详细信息

Licorice Ameliorates Cisplatin-Induced Hepatotoxicity Through Antiapoptosis, Antioxidative Stress, Anti-Inflammation, and Acceleration of Metabolism  ( SCI-EXPANDED收录)   被引量:17

文献类型:期刊文献

英文题名:Licorice Ameliorates Cisplatin-Induced Hepatotoxicity Through Antiapoptosis, Antioxidative Stress, Anti-Inflammation, and Acceleration of Metabolism

作者:Man, Qiong[2];Deng, Yi[1,3];Li, Pengjie[1];Ma, Jun[1];Yang, Zhijun[1];Yang, Xiujuan[1];Zhou, Yan[1,4];Yan, Xiao[1]

第一作者:Man, Qiong

通信作者:Deng, Y[1];Deng, Y[2]

机构:[1]Gansu Univ Chinese Med, Coll Pharm, Lanzhou, Peoples R China;[2]Chengdu Med Coll, Sch Pharm, Chengdu, Peoples R China;[3]Key Lab Pharmacol & Toxicol Tradit Chinese Med Ga, Lanzhou, Peoples R China;[4]Lanzhou Univ, Hosp 1, Dept Pharm, Lanzhou, Peoples R China

第一机构:甘肃中医药大学药学院(西北中藏药协同创新中心办公室)

通信机构:[1]corresponding author), Gansu Univ Chinese Med, Coll Pharm, Lanzhou, Peoples R China;[2]corresponding author), Key Lab Pharmacol & Toxicol Tradit Chinese Med Ga, Lanzhou, Peoples R China.|[1073501e14fb35863569f]甘肃中医药大学药学院(西北中藏药协同创新中心办公室);[10735]甘肃中医药大学;

年份:2020

卷号:11

外文期刊名:FRONTIERS IN PHARMACOLOGY

收录:;Scopus(收录号:2-s2.0-85096666104);WOS:【SCI-EXPANDED(收录号:WOS:000591649400001)】;

基金:This work was supported by National Natural Science Foundation of China (No. 81960723), Lanzhou science and the technology planning project (No. 2018-4-63), Open Foundation project of Key Laboratory of Pharmacology and Toxicology of Chinese Medicine in Gansu Province (No. ZDSYS-KJ-2018-09), and Foundation of Chengdu Medical college (No. CYZZD 20-02).

语种:英文

外文关键词:cisplatin; detoxification; hepatotoxicity; licorice; proteomics

摘要:Cisplatin (CP) is one of the most effective antitumor drugs in the clinic, but has serious adverse reactions, and its hepatotoxicity has not been fully investigated. Licorice (GC), a traditional herbal medicine, has been commonly used as a detoxifier for poisons and drugs, and may be an effective drug for CP-induced hepatotoxicity. However, its mechanism and the effector molecules remain ambiguous. Therefore, in this study, a network pharmacology and proteomics-based approach was established, and a panoramic view of the detoxification of GC on CP-induced hepatotoxicity was provided. The experimental results indicated that GC can recover functional indices and pathological liver injury, inhibit hepatocyte apoptosis, upregulate B-cell lymphoma/leukemia 2 (Bcl-2) and superoxide dismutase (SOD) levels, and downregulate cellular tumor antigen p53 (p53), caspase-3, malondialdehyde high mobility group protein B1 (HMGB1), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1 beta) levels. Proteomics indicated that GC regulates phosphatidylcholine translocator ABCB1 (ABCB1B), canalicular multispecific organic anion transporter 1 (ABCC2), cytochrome P450 4A2 (CYP4A2), cytochrome P450 1A1 (CYP1A1), cytochrome P450 1A2 (CYP1A2), estrogen receptor (ESR1), and DNA topoisomerase 2-alpha (TOP2A), inhibits oxidative stress, apoptosis, and inflammatory responses, and accelerates drug metabolism. In this study, we provide the investigation of the efficacy of GC against CP-induced hepatotoxicity, and offer a promising alternative for the clinic.

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