Endometrial carcinoma is a malignant tumor of the female genital tract. This study has been performed to evaluate the chemopreventive efficacy of vanillic acid (a bio flavonoid) on endometrial carcinoma (EC) by assessing the levels of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), cytochrome P450, antioxidants-superoxide dismutase (SOD), catalase (CAT), glutathione peroxides (GPx), reduced glutathione (GSH), vitamins C and E, matrix metalloproteinases (MMP-2 and 9) and cell cycle check point protein (cyclin D1) in -methyl-'-nitro--nitrosoguanidine (MNNG) induced carcinogenic rats. EC provoked by intravaginal detention of MNNG (150 mg/kg b.w. for 90 days), lead to enhancement of the levels of TBARS, LOOH, cytochrome P450, and decrement in the levels of antioxidants (SOD, CAT, GPx, GSH, vitamins C and E) and upregulated expression of MMP-2 and 9 and cyclin D1 (by western blot analysis). The treatment of vanillic acid (100 mg/kg b.w.) to MNNG treated rats (1) normalized the histopathological alterations, (2) reduced the levels of TBARS, LOOH and cytochrome P450 (3) increased the levels of antioxidants (SOD, CAT, GPx, GSH, vitamins C and E) in plasma and uterus and (4) down regulated the expression of MMP-2, 9 and cyclin D1. The effect of vanillic acid is more predominant in pre-treatment group than co-treated rats. Our results designate that vanillic acid inhibits the EC by elevating antioxidants and by regulating the levels of metalloproteinase and cell cycle check point protein.
We have studied the ability of quercetin (a bioflavonoid) in tackling oxidative stress to alleviate the symptoms during ammonium chloride-induced hyperammonemia. Hyperammonemia was induced by the treatment of ammonium chloride (AC) 100 mg/kg b.w for 56 days. Hyperammonemic rats exhibited reduced urea (in plasma) and increased ammonia (in blood), uric acid (in plasma), creatinine (in serum), oxidative stress markers (thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP) and decreased levels of antioxidants (enzymatic and non-enzymatic) superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) in plasma and tissues (liver and brain) vitamins E and C (in plasma)). The expression of liver inflammatory markers such as, interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS) and nuclear transcription factor-κB (NF-κB) (by western blotting) were investigated. Histological damages (in liver, brain and kidney) were observed under hyperammonemia and the administration of quercetin (1) normalized the histopathological alterations, (2) reduced the levels of TBARS and HP, (3) elevated the antioxidants (SOD, CAT, GPx, GSH, vitamins E and C), (4) declined the activities of liver marker enzymes (AST, ALT and ALP) and (5) down regulated the expression of IL-6, iNOS and NF-κB. Our results suggest that quercetin might exert defense to AC-induced hyperammonemic rats to tackle (1) oxidative stress and (2) inflammation owing to its antioxidant, anti-inflammatory and cytoprotective effects.
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