Ajayi Babajide O, Adedara Isaac A, Ajani Olumide S, Oyeyemi Matthew O, Farombi Ebenezer O
Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Department of Veterinary Surgery and Reproduction, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.
J Basic Clin Physiol Pharmacol. 2018 Jun 27;29(3):247-256. doi: 10.1515/jbcpp-2017-0140.
The deterioration of male reproductive health may represent an outcome of an active disease and environmental factors. The present study investigated the modulatory role of [6]-gingerol in spermatotoxicity resulting from colitis and benzo[a]pyrene (B[a]P), an environmental and food-borne pollutant.
Group I (control) mice received corn oil alone, while group II ([6]-gingerol alone) mice orally received [6]-gingerol alone at 100 mg/kg body weight. Group III [benzo[a]pyrene+dextran sulfate sodium (BDS) alone] mice were orally exposed to B[a]P at 125 mg/kg for 7 days followed by three cycles of 4% dextran sulfate sodium (DSS) in drinking water. A cycle consisted of seven consecutive days of exposure to DSS-treated water followed by 14 consecutive days of normal drinking water. Group IV (BDS+[6]-gingerol) mice were orally treated daily with 100 mg/kg of [6]-gingerol during exposure to B[a]P and DSS in the same manner as those of group III.
[6]-Gingerol significantly abrogated BDS-mediated increase in disease activity index and restored the colon wet weight, colon length and colon mass index to near normal when compared to BDS alone group. Moreover, [6]-gingerol significantly prevented BDS-induced decreases in the daily sperm production (DSP), testicular sperm number (TSN), epididymal sperm number, sperm progressive motility and sperm membrane integrity when compared with the control. [6]-Gingerol markedly increased the sperm antioxidant enzymes activities and decreased the sperm head, mid-piece and tail abnormalities as well as suppressed oxidative stress and inflammatory biomarkers in BDS-exposed mice.
[6]-Gingerol protected against spermatotoxicity in experimental model of interaction of colitis with environmental pollutant B[a]P.
男性生殖健康的恶化可能是一种活动性疾病和环境因素共同作用的结果。本研究调查了[6]-姜酚对结肠炎和苯并[a]芘（B[a]P，一种环境和食源性污染物）所致精子毒性的调节作用。
第一组（对照组）小鼠仅接受玉米油，第二组（仅[6]-姜酚组）小鼠以100 mg/kg体重口服[6]-姜酚。第三组（仅苯并[a]芘+葡聚糖硫酸钠（BDS）组）小鼠口服125 mg/kg B[a]P，持续7天，随后在饮用水中进行三个周期的4%葡聚糖硫酸钠（DSS）处理。一个周期包括连续7天饮用DSS处理的水，随后连续14天饮用正常饮用水。第四组（BDS+[6]-姜酚组）小鼠在与第三组相同的B[a]P和DSS暴露期间，每天口服100 mg/kg的[6]-姜酚。
与仅BDS组相比，[6]-姜酚显著消除了BDS介导的疾病活动指数升高，并使结肠湿重、结肠长度和结肠质量指数恢复到接近正常水平。此外，与对照组相比，[6]-姜酚显著预防了BDS诱导的每日精子生成量（DSP）、睾丸精子数量（TSN）、附睾精子数量、精子前向运动能力和精子膜完整性的降低。[6]-姜酚显著提高了BDS暴露小鼠精子抗氧化酶的活性，减少了精子头部、中段和尾部的异常，并抑制了氧化应激和炎症生物标志物。
[6]-姜酚在结肠炎与环境污染物B[a]P相互作用的实验模型中对精子毒性具有保护作用。
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