中文摘要：

目的：观察慢性低压性缺氧和／或重组鼠白介素-1β（traiL-1β）刺激对大鼠颈动脉体（carotidbody，CB）中酪氨酸羟化酶（ty．rosinehydroxylase，TH）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rmlL-1β刺激组。对CB进行免疫组化染色，并用westernblot法对TH进行半定量分析。结果：相对于缺氧0周组，缺氧1周、缺氧2周和缺氧3周组大鼠CB中TH的含量明显增加。相对于正常大鼠，rmlL-1β刺激引起大鼠CB中TH表达量增加。相对于单纯给予缺氧1周和缺氧2周，缺氧1周和缺氧2周同时给予mlL-1β刺激后引起大鼠CB中TH表达量的增加。结论：慢性缺氧和rmlL-1β刺激均可致颈动脉体TH上调，慢性缺氧伴rmlL-1β刺激比单纯缺氧刺激可引起TH更显著的增加。这个结果提示慢性缺氧或促炎性细胞因子tL-1β刺激不仅能够分剐促进颈动脉体中儿茶酚胺类物质的合成。而且IL-1β刺激可以促进慢性缺氧时颈动脉体中儿茶酚胺类物质的合成。这说明促炎性细胞因子可能对大鼠颈动脉体的慢性缺氧感受发挥调节作用。

英文摘要：

Objective： To observe the effects of chronic hypoxia and/or systemic administration of recombinant routine inter- leukin-1 beta （maiL-113） on the expression of tyrosine hydroxylase （TH） in the rat carotid body （CB）. Methods： Adult male Sprague-Daw- ley rats were divided into 8 groups： chronic intermittent hypobaric oxygen stimulation for 0, 1, 2 and 3 w groups, and chronic intermittent hypobaric oxygen exposure for 0, 1, 2, and 3 w paired with rmIL-1βinjection groups. Immtmohistochemistry and Western blotting tech- niques were employed to observe expressions of TH in the CB of all rats. Results： The expression of TH in the CB of the rats exposed to hypoxia for 1 w, 2 w or 3 w were up-regulated compared with that in group exposed to hypoxia for 0 w. Compared with normal rat, maiL-α can up-regulate the expression of TH in the CB. The expression of TH in the CB of the rats exposed to hypoxia for 1 w or 2 w plus rmIL-1β injection were up-regulated compared with that in groups only exposed to hypoxia for 1 w or 2 w. Conclusion： Both chronic hypoxia stimulation and maiL-1βcan up-regulate the expression of TH in the CB. The expression of TH in the CB of the rats exposed to hypoxia plus traiL-1βinjection were up-regulated compared with that in group only exposed to hypoxia. The result shows that either chronic hypoxia or proinflammatory cytokine IL-1β stimulation can promote the synthesis of catecholamines in the carotid body, and IL-1β can further promote the synthesis of catecholamines in the carotid body when the rats were exposed to chronic hypoxia. Proinflam- matory cytokine might play a regulative role in the function of the carotid body sensing chronic hypoxia.