Ghrelin在地塞米松诱发小鼠胸腺应激性萎缩中的变化

摘要

目的：观察应激状态下胸腺组织内胃饥饿素(Ghrelin)的变化,为进一步探讨Ghrelin对胸腺细胞凋亡的影响提供±据。方法 BALB/c小鼠成年雄性32只,随机均分为4组院正常对照组、地塞米松(Dex)-6 h组、Dex-12 h组和Dex-24 h组,每组各8只。用Dex腹腔注射(5 mg/kg)诱发小鼠胸腺应激性萎缩模型,正常对照组给予等量生理盐水腹腔注射。用酶免疫分析法(EIA)检测各组小鼠胸腺组织匀浆中Ghrelin含量。结果与正常对照组相比,Dex-6 h组、Dex-12 h组和Dex-24 h组小鼠胸腺重量均有不同程度下降,其中Dex-24 h组最为明显；胸腺组织匀浆Ghrelin的EIA检测结果表明,与正常对照组比较,Dex-6 h组、Dex-12 h组和Dex-24 h组小鼠胸腺组织匀浆中Ghrelin含量均增加[(5.67±1.41)ng/g比(6.94±1.80)、(8.43±2.06)、(13.59±2.39)ng/g],其中Dex-24 h组与其他三组间比较,差异均有高度统计学意义(均P<0.01)。结论 Dex诱发小鼠胸腺应激性萎缩过程中Ghrelin表达上调,为进一步探讨Ghrelin对胸腺生物学功能的调节作用提供了实验±据。%Objective To observe the alteration of Ghrelin levels in stress-related thymic atrophy in the mice, and to provide the evidence for further exploring the effects of Ghrelin on thymic cell apoptosis. Methods 32 adult male BALB/c mice were randomly divided into four groups:normal control group, Dexamethasone (DEX)-6h treated group, DEX-12h treated group and DEX-24h treated group, 8 mice in each group. The intraperitoneal injection of Dexam-ethasone(5mg/kg) was used to induce the thymic atrophy in mice, and the mice in normal control group received nor-mal saline intraperitoneal injection. Enzyme-immunoassay (EIA) was used to evaluate the Ghrelin concentration in thy-mus homogenates from different experimental animals. Results Compared with normal control group, there were differ-ent degree of decline in DEX-6h treated group, DEX-12h treated group and DEX-24h treated group, with the most deleterious effect observed in the DEX-24h treated group. EIA test of Ghrelin in thymus tissue homogenate show that, compared with normal control group, the Ghrelin concentration in DEX-6h treated group, DEX-12h treated group and DEX-24h treated group thymus homogenates was gradually increased during the recovery after Dexamethasone injec-tion [(5.67±1.41) ng/g vs (6.94±1.80), (8.43±2.06), (13.59±2.39)ng/g], with the maximum level detected at the 24h af-ter Dexamethasone treatment, the differences were statistically significant (all P<0.01). Conclusion The expression level of Ghrelin was up-regulated in Dexamethasone-induced thymic atrophy model. This study lays the foundation for the further exploration of the possible role of Ghrelin in the regulation of the thymic biological function.