甘草酸、姜黄素和肉桂对刀豆素a和对乙酰氨基酚所致小鼠肝损伤和氧化应激的预防作用

Zulfia Hussain, Haroon Rashid, Aqsa Mushtaq, R. Siddique, Ashiq Ali
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摘要

每天接触多种外源性药物是导致肝损伤的主要因素。本研究通过刀豆素a (ConA)和对乙酰氨基酚(APAP)两种不同的肝毒性模型,探讨了甘草酸、姜黄素和肉桂对肝的保护机制。为此,balb/c小鼠分别用甘草酸(200 mg/kg ig)、姜黄素(100 mg/kg ig)和肉桂(200 mg/kg ig)提取物预处理14天,然后给药ConA (15 mg/kg ig)和APAP (200 mg/kg ig) 8小时。实验结束时,解剖小鼠,取血液和肝脏标本进行生化和组织病理学分析。统计分析采用单因素方差分析,DMR检验结果的显著性。结果表明,甘草酸、姜黄素和肉桂预处理可改善ConA和APAP对肝脏的损伤作用,并可提高血清转氨酶和总蛋白水平。此外,组织病理学分析证实,ConA和APAP对肝组织有严重的损伤。然而,甘草酸、姜黄素和肉桂可能通过抗氧化机制预防肝损伤。综上所述,甘草酸、姜黄素和肉桂具有抗氧化作用,对氧化应激性肝损伤具有治疗作用。
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Glycyrrhizin, Curcumin and Cinnamon Prevent From Concanavalin-A and Acetaminophen-Induced Liver Injury and Oxidative Stress in Mouse Model
Daily exposure to a number of xenobiotics is the major contributing factor to liver injury. The present study investigated the mechanism of hepatoprotection by glycyrrhizin, curcumin and cinnamon in two distinct models of hepatotoxicity i.e., by using Concanavalin-A (ConA) and Acetaminophen (APAP). For this evaluation, balb/c mice were pretreated with glycyrrhizin (200 mg/kg i.g.), curcumin (100 mg/kg i.g.) and cinnamon (200 mg/kg i.g.) extracts for 14 days followed by administration of ConA (15 mg/kg i.v.) and APAP (200 mg/kg i.p.) for 8 hours. At the end of the experiment, mice were dissected and blood and liver samples were collected for biochemical and histopathological analysis. Statistical analysis by using one-way ANOVA followed by DMR test was performed for the significance of results. The results showed that pre-treatment of glycyrrhizin, curcumin and cinnamon ameliorated the damaging effects of ConA and APAP on the liver as indicated by the serum transaminase enzymes and total protein levels. In addition, ConA and APAP exerted severe damage on liver tissues as confirmed from the histopathological analysis. However, glycyrrhizin, curcumin and cinnamon prevented liver injury, possibly through antioxidant mechanism. In conclusion, glycyrrhizin, curcumin and cinnamon possessed antioxidant properties with therapeutic potential in liver injury related to oxidative stress.
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