Author/Authors :
-، - نويسنده Department of Technology Management, Chung Hua University, Hsinchu, Taiwan Lin, Wen-Hung , -، - نويسنده Department of Finance, Chung Hua University, Hsinchu, Taiwan Kuo, Heng-Hung , -، - نويسنده Department of Technology Management, Chung Hua University, Hsinchu, Taiwan Ho, Li-Hsing , -، - نويسنده Department of Biotechnology, Yuanpei University, Hsinchu, Taiwan Tseng, Ming-Lang , -، - نويسنده Office of Physical Education, Chung Hua University Hsinchu, Taiwan Siao, An-Ci , -، - نويسنده Department of Health and Leisure Management, Yuanpei University, Hsinchu, Taiwan Hung, Chang-Tsen , -، - نويسنده Department of Medical Research, Tungs’ Taichung Metro Harbor Hospital, Taichung, Taiwan Jeng, Kee-Ching , -، - نويسنده Office of Physical Education, Chung Hua University Hsinchu, Taiwan Hou, Chien-Wei
Abstract :
Objective(s): Gardenia jasminoides Ellis (GJ, Cape Jasmine Fruit, Zhi Zi) has been traditionally used for the treatment of infectious hepatitis, aphthous ulcer, and trauma; however, the direct evidence is lacking.
Materials and Methods:We investigated the effect of the GJ extract(GJ) and gallic acid (GA) on lipopolysaccharide (LPS) induced inflammation of BV-2 microglial cells and acute liver injury in Sprague-Dawley (SD) rats.
Results:Our results showed that the GJ extract and GA reduced LPS-induced nitric oxide (NO), interleukin (IL)-1, IL-6, reactive oxygen species (ROS), and prostaglandin (PGE2) production in BV-2 cells. The GJ extract and GA significantly decreased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in LPS-treated rats. Furthermore, the water extract, but not the ethanol extract, of the GJ dose-dependently inhibited LPS-induced JNK2/1 and slightly p38 mitogen-activated protein kinases (MAPK), and cyclooxygenase-2 (COX-2) expression in BV-2 cells.
Conclusion:Taken together, these results indicate that the protective mechanism of the GJ extract involves an antioxidant effect and inhibition of JNK2/1 MAP kinase and COX-2 expressions in LPS-induced inflammation of BV-2 cells.
