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辣椒素对2,3,7,8-四氯二苯并对二恶英诱导的大鼠氧化损伤的保护作用。

The protective effects of capsaicin on oxidative damage-induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats.

作者信息

Doğan Muhammed Fatih, Başak Türkmen Neşe, Taşlıdere Aslı, Şahin Yasemin, Çiftçi Osman

机构信息

Department of Pharmacology, Faculty of Medicine, University of Pamukkale, Denizli, Turkey.

Department of Pharmaceutical Toxicology, Faculty of Pharmacy, University of Inonu, Malatya, Turkey.

出版信息

Drug Chem Toxicol. 2022 Nov;45(6):2463-2470. doi: 10.1080/01480545.2021.1957912. Epub 2021 Jul 26.

DOI:10.1080/01480545.2021.1957912
PMID:34308744
Abstract

The present study aimed to investigate the protective role of capsaicin in a rat model of 2,3,7,8-tetracholorodibenzo-p-dioxin (TCDD)-induced toxicity. Exposure to TCDD which is an environmental toxicant causes severe toxic effects in the animal and human tissues. Therefore, the potential protective effect of capsaicin in TCDD-induced organ damage was investigated in rats by measuring thiobarbituric acid reactive substances (TBARS) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the heart, liver, and kidney tissues for oxidant/antioxidant balance. Thirty-two healthy adults (250-300 g weight and 3-4 months old) male Wistar albino rats were randomly distributed into four equal groups ( = 8): Control, CAP, TCDD, TCDD + CAP. A dose of 2 μg/kg TCDD or a dose of 25 mg/kg capsaicin were dissolved in corn oil and orally administered to the rats for 30 days. The results indicated that TCDD-induced oxidative stress by increasing the level of TBARS and by decreasing the levels of GSH, and SOD activity in the tissues of rats. However, capsaicin treatment was significantly decreased TBARS levels and was significantly increased GSH level and SOD activity ( < 0.05). In addition, capsaicin (25 mg/kg) significantly attenuated TCDD-induced histopathological alteration associated with oxidative stress in the heart, liver, and kidney tissues ( < 0.05). As capsaicin regulates oxidative imbalance and attenuates histopathological alterations in the rat tissues, it may be preventing agents in TCDD toxicity.

摘要

本研究旨在探讨辣椒素在2,3,7,8-四氯二苯并对二恶英(TCDD)诱导的大鼠毒性模型中的保护作用。TCDD作为一种环境毒物,暴露于其中会对动物和人体组织造成严重的毒性作用。因此,通过测量大鼠心脏、肝脏和肾脏组织中的硫代巴比妥酸反应物质(TBARS)水平、超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)水平,以研究辣椒素对TCDD诱导的器官损伤的潜在保护作用,从而评估氧化/抗氧化平衡。将32只健康成年雄性Wistar白化大鼠(体重250-300克,3-4个月大)随机分为四组(每组8只):对照组、辣椒素组、TCDD组、TCDD+辣椒素组。将2μg/kg的TCDD或25mg/kg的辣椒素溶解于玉米油中,经口给予大鼠,持续30天。结果表明,TCDD通过提高TBARS水平、降低GSH水平和SOD活性,诱导大鼠组织产生氧化应激。然而,辣椒素治疗显著降低了TBARS水平,显著提高了GSH水平和SOD活性(P<0.05)。此外,辣椒素(25mg/kg)显著减轻了TCDD诱导的心脏、肝脏和肾脏组织中与氧化应激相关的组织病理学改变(P< 0.05)。由于辣椒素可调节大鼠组织中的氧化失衡并减轻组织病理学改变,它可能是预防TCDD毒性的药物。

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