Drug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Drug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Chem Biol Interact. 2019 Jul 1;307:1-7. doi: 10.1016/j.cbi.2019.04.026. Epub 2019 Apr 18.
Exposure to benzo[a]pyrene (BaP), the most toxic polycyclic aromatic hydrocarbon and a procarcinogen, is a global health concern which necessitates preventive measures. [6]-Gingerol (6-G), the most pharmacologically active constituent of ginger has been reported to promote gut health in various experimental settings. This study investigated the role of 6-G in BaP-induced colonic oxidative and inflammatory stress responses in mice. Experimental mice were randomly assigned into five groups of eight mice each and were orally gavage with BaP (125 mg/kg) singly or in combination with 6-G at 50 and 100 mg/kg for 14 consecutive days. Following sacrifice, the colonic activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), myeloperoxidase (MPO) as well as levels of glutathione (GSH), nitrites and lipid peroxidation (LPO) were assessed spectrophotometrically. Moreover, colonic concentration of epoxide hydrolase (EPXH), tumor necrosis factor alpha (TNF-α), interleukin-1 β (IL-1β), cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were assessed using ELISA. Administration of 6-G augmented BaP detoxification and colonic antioxidant status by increasing the EPXH, GST, SOD and CAT activities, GSH level with concomitant decrease in MDA level when compared with BaP alone group. In addition, 6-G suppressed BaP-induced colonic inflammation by decreasing MPO activity as well as nitrites, TNF-α, IL-1β, COX-2 and iNOS levels when compared with BaP alone group. In conclusion, 6-G protected against a decrease in colonic epoxide detoxifying enzymes and antioxidant defense mechanisms caused by BaP.
暴露于苯并[a]芘(BaP),这是最具毒性的多环芳烃和前致癌物,是全球关注的健康问题,需要采取预防措施。[6]-姜酚(6-G)是生姜中最具药理活性的成分,据报道在各种实验环境中可促进肠道健康。本研究调查了 6-G 在 BaP 诱导的小鼠结肠氧化和炎症应激反应中的作用。实验小鼠随机分为五组,每组 8 只,连续 14 天每天口服 BaP(125mg/kg)单独或与 6-G(50 和 100mg/kg)联合给药。处死小鼠后,用分光光度法测定结肠中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽 S-转移酶(GST)、髓过氧化物酶(MPO)的活性以及谷胱甘肽(GSH)、亚硝酸盐和脂质过氧化(LPO)的水平。此外,用 ELISA 测定环氧水解酶(EPXH)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)在结肠中的浓度。与 BaP 单独给药组相比,6-G 给药增加了 EPXH、GST、SOD 和 CAT 活性、GSH 水平,并降低了 MDA 水平,从而增强了 BaP 的解毒和结肠抗氧化状态。此外,与 BaP 单独给药组相比,6-G 降低了 MPO 活性以及 nitrites、TNF-α、IL-1β、COX-2 和 iNOS 水平,从而抑制了 BaP 诱导的结肠炎症。总之,6-G 防止了 BaP 引起的结肠环氧解毒酶和抗氧化防御机制的降低。