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目的研究肥胖诱导的雄性小鼠生殖系统炎症反应以及相关分子机制。方法建立肥胖小鼠模型。通过Real-time PCR检测其睾丸和附睾内促炎细胞因子白细胞介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(tumor necrosis factor,TNF-α),炎症小体3(NOD-like receptor family pyrin domain containing-3,NLRP3)的m RNA表达水平,运用HE染色观察肥胖小鼠睾丸组织的结构变化,采用ELISA实验检测小鼠血清中性激素,IL-6,TNF-α,皮质酮,免疫球蛋白G(immunoglobulin G,Ig G)以及免疫球蛋白M(Immunoglobulin M,Ig M)浓度变化,最后通过Western blot检测肥胖小鼠睾丸中炎症反应相关信号通路蛋白p38,核转录因子-κB(nuclear factor-κB,NF-κB),细胞外调节蛋白激酶(extracellular signal-regulated kinase,ERK),c-Jun氨基末端激酶(Jun N-terminal kinase,JNK)的含量变化。结果与正常组小鼠相比,肥胖小鼠睾丸和附睾内IL-6,TNF-α和NLRP3的含量显著上升,肥胖小鼠血清中性激素水平紊乱,表现为雌激素水平上升,睾酮和孕酮水平下降。血清中IL-6、TNF-α、皮质酮、Ig G和Ig M浓度也明显增高。此外,肥胖小鼠睾丸发育异常,且睾丸中p38、NF-κB、ERK和JNK含量显著上升。结论肥胖会诱导雄性小鼠睾丸和附睾发生炎症反应,而该炎症反应可导致小鼠生育力的损伤。
Objective To study the reproductive system inflammatory response and its molecular mechanism in obesity-induced male mice. Methods Obesity mouse model was established. Real-time PCR was used to detect the expression of pro-inflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor (TNF-α) and inflammasome 3 The expression of m RNA of NOD-like receptor (NLRP3) and NO in the obese mice were detected by HE staining. The changes of serum testosterone, IL-6, TNF-α, Corticosterone, immunoglobulin G (Ig G) and immunoglobulin M (Ig M) were detected by Western blotting. The expressions of p38, NF-κB, (NF-κB), extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) Results The levels of IL-6, TNF-α and NLRP3 in testis and epididymis were significantly increased in obese mice compared with those in normal mice. Serum levels of sex hormones in obese mice were disturbed, showing the increase of estrogen levels. The levels of testosterone and progesterone Level down. Serum IL-6, TNF-α, corticosterone, Ig G and Ig M concentrations were also significantly higher. In addition, testicular dysplasia was observed in obese mice, and the content of p38, NF-κB, ERK and JNK in testis increased significantly. Conclusion Obese can induce inflammation in testis and epididymis of male mice, which can lead to impaired fertility in mice.