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目的:观察慢性低压性缺氧和/或重组鼠白介素-1β(rmIL-1β)刺激对大鼠颈动脉体(carotid body,CB)中酪氨酸羟化酶(tyrosine hydroxylase,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rmIL-1β刺激组。对CB进行免疫组化染色,并用western blot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,rmIL-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rmIL-1β刺激后引起大鼠CB中TH表达量的增加。结论:慢性缺氧和rmIL-1β刺激均可致颈动脉体TH上调,慢性缺氧伴rmIL-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IL-1β刺激不仅能够分别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。
AIM: To observe the effect of chronic hypobaric hypoxia and / or recombinant murine interleukin-1β (rmIL-1β) on tyrosine hydroxylase (TH) expression in carotid body (CB) of rats . Methods: Male SD rats were divided into 8 groups: hypoxia-stimulated group 0, 1, 2, 3 and hypoxia 0, 1, 2, and 3 weeks combined with rmIL-1β stimulation group. Immunohistochemical staining of CB was performed and semi-quantitative analysis of TH was performed by western blot. Results: Compared with 0 week group, the content of TH in CB of hypoxia group was significantly increased at 1 week hypoxia, 2 weeks hypoxia and 3 weeks hypoxia. RmIL-1 [beta] stimulation caused an increase in TH expression in rat CB relative to normal rats. Compared with the simple administration of hypoxia for 1 week and hypoxia for 2 weeks, hypoxia for 1 week and hypoxia for 2 weeks simultaneously given rmIL-1β stimulation induced increased expression of TH in rat CB. CONCLUSION: Chronic hypoxia and rmIL-1βhad both up-regulated TH in carotid artery. Chronic hypoxia with rmIL-1βstimulation induced a more significant increase of TH than simple hypoxic stimulation. This result suggests that chronic hypoxia or proinflammatory cytokine IL-1β stimulation can not only promote the synthesis of catecholamines in the carotid body, respectively, but that IL-1β stimulation can promote the synthesis of catecholamines in the carotid body during chronic hypoxia . This suggests that proinflammatory cytokines may play a regulatory role in chronic hypoxia in the carotid body of rats.