Zhao Bin-Bin, Meng Jun, Zhang Qiu-Xiang, Kang Ting-Ting, Lu Rong-Rong
School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi, Jiangsu 214122, China.
School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi, Jiangsu 214122, China; School of Food Science and Technology, Henan University of Technology, Zhengzhou, Henan Province 450001, China.
Int J Biol Macromol. 2017 Sep;102:76-83. doi: 10.1016/j.ijbiomac.2017.03.160. Epub 2017 Mar 30.
The objective of this study was to explore the antioxidant effect of the surface layer proteins (SLPs) and their mechanism. We investigated four SLPs which were extracted from L. casei zhang, L. rhamnosus, L. gasseri and L. acidophilus NCFM respectively using LiCl. The protective effect of SLPs on HO-induced HT-29 cells oxidative injury was investigated. As results, SLPs (100μg/mL) could significantly mitigate HT-29 cells cytotoxicity, improve the activities of total antioxidant capacity (T-AOC), catalase (CAT) and superoxide dismutase (SOD), decrease the contents of malondialdehyde (MDA) and lactate dehydrogenase (LDH), compared with HO-induced group (P<0.05). Furthermore, SLPs were also shown to attenuate the apoptosis rate (10.94-24.03%, P<0.01), suppress the elevation of intracellular reactive oxygen species (ROS) and calcium levels, restore mitochondrial membrane potential (MMP) and block the activation of apoptosis-related proteins of caspase-3 and caspase-9 (P<0.05). Considering all the parameters analyzed, we concluded that Lactobacillus SLPs play an essential role in the antioxidant capacity of HT-29 cells induced by HO, and the mechanism could be attributed to SLPs' ability to enhance the activity of the intracellular antioxidant enzyme system, reduce ROS accumulation and to inhibit apoptosis by regulating mitochondrial pathway.
本研究的目的是探讨表层蛋白（SLPs）的抗氧化作用及其机制。我们研究了分别用LiCl从干酪乳杆菌zhang、鼠李糖乳杆菌、加氏乳杆菌和嗜酸乳杆菌NCFM中提取的四种SLPs。研究了SLPs对过氧化氢（HO）诱导的HT-29细胞氧化损伤的保护作用。结果显示，与HO诱导组相比，SLPs（100μg/mL）可显著减轻HT-29细胞的细胞毒性，提高总抗氧化能力（T-AOC）、过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性，降低丙二醛（MDA）和乳酸脱氢酶（LDH）的含量（P<0.05）。此外，SLPs还可降低凋亡率（10.94-24.03%，P<0.01），抑制细胞内活性氧（ROS）水平和钙水平的升高，恢复线粒体膜电位（MMP），并阻断凋亡相关蛋白caspase-3和caspase-9的激活（P<0.05）。综合分析所有参数，我们得出结论，乳酸菌SLPs在HO诱导的HT-29细胞抗氧化能力中起重要作用，其机制可能归因于SLPs增强细胞内抗氧化酶系统活性、减少ROS积累以及通过调节线粒体途径抑制凋亡的能力。
