Zhou Xing, Zhang Guo-Wei, Liang Wei-Ning, Li Yi-Ze, Xu Song, Yan Ling-Ling, Li Hong-Jun, Shang Xue-Jun
Department of Andrology, Jinling Hospital Affiliated to Nanjing University School of Medicine, No. 305, East Zhongshan Road, Nanjing, Jiangsu 210002, China.
Department of Andrology, The First Affiliated Hospital of Hunan University of Chinese Medicine, No. 95, Shaoshan Middle Road, Changsha, Hunan 410007, China.
Evid Based Complement Alternat Med. 2021 Jun 8;2021:4059248. doi: 10.1155/2021/4059248. eCollection 2021.
To investigate the effect and mechanism of action of Moriamin Forte (MF) on oligoasthenospermia (OA) in rats exposed to multiglycosides of (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.
为研究福斯多维生素（MF）对雷公藤多苷（GTW）致大鼠少弱精子症（OA）的作用及作用机制，将40只雄性Sprague Dawley大鼠随机分为四组。对照组大鼠给予0.5%羧甲基纤维素钠。其余大鼠给予GTW（30 mg/kg/d）连续40天以建立OA模型。同时，各实验组分别给予生理盐水、低剂量（100 mg/kg/d）和高剂量（200 mg/kg/d）MF治疗。治疗后，检测精子细胞数量和活力。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（超氧化物歧化酶、过氧化氢酶、丙二醛、总抗氧化能力和核因子E2相关因子2）。通过免疫组化法检测睾丸组织中的凋亡和抗凋亡指标（Bax和Bcl2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丙二醛水平。同时，GTW上调Bax表达并下调Bcl2表达。蛋白质免疫印迹分析显示模型组核因子E2相关因子2表达降低。MF治疗可改善精子数量和活力，并抑制大鼠生殖系统的凋亡率。此外，MF提高抗氧化剂活性并增加抗氧化途径相关蛋白核因子E2相关因子2的相对表达。总之，MF可能通过调节凋亡和抗氧化途径相关蛋白的表达来逆转GTW诱导的OA。本研究可能为MF用于OA治疗提供药理学依据。
