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Chun Pang Yu-chen Sheng Ping Jiang Hai Wei Li-li Ji 《Journal of Zhejiang University. Science. B》2015,16(7):602-610
Chlorogenic acid (CGA), a polyphenolic compound, is abundant in fruits, dietary vegetables, and some medicinal herbs. This study investigated the prevention of CGA against acetaminophen (AP)-induced hepatotoxicity and its engaged mechanisms. CGA reversed the decreased cell viability induced by AP in L-02 cells in vitro. In addition, CGA reduced the AP-induced increased serum levels of alanine/aspartate aminotransferase (ALT/AST) in vivo. The effect of CGA on cytochrome P450 (CYP) enzymatic (CYP2E1, CYP1A2, and CYP3A4) activities showed that CGA caused very little inhibition on CYP2E1 and CYP1A2 enzymatic activities, but not CYP3A4. The measurement of liver malondialdehyde (MDA), reactive oxygen species (ROS), and glutathione (GSH) levels showed that CGA prevented AP-induced liver oxidative stress injury. Further, CGA increased the AP-induced decreased mRNA expression of peroxiredoxin (Prx) 1, 2, 3, 5, 6, epoxide hydrolase (Ephx) 2, and polymerase (RNA) II (DNA directed) polypeptide K (Polr2k), and nuclear factor erythroid-2-related factor 2 (Nrf2). In summary, CGA ameliorates the AP-induced liver injury probably by slightly inhibiting CYP2E1 and CYP1A2 enzymatic properties. In addition, cellular important antioxidant signals such as Prx1, 2, 3, 5, 6, Ephx2, Polr2k, and Nrf2 also contributed to the protection of CGA against AP-induced oxidative stress injury. 相似文献
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Munzir M. E. Ahmed J. A. S. Al-Obosi H. M. Osman M. E. Shayoub 《Indian journal of clinical biochemistry : IJCB》2016,31(2):162-170
Acetaminophen (APAP) a commonly used drug for decrease the fever and pain but is capable to induced hepatotoxicity at over dose. This study was carried out to investigate the effect of APAP on the expression of anti-apoptotic and antioxidative defense genes, and whether aldose reductase over-expressing plasmid capable to protect against APAP-induced oxidative stress and cell death. APAP treatment induced oxidative stress and hepatotoxicity, and significantly increased aldose reductase mRNA and protein expression in mouse hepatocyte (AML-12). Unexpectedly, AML-12 cells over-expressing aldose reductase augmented APAP-induced reduction in cell viability, reactive oxygen species (ROS) production, glutathione (GSH) depletion and glutathione S-transferase A2 expression. Moreover, over-expression of aldose reductase potentiated APAP induced reduction on proliferating cell nuclear antigen, B cell lymphoma-extra large (bcl-xL), catalase, glutathione peroxidase-1 (GPx-1) and abolished APAP-induced B-cell lymphoma 2 (bcl-2) inductions. Further, over-expression of aldose reductase significantly abolished AMP activated protein kinase (AMPK) activity in APAP-treated cells and induced p53 expression. This results demonstrate that APAP induced toxicity in AML-12, increased aldose reductase expression, and over-expression of aldose reductase render this cell more susceptible to APAP induced oxidative stress and cell death, this probably due to inhibition AMPK or bcl-2 activity, or may due to competition between aldose reductase and glutathione reductase for NADPH. 相似文献
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本文以微渗析取样技术与高效液相色谱—电化学检测（HPLC—CED）相结合研究对乙酰氨基酚的药物动力学,流动相的磷酸盐缓冲溶液CPBS,PH＝7．07中,以四氛酞菁酮（CaTAPC）化学修饰电极作为工作电极,检测限为2．oXI0。VL,在6．0x10-7mol／L～1．0x10-4mol／L的线性浓度范围内,恒电位为＋500mV（对Agcl参比电极）,对乙酰氢基酚与峰线电流呈良好的线性（有限好的电催化氧化性能）,应用这个方法研究对乙酰氨基酚（ACE）的药物动力学,测得对乙酰氢酚与蛋白质结合参数（K）及结合因子（n）分别为5.37x103（mol／L）和257。测得（药物在血液中的）吸附半衰期为33．0±1．0min,消去半衰期为45．0±2．0min 相似文献
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