Emodin attenuates CY-induced oxidative injury in PBLs of the blunt snout bream (Megalobrama amblycephala) though the Nrf2-Keap1 signaling pathway

文献类型： 外文期刊

第一作者： Zhao, Zhenxin

作者： Zhao, Zhenxin;Li, Zhengyou;Yang, Xing;Zhou, Zhou;Zhao, Feng;Zhao, Zhenxin;Li, Zhengyou;Yang, Xing;Zhou, Zhou;Zhao, Feng;Liu, Bo;Ge, Xianping;Liu, Bo;Ge, Xianping

作者机构：

关键词： Cyclophosphamide; Emodin; Protective mechanism; Oxidative injury; Megalobrama amblycephala

期刊名称：AQUACULTURE （ 影响因子：5.135； 五年影响因子：5.125 ）

ISSN： 0044-8486

年卷期： 2021 年 545 卷

页码：

收录情况： SCI

摘要： The present study aimed to evaluate the protective effects of emodin on cyclophosphamide (CY)-induced oxidative injury in peripheral blood leukocytes (PBLs) of blunt snout bream and the potential mechanisms. We examined the cell viability, lactate dehydrogenase (LDH) release, apoptosis, mitochondrial membrane potential (Delta psi m), reactive oxygen species (ROS) generation and correlative gene expression of nuclear factor-erythroid 2 related factor-2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) signaling molecules. For the control group, PBLs were maintained in normal cell culture medium for 12 h. For the CY group, cells were exposed to 0.32 mg/ mL CY for 6 h, followed by maintaining in RPMI-1640 complete medium for an additional 6 h. Cells in the CY + Emodin group were exposed to 0.32 mg/mL CY for 6 h, and then exposed to 0.20 mu g/mL emodin for 6 h. We observed that emodin significantly inhibited CY-induced apoptosis in PBLs through increasing cell viability and decreasing LDH release. Emodin also inhibited Delta psi m disruption and respiratory burst in CY-induced PBLs. In consistent with these results, emodin attenuated oxidative stress in CY-induced PBLs by significantly upregu-lating Nrf2, BTB and CNC homolog 1 (Bach1), superoxide dismutase (SOD) and catalase (CAT) genes while significantly downregulates Keap1 in Nrf2-Keap1 signaling pathway. These results collectively demonstrate that emodin can alleviate CY-induced oxidative stress in the PBLs of blunt snout bream, possibly through activating Nrf2-Keap1 signaling pathway. Our findings also suggest that emodin might be developed as a promising therapeutic agent for treating oxidative injury in blunt snout bream.

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