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Background and Aim: Fibrosis, which develops during the progression of liver damage, is the previous stage of cirrhosis. Carbon tetrachloride is one of the most commonly used hepatic toxins in experimental animal models of liver fibrosis. It was investigated the hepatoprotective effects of Tribulus terrestris, Ashwagandha and N-acetylcysteine in an experimental model of liver fibrosis induced by carbon tetrachloride in this study. Methods: Fifty Wistar rats were divided into five groups of 10 each, as follows: 1) control, 2) carbon tetrachloride, 3) carbon tetrachloride plus N-acetylcysteine, 4) carbon tetrachloride plus T. terrestris, and 5) carbon tetrachloride plus Ashwagandha group. At the end of 6 weeks, the rats were sacrificed, and serum and tissue samples were collected. Aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase, malondialdehyde, NF-κB, collagen 1, nuclear factor erythroid-2-related factor 2, tumor necrosis factor-α were analyzed, and histopathological evaluation was performed. Results: There were no significant differences in serum aspartate aminotransferase and alanine aminotransferase levels of the N-acetylcysteine-treated group versus those in the T. terrestris- and Ashwagandha-treated groups (p>0.05). Liver malondialdehyde levels were lower in the N-acetylcysteine-, T. terrestris- and Ashwagandha-treated groups than in the carbon tetrachloride-administered group (p<0.001). There were differences between groups in NF-κB, collagen 1, nuclear factor erythroid-2-related factor 2 and tumor necrosis factor-α levels (p<0.05). Conclusions: In conclusion, T. terrestris, Ashwagandha and N-acetylcysteine had protective effects on the liver in this experimental fibrosis model. T.Terrestris was a little more effective than Ashwagandha in combating liver fibrosis.
EN
Mango ginger (MG) has antiinflammatory and antioxidant properties. The objective of this study was to investigate the potential protective role of MG and the mechanisms against methotrexate (MTX) induced bone damage in rats. A total of 28 Sprague-Dawley rats were divided into four groups: i) control; ii) MG, rats were treated orally with 50 mg/kg/day of MG, iii) MTX, rats were injected with 0.75 mg/kg of MTX from 8th to 12th day for 5 days and iv) MTX+MG group, rats were treated with 50 mg/kg/day of MG and injected with MTX from 8th to 12th day for 5 days. MTX pretreatment increased blood urea nitrogen and creatinine levels and aminotransferase enzyme activities, while tibia osteocalcin levels and bone mineral density (BMD) decreased (p < 0.001). MG pretreatment markedly attenuated aminotransferases activities and creatinine levels and increased tibia osteocalcin levels and femur BMD in the MTX + MG groups. MTX treatment increased levels of bone nuclear factor kappa beta ligand receptor-activator (RANKL), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) and decreased the bone osteoprotegerin (OPG) and type1 collagen levels (p < 0.001). The effect of MG treatment on RANKL, IL-6, TNF-α, OPG and type1 collagen levels induced by MTX was observed actual effects (p < 0.05). Similarly, the protective effect of MG against MTX was confirmed by histological examination. In conclusion, MG pretreatment reduced the negative effects of MTX on bone damage by improving BMD and modulation of RANKL, IL-6, TNF-α, OPG and type1 collagen expressions in the rats.
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