Antioxidant activities of ginsenoside Rg1 against cisplatin-induced hepatic injury through Nrf2 signaling pathway in mice
| Autor: | Nai-Hong Chen, Cong-Yuan Xia, Yan Gao, Qianhang Shao, Yu-Xia Lou, Yueting Li, Ying-ying Wang, Hui-Yong Huang, Shi-Feng Chu, Mei-Jin Zhang |
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| Rok vydání: | 2016 |
| Předmět: |
Male
Transcriptional Activation 0301 basic medicine Antioxidant Ginsenosides NF-E2-Related Factor 2 medicine.medical_treatment Drug Evaluation Preclinical Antineoplastic Agents Pharmacology medicine.disease_cause Biochemistry Antioxidants 03 medical and health sciences chemistry.chemical_compound Ginseng medicine Animals chemistry.chemical_classification Liver injury Reactive oxygen species Tyrosine phosphorylation General Medicine medicine.disease KEAP1 Mice Inbred C57BL Oxidative Stress 030104 developmental biology Liver chemistry Proteolysis Chemical and Drug Induced Liver Injury Cisplatin Signal transduction Reactive Oxygen Species Oxidative stress Signal Transduction |
| Zdroj: | Free Radical Research. 51:1-13 |
| ISSN: | 1029-2470 1071-5762 |
| DOI: | 10.1080/10715762.2016.1234710 |
| Popis: | Oxidative stress is mainly caused by reactive oxygen species (ROS). The damage causes a net stress on normal organs, leading to a gradual loss of vital physiological function. ROS, such as free radicals, represent a class of molecules which are derived from the metabolism of oxygen and exist inherently. However, excessive produced ROS can damage all aerobic organisms. Ginseng is one of the most commonly used alternative herbal medicines, also as a traditional Chinese medicine. The aim of this study is to investigate the antioxidant potential function of ginsenoside Rg1 against cisplatin-caused hepatic damage. Male mice were treated with cisplatin to induce oxidative stress to mimic the side effect of anti-cancer drug cisplatin. Ginsenoside Rg1 effectively prevented against cisplatin-induced hepatotoxicity, alleviating histological lesions. Antioxidant functions of Rg1 were restrained by the activation of p62-Keap1-Nrf2 signaling pathway, simultaneously accompanied with expression of protein products. Accumulative p62 and increased activation of JNK in hepatocytes promoted the activation of Nrf2. For the other, degradation of Nrf2 was guided by tyrosine phosphorylation, ubiquitin, and Keap1. In summary, Rg1 prevents hepatotoxicity mainly by inhibiting the binding of Keap1 and Nrf2, partly by p62 accumulation, and more importantly by increasing the production of antioxidative proteins associated to Nrf2. Pharmacological activation of Nrf2 is an effective way in combating against liver injury. |
| Databáze: | OpenAIRE |
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