Freshwater Biosources Utilization Bureau, Bioresources Industrialization Support Division, Nakdonggang National Institute of Biological Resources (NNIBR), Sangju, Republic of Korea.
Department of Food Technology and Nutrition, Chonnam National University, Yeosu, Republic of Korea.
Adv Exp Med Biol. 2019;1155:583-596. doi: 10.1007/978-981-13-8023-5_53.
In this study, we evaluated the protective effects of an aqueous extract from Batillus cornutus meat (BM) against cellular oxidative damage caused by hydrogen peroxide (HO) in human hepatocyte, Chang cells. First, we prepared an aqueous extract of BM meat (BMW) showing the highest taurine content among free amino acid contents. BMW led to high antioxidant activity showing 2,2-azino-bis(3-ethylbenzthiazoline)-6-sulfonic acid (ABTS) radical scavenging activity, good reducing power and an oxygen radical absorbance capacity (ORAC) value. Also, BMW improved cell viability that was diminished by HO exposure, as it reduced the generation of intracellular reactive oxygen species (ROS) in Chang cells. In addition, BMW up-regulated the production of antioxidant enzymes, such as catalase and superoxide dismutase (SOD), compared to HO-treated Chang cells lacking BMW. Moreover, BMW induced the expressions of nuclear Nrf2 and cytosolic HO-1 in HO-treated Chang cells. Interestingly, the treatment of ZnPP, HO-1 inhibitor, abolished the improvement in cell viability and intracellular ROS generation mediated by BMW treatment. In conclusion, this study suggests that BMW protects hepatocytes against HO-mediated cellular oxidative damage via up-regulation of the Nrf2/HO-1 signal pathway.
在这项研究中,我们评估了来自角雉肉(BM)的水提取物对人肝细胞Chang 细胞中过氧化氢(HO)引起的细胞氧化损伤的保护作用。首先,我们制备了一种水提取物,其中肉碱的游离氨基酸含量最高。BMW 具有较高的抗氧化活性,表现出 2,2-氮杂双(3-乙基苯并噻唑啉)-6-磺酸(ABTS)自由基清除活性、良好的还原能力和氧自由基吸收能力(ORAC)值。此外,BMW 改善了因 HO 暴露而降低的细胞活力,因为它减少了 Chang 细胞内活性氧物种(ROS)的产生。此外,与缺乏 BMW 的 HO 处理的 Chang 细胞相比,BMW 上调了过氧化氢酶和超氧化物歧化酶(SOD)等抗氧化酶的产生。此外,BMW 诱导了 HO 处理的 Chang 细胞中核 Nrf2 和胞质 HO-1 的表达。有趣的是,HO-1 抑制剂 ZnPP 的处理消除了 BMW 处理介导的细胞活力和细胞内 ROS 生成改善。总之,本研究表明,BMW 通过上调 Nrf2/HO-1 信号通路来保护肝细胞免受 HO 介导的细胞氧化损伤。