Park Hyun Jun, Koo Yean Kyoung, Park Min Jung, Hwang Yoon Kyung, Hwang Sung Yeoun, Park Nam Cheol
Department of Urology, Pusan National University School of Medicine, Busan, Korea.
Biomedical Research Institute of Pusan National University Hospital, Busan, Korea.
World J Mens Health. 2017 Dec;35(3):170-177. doi: 10.5534/wjmh.17031. Epub 2017 Oct 25.
We investigated the protective effect of a mixture of 2 herbal extracts, KH-465, which consisted of Epimedium koreanum Nakai and Angelica gigas Nakai, on spermatogenesis in a luteinizing hormone-releasing hormone (LHRH) agonist-induced rat model of male infertility.
Seventy-five 12-week-old male Sprague-Dawley rats were randomly divided into 5 groups, containing 15 rats each: a normal control group that received no treatment and 4 experimental groups (I, II, III, and IV) in which an LHRH agonist was administered for 4 weeks to induce spermatogenic failure. Group I received distilled water, and groups II, III, and IV received 200 mg/kg/day of KH-465, 400 mg/kg/day KH-465, and depo-testosterone for 4 weeks, respectively. Weight changes of the testis and epididymis, sperm count motility, and levels of testosterone (T), free T, follicle-stimulating hormone (FSH), luteinizing hormone (LH), superoxide dismutase (SOD), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were estimated.
Body, testis, and epididymis weight showed no significant differences among the control and experimental groups. Treatment with KH-465 increased the sperm count and motility. Serum hormone levels of T, free T, and FSH were not significantly different in the experimental groups, while the LH level was higher than in the LHRH agonist-induced control group, but not to a significant extent. Levels of SOD were higher and 8-OHdG were lower in the groups that received KH-465 than in the LHRH agonist-induced control group.
Our results suggest that KH-465 increased sperm production via reducing oxidative stress and had a positive effect in a male infertility model.
我们研究了由朝鲜淫羊藿和当归组成的两种草药提取物混合物KH - 465对促黄体生成素释放激素(LHRH)激动剂诱导的雄性不育大鼠模型精子发生的保护作用。
75只12周龄雄性Sprague - Dawley大鼠随机分为5组,每组15只:一个未接受治疗的正常对照组和4个实验组(I、II、III和IV),其中LHRH激动剂给药4周以诱导生精功能衰竭。I组接受蒸馏水,II、III和IV组分别接受200 mg/kg/天的KH - 465、400 mg/kg/天的KH - 465和长效睾酮,持续4周。评估睾丸和附睾的重量变化、精子计数活力以及睾酮(T)、游离T、促卵泡激素(FSH)、促黄体生成素(LH)、超氧化物歧化酶(SOD)和8 - 羟基 - 2'-脱氧鸟苷(8 - OHdG)的水平。
对照组和实验组之间的体重、睾丸和附睾重量无显著差异。KH - 465治疗增加了精子计数和活力。实验组中血清T、游离T和FSH激素水平无显著差异,而LH水平高于LHRH激动剂诱导的对照组,但差异不显著。接受KH - 465的组中SOD水平较高,8 - OHdG水平低于LHRH激动剂诱导的对照组。
我们的结果表明,KH - 465通过降低氧化应激增加精子生成,并对雄性不育模型有积极作用。