛋白体的活性显著升高(P<0.01)。结论泛素-蛋白酶体途径参与急性炎症状态下大鼠肝P-糖蛋白的下调。
Objective To study the mechanism of posttranslational modification of rat liver P-glycoprotein in acute inflammatory state. Methods Twenty rats were randomly divided into two groups: model group (n = 10) and control group (n = 10). The model group was given intraperitoneal injection of 5 mg · kg-1 lipopolysaccharide, and the control group was given a single intraperitoneal injection of 0.9% sodium chloride. Twenty-four hours later, the liver tissues were harvested and homogenized. The expression of P-glycoprotein, P-glycoprotein ubiquitination and 26S proteasome in model group and control group were detected by Western blot, immunoprecipitation and fluorescence. Changes in activity. Results Compared with the control group, the expression of P-glycoprotein in the model group was significantly lower (P <0.01) and the level of hepatic P-glycoprotein ubiquitination was significantly increased (P <0.01), and the activity of 26S protein body was significantly increased High (P <0.01). Conclusion The ubiquitin-proteasome pathway is involved in the down-regulation of rat liver P-glycoprotein in acute inflammatory state.