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目的观察外源性褪黑素对缺氧缺血性脑损伤(HIBD)新生大鼠干预后不同时间点肾上腺组织中褪黑素受体1及糖皮质激素受体mRNA和血浆皮质酮水平的变化。方法7日龄SD大鼠随机分为治疗组、模型组、假手术组和正常组。常压低体积分数氧建立HIBD模型。治疗组新生大鼠腹腔注射褪黑素10mg/kg;模型组和假手术组新生大鼠注射乙醇载体溶液(0.05g/L)10mg/kg;正常组不作任何干预。各组分别于HIBD完成2、4、8、12、24、48h6个时间点摘取其肾上腺组织,采用反转录多聚酶链式反应法半定量测定各组褪黑素受体1及糖皮质激素受体mRNA的表达;暴露心脏,右心室采血,采用放射免疫分析法检测各组血浆皮质酮水平。结果模型组2h肾上腺组织中褪黑素受体1及糖皮质激素受体mRNA表达下调,血浆皮质酮水平显著升高,4h达高峰(Pa<0.05);治疗组血浆皮质酮及肾上腺组织中褪黑素受体1变化均不明显(Pa>0.05),糖皮质激素受体在24h恢复正常生理水平。结论缺氧缺血应激反应刺激下丘脑-垂体-肾上腺皮质系统过度兴奋,引发机体的应激损伤,血浆皮质酮和肾上腺组织的糖皮质激素受体参与HIBD的病理生理过程,外源性褪黑素可能通过自身受体调控应激激素,降低内源性皮质酮水平,使糖皮质激素受体表达上调,减轻HIBD后的过度应激损伤。
Objective To observe the changes of melatonin receptor 1, glucocorticoid receptor mRNA and plasma corticosterone in adrenal glands at different time points after exposure to exogenous melatonin in neonatal rats with hypoxic-ischemic brain damage (HIBD) . Methods 7-day-old SD rats were randomly divided into treatment group, model group, sham operation group and normal group. HIBD model was established by atmospheric pressure and low volume fraction of oxygen. Neonatal rats in the treatment group were intraperitoneally injected with 10 mg / kg of melatonin. Neonatal rats in the model group and sham operation group were injected with 10 mg / kg of ethanol vehicle solution (0.05 g / L). Normal rats received no intervention. The adrenal tissues were harvested at 6, 8, 12, 24, and 48 h after HIBD treatment respectively. The levels of melatonin receptor 1 and glucocorticoids were determined by semi-quantitative reverse transcriptase-polymerase chain reaction Receptor mRNA expression; exposed heart, right ventricle blood collection, radioimmunoassay to detect plasma corticosterone levels in each group. Results The expression of melatonin receptor 1 and glucocorticoid receptor mRNA in the adrenal gland of model group was down-regulated at 2 hours, and the plasma corticosterone level was significantly increased at 4 hours (P <0.05). The corticosterone and adrenal tissue faded Melanocyte receptor 1 changes were not significant (Pa> 0.05), glucocorticoid receptor returned to normal physiological levels at 24h. CONCLUSION: Hypoxia-ischemic stress stimulates hyperactivity in hypothalamus-pituitary-adrenal system and triggers stress injury. Glucocorticoid receptor in plasma corticosterone and adrenal gland is involved in the pathophysiological process of HIBD. Melanin may regulate stress hormones through its own receptors, reduce the level of endogenous corticosterone, up-regulate the expression of glucocorticoid receptor and reduce the excessive stress injury after HIBD.