A number of liver diseases are known to be caused by oxidative stress. Petroselinum sativum (P. sativum; parsley) is popular for its anti-inflammatory, antimicrobial, anticancer, antioxidant and antidiabetic activities. However, till date the hepatoprotective potential of chloroform extract of P. sativum (PSA) on hydrogen peroxide (H2O2) induced cytotoxicity and oxidative stress in human liver (HepG2) cells have not been studied. Therefore, this study was framed to evaluate whether the levels of hydrogen peroxide (H2O2) induced cytotoxicity and oxidative stress in HepG2 cells could be diminished by pretreating the cells with PSA. MTT assay, NRU assay, morphological alterations, glutathione (GSH) depletion, lipid peroxidation (LPO), ROS generation and loss of mitochondrial membrane potential (MMP) were assessed by using non-cytotoxic concentrations (5, 10 and 25 μg/mL) of PSA against H2O2 (0.25 mM) induced damage in HepG2 cells. The results demonstrated that pretreatment of HepG2 cells with PSA offered protective properties by lowering the LPO and ROS generation and elevating the cell viability, GSH and MMP levels. Together, these results suggest that PSA has the hepatoprotective effect on H2O2 induced cell death in HepG2 cells.

中文翻译：

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石油白僵菌保护HepG2细胞免受过氧化氢诱导的细胞毒性和氧化应激。

已知许多肝脏疾病是由氧化应激引起的。石油Petroselinum sativum（P. sativum;荷兰芹）因其抗炎，抗微生物，抗癌，抗氧化和抗糖尿病作用而广受欢迎。然而，迄今为止，尚未研究过辣椒（Psa Sativum）的氯仿提取物（PSA）对过氧化氢（H2O2）诱导的人肝细胞（HepG2）细胞毒性和氧化应激的保护作用。因此，本研究旨在评估过氧化氢（H2O2）诱导的HepG2细胞细胞毒性和氧化应激水平是否可以通过用PSA预处理细胞而降低。MTT分析，NRU分析，形态学改变，谷胱甘肽（GSH）耗竭，脂质过氧化（LPO），通过使用非细胞毒性浓度（5、10和25μg/ mL）的PSA对抗H2O2（0.25 mM）诱导的HepG2细胞损伤，评估ROS的产生和线粒体膜电位（MMP）的损失。结果表明，用PSA预处理HepG2细胞可通过降低LPO和ROS生成并提高细胞活力，GSH和MMP水平来提供保护性能。总之，这些结果表明PSA对H2O2诱导的HepG2细胞死亡具有肝保护作用。