Sebai Hichem, Jabri Mohamed-Amine, Souli Abdelaziz, Hosni Karim, Rtibi Kais, Tebourbi Olfa, El-Benna Jamel, Sakly Mohsen
Laboratoire de Physiologie Intégrée, Département des Sciences de la Vie, Faculté des Sciences de Bizerte, 7021 Zarzouna, Tunisia.
Gen Physiol Biophys. 2015 Jul;34(3):263-75. doi: 10.4149/gpb_2014039. Epub 2015 Mar 27.
The present study assessed the chemical composition, antioxidant properties, and hepatoprotective effects of subacute pre-treatment with chamomile (Matricaria recutita L.) decoction extract (CDE) against ethanol (EtOH)-induced oxidative stress in rats. The colorimetric analysis demonstrated that the CDE is rich in total polyphenols, total flavonoids and condensed tannins, and exhibited an important in vitro antioxidant activity. The use of LC/MS technique allowed us to identify 10 phenolic compounds in CDE. We found that CDE pretreatment, in vivo, protected against EtOH-induced liver injury evident by plasma transaminases activity and preservation of the hepatic tissue structure. The CDE counteracted EtOH-induced liver lipoperoxidation, preserved thiol -SH groups and prevented the depletion of antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). We also showed that acute alcohol administration increased tissue and plasma hydrogen peroxide (H(2)O(2)), calcium and free iron levels. More importantly, CDE pre-treatment reversed all EtOH-induced disturbances in intracellular mediators. In conclusion, our data suggest that CDE exerted a potential hepatoprotective effect against EtOH-induced oxidative stress in rat, at least in part, by negatively regulating Fenton reaction components such as H(2)O(2) and free iron, which are known to lead to cytotoxicity mediated by intracellular calcium deregulation.
本研究评估了亚急性预处理洋甘菊(母菊)水煎提取物(CDE)对乙醇(EtOH)诱导的大鼠氧化应激的化学成分、抗氧化特性及肝脏保护作用。比色分析表明,CDE富含总多酚、总黄酮和缩合单宁,并表现出重要的体外抗氧化活性。采用LC/MS技术使我们能够鉴定出CDE中的10种酚类化合物。我们发现,CDE体内预处理可预防EtOH诱导的肝损伤,这可通过血浆转氨酶活性及肝组织结构的保存得以证明。CDE可抵消EtOH诱导的肝脏脂质过氧化,保留巯基-SH基团,并防止超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的抗氧化酶活性耗竭。我们还表明,急性酒精给药会增加组织和血浆中的过氧化氢(H₂O₂)、钙和游离铁水平。更重要的是,CDE预处理可逆转所有EtOH诱导的细胞内介质紊乱。总之,我们的数据表明,CDE对EtOH诱导的大鼠氧化应激具有潜在的肝脏保护作用,至少部分是通过负向调节Fenton反应成分如H₂O₂和游离铁来实现的,已知这些成分会导致细胞内钙失调介导的细胞毒性。