Modulatory effects of Crataeva nurvala bark against testosterone and N-methyl-N-nitrosourea-induced oxidative damage in prostate of male albino rats

岩蔷薇树皮对雄性白化大鼠前列腺中睾酮和N-甲基-N-亚硝基脲诱导的氧化损伤的调节作用

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Abstract

BACKGROUND: Antioxidant properties of Crataeva nurvala bark contains a variety of the bioactive phytochemical constituents in medicinal plants which include flavonoids, phenolic compounds, tannins, anthracene derivatives, and essential oils. Components from Crataeva nurvala bark have been accounted to play an important role in scavenging free radicals generated by mutagens and carcinogens. Androgens are the key factors in either the initiation or progression of prostate cancer by inducing oxidative stress. In the present set of investigations, the antioxidative potential of Crataeva nurvala bark extract against androgen-mediated oxidative stress in male Wistar rats has been studied. MATERIALS AND METHODS: Oxidative damage in prostate was induced in rats by the injection of testosterone (100 mg/kg body weight [bw]) for 3 days followed by injection of chemical carcinogen N-Methyl N-Nitroso Urea (50 mg/kg bw) for 1 week. The oxidative damage in prostate-induced rats were treated with the ethanolic extract of Crataeva nurvala bark (150 mg/kg bw) and testosterone injection (2 mg/ kg bw) was also continued through the experimental period of 4 months. The prostate tissue was dissected out for biochemical analysis of lipid peroxidation and enzymic-antioxidants viz. catalase, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, and glutathione reductase; the non-enzymic antioxidants viz. reduced glutathione, and Vitamin C. RESULTS: The results revealed that testosterone administration induced the oxidative stress in rat prostate; however, in drug (150 mg/kg bw) supplemented groups, a significant protective effect of Crataeva nurvala bark against testosterone-induced oxidative injury was recorded. CONCLUSION: Hence, the study reveals that constituents present in Crataeva nurvala bark impart protection against androgen-induced oxidative injury in prostate.

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