CONTEXT: Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is one of the most extensively used herbs for stroke and chronic debilitating conditions in East Asian countries. Ginsenosides (GS) are the main bioactive compounds for ginseng's efficacy, but the mechanisms have not been fully clarified. OBJECTIVE: To investigate hepatoprotective effects of GS against ischemia/reperfusion (IR) injury in the experimental obstructive jaundice rats. MATERIALS AND METHODS: GS was fed to cholestatic rats with IR injury daily for 6 d at a dose of 1.10 g/kg. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by colorimetric method. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling method. Protein expression of Bax and Bcl-2 was detected by immunohistochemistry. RESULTS AND DISCUSSION: After intervention of GS to cholestatic rats with IR injury, the levels of activating blood flow were significantly improved, and the levels of serum ALT were decreased 1.7-times, AST decreased 1.3-times, but SOD activities were increased 1.1-times compared with those of the model rats. It could also reverse histopathological changes and inhibit IR-induced apoptosis of hepatic tissues via decrease of Bax/Bcl-2 ratio (from 2.87 ± 0.57 to 1.65 ± 0.29). Oral administration of GS in a dosage of 26.4 g/kg did not lead to toxic effects in rats. CONCLUSION: GS attenuated the IR injury in the presence of cholestasis and could be considered for the clinical treatment of cholestasis.
CONTEXT: Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is one of the most extensively used herbs for stroke and chronic debilitating conditions in East Asian countries. Ginsenosides (GS) are the main bioactive compounds for ginseng's efficacy, but the mechanisms have not been fully clarified. OBJECTIVE: To investigate hepatoprotective effects of GS against ischemia/reperfusion (IR) injury in the experimental obstructive jaundicerats. MATERIALS AND METHODS: GS was fed to cholestaticrats with IR injury daily for 6 d at a dose of 1.10 g/kg. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by colorimetric method. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling method. Protein expression of Bax and Bcl-2 was detected by immunohistochemistry. RESULTS AND DISCUSSION: After intervention of GS to cholestaticrats with IR injury, the levels of activating blood flow were significantly improved, and the levels of serum ALT were decreased 1.7-times, AST decreased 1.3-times, but SOD activities were increased 1.1-times compared with those of the model rats. It could also reverse histopathological changes and inhibit IR-induced apoptosis of hepatic tissues via decrease of Bax/Bcl-2 ratio (from 2.87 ± 0.57 to 1.65 ± 0.29). Oral administration of GS in a dosage of 26.4 g/kg did not lead to toxic effects in rats. CONCLUSION: GS attenuated the IR injury in the presence of cholestasis and could be considered for the clinical treatment of cholestasis.
Authors: Su Kang Kim; Joo-Ho Chung; Byung-Cheol Lee; Sang Won Lee; Kang Hyo Lee; Young Ock Kim Journal: Int Neurourol J Date: 2014-12-29 Impact factor: 2.835
Authors: Ahmet Caliskan; Oguz Karahan; Suleyman Yazici; Sinan Demirtas; Orkut Guclu; Orhan Tezcan; Celal Yavuz Journal: Cardiovasc J Afr Date: 2015 Nov-Dec Impact factor: 1.167