Gastrodin Alleviates Acetaminophen-Induced Liver Injury in a Mouse Model Through Inhibiting MAPK and Enhancing Nrf2 Pathways

天麻素 丙二醛 药理学 对乙酰氨基酚 MAPK/ERK通路 肝损伤 氧化应激 化学 超氧化物歧化酶 腹腔注射 丙氨酸转氨酶 髓过氧化物酶 医学 炎症 生物化学 信号转导 免疫学 内科学 色谱法
作者
Chia-Chih Liao,Huang‐Ping Yu,An‐Hsun Chou,Hung-Chen Lee,Limin Hu,Fu-Chao Liu
出处
期刊:Inflammation [Springer Science+Business Media]
卷期号:45 (4): 1450-1462 被引量:10
标识
DOI:10.1007/s10753-021-01557-1
摘要

Gastrodin is a major active phenolic glycoside extract from Gastrodia elata, an important herb used in traditional medicine. Previous research has reported that gastrodin possesses anti-inflammatory and anti-oxidant properties. Therefore, we aimed to investigate its hepatoprotective effects and mechanisms on acetaminophen (APAP)-induced liver injury in a mouse model. Mice included in this study were intraperitoneally administered with a hepatotoxic APAP dose (300 mg/kg). At 30 min after APAP administration, gastrodin was intraperitoneally injected at concentrations of 0, 15, 30, and 45 mg/kg. Then, all mice were sacrificed at 16 h after APAP injection for further analysis. The results showed that gastrodin treatment ameliorated acute liver injury caused by APAP, as indicated by serum alanine aminotransferase level, hepatic myeloperoxidase activity, and cytokine (TNF-α, IL-1β, and IL-6) production. It also significantly decreased hepatic malondialdehyde activity but increased superoxide dismutase activity. In addition, gastrodin decreased ERK/JNK MAPK expression but promoted Nrf2 expression. These results demonstrated that gastrodin may be a potential therapeutic target for the prevention of APAP-induced hepatotoxicity via amelioration of the inflammatory response and oxidative stress, inhibition of ERK/JNK MAPK signaling pathways, and activation of Nrf2 expression levels.
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