Overuse of therapeutic drugs such as acetaminophen often affects liver, and may lead to inflammatory mediated liver cell death. Here, we studied the effect of Terminalia arjuna (TA) bark against acetaminophen (APAP) induced liver cell death/injury by testing the antioxidant levels, oxidative stress, and inflammation and apoptosis markers. Wistar albino male rats weighing 180-280 mg/kg were made into 5 groups of 6 animals each and were treated as follows: Gr. I, control; Gr. II, acetaminophen (APAP); GR. III, N-acetylcysteine (NAC); Gr. IV & V, Terminalia arjuna (TA) 250 and mg/kg. The antioxidant glutathione (GSH), lipid peroxidation (MDA), interleukin 1β (IL-1β) levels, caspase-9 levels, and Protein kinase B (P-AKT) gene expression levels were assessed. The rGr. V animals pre-treated with Terminalia arjuna high dose bark showed increased glutathione (GSH) levels, but decreased malondialdehyde (MDA) levels; inhibited IL-1β and caspase-9 levels; and also elevated gene expression level of P-AKT to regulate the cell signaling pathway. Apparently, the results demonstrated that a high dose of TA 500 mg/kg ameliorated acetaminophen-induced hepatotoxicity.

中文翻译：

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榄仁提取物对对乙酰氨基酚诱导的Wistar白化病大鼠肝毒性的氧化应激，炎症和细胞凋亡的抑制作用

对乙酰氨基酚等治疗药物的过度使用通常会影响肝脏，并可能导致炎症介导的肝细胞死亡。在这里，我们通过测试抗氧化剂水平，氧化应激以及炎症和凋亡标记物，研究了榄仁（TA）树皮对乙酰氨基酚（APAP）诱导的肝细胞死亡/伤害的影响。将体重为180-280 mg / kg的Wistar白化病雄性大鼠分为5组，每组6只动物，并进行如下处理：我，控制；Gr。II，对乙酰氨基酚（APAP）; GR。III，N-乙酰半胱氨酸（NAC）；Gr。IV和V，阿特那榄仁（TA）250和mg / kg。抗氧化剂谷胱甘肽（GSH），脂质过氧化（MDA），白介素1β（IL-1β）水平，caspase-9水平和蛋白激酶B（P-AKT）基因表达水平进行了评估。rGr。用Terminalia arjuna高剂量树皮进行预处理的V动物的谷胱甘肽（GSH）水平升高，但丙二醛（MDA）水平降低；抑制IL-1β和caspase-9水平；P-AKT的基因表达水平升高，从而调节细胞信号通路。显然，结果表明，大剂量TA 500 mg / kg改善了对乙酰氨基酚引起的肝毒性。