Department of Surgery, Taipei City Hospital, Taipei, Taiwan, Republic of China.
J Cell Biochem. 2010 May 15;110(2):333-42. doi: 10.1002/jcb.22541.
Catechins have been reported to have many pharmacological properties such as the effects of anti-oxidative, anti-inflammatory, anti-carcinogenic, anti-ultraviolet, and reduction of blood pressure as well as glucose and cholesterol levels. However, the effect of catechins on the reproductive mechanism is still unknown. In the present study, the effects of catechins on testosterone secretion in rat testicular Leydig cells (LCs) were explored. Both in vivo and in vitro investigations were performed. Purified LCs were incubated with or without catechin (CCN), epicatechin (EC), epigallocatechin gallate (EGCG, 10(-10)-10(-8) M) under challenge with human chorionic gonadotropin (hCG, 0.01 IU/ml), forskolin, SQ22536 (an adenylyl cyclase inhibitor), 8-bromo-adenosine 3':5'-cyclic monophosphate (8-Br-cAMP), A23187 (a calcium ionophore), and nifedipine (10(-5) M), respectively. To study the effects of catechins on steroidogenesis, steroidogenic precursors-stimulated testosterone release was examined. The functions of the steroidogenic enzymes including protein expression of cytochrome P450 side chain cleavage enzyme (P450scc) and steroidogenic acute regulatory (StAR) protein were investigated and expressed by Western blotting. Catechins increased plasma testosterone in vivo in male rats. In vitro, low-dose concentration of catechins increased gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release by anterior pituitary gland and hCG-stimulated testosterone release by LCs of male rats. These results suggested that catechins stimulated testosterone production by acting on rat LCs via the mechanism of increasing the action of cAMP, but not P450scc, StAR protein or the activity of intracellular calcium. EC, one of the catechins increased the testosterone secretion by rat LCs via the enzyme activities of 17beta-hydroxysteroid dehydrogenase (17beta-HSD).
儿茶素已被报道具有许多药理学特性,如抗氧化、抗炎、抗癌、抗紫外线、降低血压以及血糖和胆固醇水平。然而,儿茶素对生殖机制的影响尚不清楚。在本研究中,探讨了儿茶素对大鼠睾丸间质细胞(LCs)中睾丸酮分泌的影响。进行了体内和体外研究。用或不用儿茶素(CCN)、表儿茶素(EC)、表没食子儿茶素没食子酸酯(EGCG,10(-10)-10(-8)M)孵育纯化的 LCs,分别用绒毛膜促性腺激素(hCG,0.01IU/ml)、福司可林、SQ22536(腺苷酸环化酶抑制剂)、8-溴-腺苷 3':5'-环单磷酸(8-Br-cAMP)、A23187(钙离子载体)和硝苯地平(10(-5)M)刺激。为了研究儿茶素对类固醇生成的影响,检查了类固醇生成前体刺激的睾丸酮释放。通过 Western 印迹法研究了类固醇生成酶的功能,包括细胞色素 P450 侧链裂解酶(P450scc)和类固醇急性调节蛋白(StAR)蛋白的蛋白质表达。儿茶素增加了雄性大鼠体内的血浆睾丸酮。在体外,儿茶素的低剂量浓度增加了促性腺激素释放激素(GnRH)刺激的促黄体生成素(LH)释放和 hCG 刺激的雄性大鼠 LCs 的睾丸酮释放。这些结果表明,儿茶素通过增加 cAMP 的作用刺激大鼠 LCs 产生睾丸酮,而不是 P450scc、StAR 蛋白或细胞内钙的活性。儿茶素之一的 EC 通过大鼠 LCs 的 17β-羟甾脱氢酶(17β-HSD)的酶活性增加了睾丸酮的分泌。