Alterations in gene expression and steroidogenesis in the testes of transient cerebral ischemia in male rats.
Alterations in gene expression and steroidogenesis in the testes of transient cerebral ischemia in male rats.
复制标题
雄性大鼠短暂性脑缺血睾丸基因表达和类固醇生成的改变。
DOI：
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发表时间：
2012-06
期刊：
影响因子：
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通讯作者：
郭艳芹
中科院分区：
文献类型：
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作者：
郭艳芹
背景
急性缺血性中风男性患者血清睾酮水平较低。然而，确切的机制仍不清楚。本研究通过检测实验性短暂性脑缺血雄性大鼠血清睾酮水平、类固醇生成相关基因和间质细胞数量来阐明其机制。
方法
将成年雄性Sprague-Dawley大鼠的大脑中动脉缝合120分钟，然后在24小时后处死。采集血液测量血清睾酮、促卵泡激素和雌二醇水平，采集睾丸测量类固醇生成相关基因mRNA水平和Leydig细胞数量。
结果
脑缺血后大鼠血清睾酮水平（0.53 ± 0.16）ng/ml，n = 7）显著低于对照组（2.33 ± 0.60）ng/ml，n = 7，而雌二醇和卵泡刺激素水平无明显变化。促黄体生成素受体（Lhcgr）、清道夫受体B类成员1（Scarb 1）、类固醇生成急性调节蛋白（星星）、胆固醇侧链裂解酶（Cyp 11 a1）、3β-羟基类固醇脱氢酶1（HSD 3 β1）、17α-羟化酶/20-裂解酶（Cyp 17 a1）和膜受体c-kit（kit）的mRNA水平在脑缺血后显著下调，而促黄体生成素、Kit配体（KitL）、17β-氢化类固醇脱氢酶3（HSD 17 β3）和5α-还原酶（Srd 5a 1）未受影响。我们还观察到，相对于对照，Leydig细胞数量没有变化。
结论
这些结果表明，大脑中的短暂脑缺血导致类固醇生成相关基因的表达水平降低，从而降低血清睾酮水平。短暂性脑缺血并没有降低Leydig细胞的数量。
BACKGROUND
Serum testosterone levels have been found lower in acute ischemic stroke male patients. However, the exact mechanism remains unclear. In the present study, we measured serum testosterone levels, steroidogenesis- related genes and Leydig cells number in experimental transient cerebral ischemia male rats to elucidate the mechanism.
METHODS
The middle cerebral arteries of adult male Sprague-Dawley rats were sutured for 120 minutes and then sacrificed after 24 hours. Blood was collected for measurement of serum testosterone, follicular stimulating hormone and estradiol levels, and testes were collected for measurement of steroidogenesis-related gene mRNA levels and number of Leydig cells.
RESULTS
Serum testosterone levels in rats after cerebral ischemia were significantly lower (0.53 ± 0.16) ng/ml, n = 7, mean ± SE) compared with control ((2.33 ± 0.60) ng/ml, n = 7), while serum estradiol and follicular stimulating hormone levels did not change. The mRNA levels for luteinizing hormone receptor (Lhcgr), scavenger receptor class B member 1 (Scarb1), steroidogenic acute regulatory protein (StAR), cholesterol side chain cleavage enzyme (Cyp11a1), 3β-hydroxysteroid dehydrogenase 1 (HSD3β1), 17α-hydroxylase/20-lyase (Cyp17a1) and membrane receptor c-kit (kit) were significantly downregulated by cerebral ischemia, while luteinizing hormone, Kit ligand (KitL), 17β-hydrosteroid dehydrogenase 3 (HSD17β3) and 5α-reductase (Srd5a1) were not affected. We also observed that, relative to control, the Leydig cell number did not change.
CONCLUSIONS
These results indicate that transient cerebral ischemia in the brain results in lower expression levels of steroidogenesis-related genes and thus lower serum testosterone level. Transient cerebral ischemia did not lower the number of Leydig cells.