慢性缺氧和炎性细胞因子刺激对大鼠颈动脉体中IL-1β表达的影响

THE EFFECTS OF CHRONIC HYPOXIA AND PRO-INFLAMMATORY CYTOKINE STIMULATION ON THE EXPRESSION OF INTERLEUKIN-1β IN THE CAROTID BODY OF THE RAT

采用免疫组织化学染色和图像分析方法观察慢性低压性缺氧和腹腔注射重组鼠IL-1β(rmIL-1β)对颈动脉体中IL-1β表达的影响。雄性SD大鼠20只,随机分为4组:T1组缺氧并腹腔注射rmIL-1β;T2组单纯缺氧;T3组仅腹腔注射rmIL-1β;T4组不缺氧也未腹腔注射rmIL-1β。T1组和T2组采用慢性低压性缺氧模型,大鼠在低压氧舱内连续缺氧2周,每天9h(PB=375Torr)。T3组和T4组也每天放入低压氧舱内9h,但不给予低压缺氧。T1组和T3组在第13d放入低压氧舱前,给予腹腔注射rmIL-1β1000ng/kg,T2组和T4组给予腹腔注射相同体积的生理盐水。第14d四组动物分别在低压缺氧舱中缺氧或常氧处理6h后,注射与前一天相同量的rmIL-1β或生理盐水,然后继续低氧或对照处理3h。处理完毕后麻醉处死动物。结果显示:与未给予缺氧和rmIL-1β刺激的T4组相比,T2组(单纯缺氧组)或T3组(单纯注射rmIL-1β)颈动脉体中IL-1β表达均上调(P<0.05);双因素方差分析的结果表明,缺氧和腹腔注射rmIL-1β之间无交互作用(P>0.05)。以上结果提示:慢性缺氧和炎性细胞因子刺激均可导致颈动脉体内IL-1β的上调,IL-1β可能与颈动脉体的功能调节有关。

The effects of chronic hypoxia and intraperitoneal injection of recombinant murine interleukin-1 β（ rmIL-1β） on the expression of IL-1β in the carotid body were studied by using immunohistochemistry and image analysis. Twenty adult male Sprague-Dawley rats were used and divided into four groups. The rats in the T1 group were exposed to hypoxia and injected with rmIL-1β. The rats in the T2 group and T3 group were only exposed to hypoxia or injected with rmIL-1β, respectively. The rats in the T4 group were exposed to normoxia and not subjected to an injection of rmIL-1β. For producing hypoxia, the rats in T1 and T2 groups were exposed to hypobaric apparatus （PB =375 Torr 9 h per day for consecutive 2 weeks. The rats in T3 and T4 groups were also placed in the apparatus but with a normoxia. At the thirteenth day, before placed in the hypobaric chamber, the rats in T1 and T3 groups received an intraporitoneal injection of rmIL-1β, while the rats in T2 and T4 groups, injection with saline. At the fourteenth day, after exposed to hypobaric hypoxia or normoxia in the chamber for 6 h, the rats in four groups received an injection of rmIL-1β or saline, then continued to be exposed to hypobaric hypoxia or normoxia in chamber for another 3 h and were killed. The results showed that the expression of IL-1β in the carotid body in the T2 group or the T3 group was up-regulated compared with that of the T4 group （ P〈0.05 ）, and there was no interaction between hypoxia and intraperitoneal injection of rmIL-1β （P〉0.05 ）. The above results indicate that either the chronic hypoxia or pro-inflammatory cytokine stimulation can up-regulate the expression of IL-1β in the carotid body. IL-1β might play a role in regulation of carotid body function.