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Regulatory mechanism of Cordyceps sinensis mycelium on mouse Leydig cell steroidogenesis

机译:冬虫夏草菌丝体对小鼠Leydig细胞类固醇生成的调控机制

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>We demonstrate the mechanism by which Cordyceps sinensis (CS) mycelium regulates Leydig cell steroidogenesis. Mouse Leydig cells were treated with forskolin, H89, phorbol 12-myristate 13-acetate, staurosporine, or steroidogenic enzyme precursors with or without 3 mg/ml CS; then testosterone production was determined. H89, but not phorbol 12-myristate 13-acetate or staurosporine, decreased CS-treated Leydig cell steroidogenesis. CS inhibited Leydig cell steroidogenesis by suppressing the activity of P450scc enzyme, but not 3β-hydroxysteroid dehydrogenase, 17α-hydroxylase, 20α-hydroxylase, or 17β-hydroxysteroid dehydrogenase enzymes. Thus, CS activated the cAMP–protein kinase A signal pathway, but not protein kinase C, and attenuated P45scc enzyme activity to reduce human chorionic gonadotropin-stimulated steroidogenesis in purified mouse Leydig cells.
机译:>我们证明了 Cordyceps sinensis (CS)菌丝体调节Leydig细胞类固醇生成的机制。用福司柯林,H89,佛波醇12-肉豆蔻酸酯13-乙酸酯,星形孢菌素或类固醇生成酶前体处理或不使用3 mg / ml CS处理小鼠Leydig细胞;然后确定睾丸激素的产生。 H89,而不是佛波醇12-肉豆蔻酸酯13-乙酸酯或星形孢菌素,减少了CS治疗的Leydig细胞类固醇生成。 CS通过抑制P450scc酶的活性抑制Leydig细胞的类固醇生成,但不抑制3β-羟基类固醇脱氢酶,17α-羟基化酶,20α-羟基化酶或17β-羟基类固醇脱氢酶的活性。因此,CS激活了cAMP-蛋白激酶A的信号通路,但不激活蛋白激酶C,并减弱了P45scc酶的活性,以减少人绒毛膜促性腺激素刺激的纯净小鼠Leydig细胞中的类固醇生成。

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