目的:观察慢性低压性缺氧和重组鼠白介素-1β(rmlL-1β)刺激对大鼠颈动脉体(carotid body,CB)中磷酸化细胞外信号调节蛋白激1/2(p-ERKI/2)表达的影响。方法:雄性sD大鼠分为8组,分别为缺氧刺激0、1、2、3周组和缺氧0、1、2、3周的同时伴maiL-1β刺激组。对cB进行免疫组化染色,并用Western Blot法对p-ERK1/2进行半定量分析。结果:相对于缺氧0周组,缺氧2周和缺氧3周组大鼠CB中p-ERKI/2的含量明显增加。相对于单纯给予缺氧,缺氧同时给予maiL-1β刺激后引起大鼠CB体中p-ERKI/2表达量的增加。结论:慢性缺氧和rmIL-1β刺激均可致颈动脉体p-ERK1/2上调;慢性缺氧伴rmIL-1β刺激比单纯缺氧或rmIL-1β刺激可引起P-ERK1/2更显著的增加。
Objective: To observe the effects of chronic hypoxia and systemic administration of recombinant marine in- terleukin-1 beta(rmIL-1β) on the expression of phosphorylated extracelluar sigual-regulated kinase1/2 ( p-ERK1/2 ) in the rat carotid body(CB). Methods: Adult male Sprague-Dawley rats were divided into 8 groups: chronic intermittent hypobaric oxygen stimulation for 0, 1, 2 and 3 weeks groups, and chronic intermittent hypobaric oxygen exposure for 0, 1,2, and 3 weeks paired with rmIL-1βinjection groups. Immunohistochemistry and Western Blot techniques were em- ployed to observe expressions of p-ERK1/2 in the CB of all rats. Results: The expression of p-ERK1/2 in the CB of the rats exposed to hypoxia for 2 weeks or 3 weeks were up-regulated compared with that in group exposed to hypoxia for 0 week. The expression of p-ERK1/2 in the CB of the rats exposed to hypoxia plus rmIL-1βinjection were up-regulated compared with that in group only exposed to hypoxia. Conclusion: Both chronic hypoxia stimulation and rmIL-113 can up- regulate the expression of p-ERK1/2 in the CB ; the combination of hypoxia and rmIL-113 stimulation can significantly en- hance the expression of p-ERK1/2 in CB compared with single treatment by hypoxia or rmIL-1β.