Impact of Moriamin Forte on Testicular and Epididymal Damage in Rats with Oligoasthenospermia.

Impact of Moriamin Forte on Testicular and Epididymal Damage in Rats with Oligoasthenospermia.
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Moriamin Forte 对少弱精子症大鼠睾丸和附睾损伤的影响

DOI:
10.1155/2021/4059248
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发表时间:
2021
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Shang XJ
Shang XJ
中科院分区:
其他
文献类型:
--
作者:
Zhou X;Zhang GW;Liang WN;Li YZ;Xu S;Yan LL;Li HJ;Shang XJ

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为探讨莫里亚明(MF)对雷公藤多甙(GTW)致大鼠少弱精子症(OA)的治疗作用及其机制,将40只雄性Sprague道利大鼠随机分为4组。对照组给予0.5%羧甲基纤维素钠。其余大鼠给予雷公藤多甙(30 mg/kg/d)40 d,建立OA模型。同时,各组分别给予生理盐水和低剂量(100 mg/kg/d)和高剂量(200 mg/kg/d)MF。治疗后,检查精子细胞的数量和活力。观察睾丸和附睾组织形态学变化。检测睾丸和附睾组织中的抗氧化指标(SOD、CAT、MDA、TAC和Nrf 2)。用免疫组化法检测睾丸组织中凋亡和抗凋亡指标(Bax和Bcl 2表达)。GTW降低精子数量和活力,损伤睾丸和附睾组织,损害抗氧化酶活性,并增加组织MDA水平。GTW可上调Bax的表达,下调Bcl 2的表达。Western blot分析显示模型组Nrf 2表达降低。MF处理改善了精子数量和活力,并抑制了大鼠生殖系统的凋亡率。此外,MF提高了抗氧化剂的活性,并增加了抗氧化途径相关蛋白Nrf 2的相对表达。总之,MF可能通过调节细胞凋亡和抗氧化途径相关蛋白的表达来逆转GTW诱导的OA。本研究为MF在OA治疗中的应用提供了药理学基础。
To investigate the effect and mechanism of action of Moriamin Forte (MF) on oligoasthenospermia (OA) in rats exposed to multiglycosides of Tripterygium wilfordii (GTW), forty male Sprague Dawley rats were randomly divided into four groups. Rats in the control group were treated with 0.5% sodium carboxymethyl cellulose. The remaining rats were administered GTW (30 mg/kg/d) for 40 d to establish an OA model. Concurrently, the groups were treated with normal saline and low-dose (100 mg/kg/d) and high-dose (200 mg/kg/d) MF, respectively. After treatment, the number and motility of sperm cells were examined. Testicular and epididymal histomorphology changes were observed. Antioxidant indicators (SOD, CAT, MDA, TAC, and Nrf2) in testicular and epididymal tissues were detected. Apoptotic and antiapoptotic indicators (Bax and Bcl2 expression) in the testicular tissue were measured by immunohistochemistry. GTW decreased sperm count and motility, damaged testicular and epididymis tissues, impaired antioxidase activity, and increased tissue MDA levels. Meanwhile, GTW upregulated the expression of Bax and downregulated the expression of Bcl2. Western blot analysis demonstrated a decrease in the Nrf2 expression in the model group. Treatment with MF improved sperm count and motility, as well as inhibited the rate of apoptosis in the rat reproductive system. Moreover, MF improved the activity of antioxidants and increased the relative expression of the antioxidant pathway-related protein Nrf2. In conclusion, MF may reverse the GTW-induced OA by modulating the expression of apoptotic and antioxidant pathway-related proteins. This study may provide a pharmacological foundation for the use of MF in OA treatment.
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