The Prophylactic Activity of Punica granatum L. mesocarp Protects Preadipocytes against Ribosylated BSA-Induced Toxicity

被引:1
作者
Ramlagan, P. [1 ,2 ]
Rondeau, P. [3 ]
Neergheen, V. S. [1 ,2 ]
Bourdon, E. [3 ]
Bahorun, T. [2 ,4 ]
机构
[1] Univ Mauritius, Dept Hlth Sci, Fac Sci, Reduit, Mauritius
[2] Univ Mauritius, Ctr Biomed & Biomat Res, Biopharmaceut Unit, Reduit, Mauritius
[3] Univ Reunion, UMR DETROIT INSERM U1188, Diabete Atherothrombose Therapies Reunion Ocean I, St Denis, Reunion, France
[4] Univ Mauritius, Fac Sci, Dept Biosci & Ocean Studies, Reduit, Mauritius
关键词
Pomegranate mesocarp; prophylactic activity; preadipocytes; BSA(RIB); oxidative damage;
D O I
10.1080/07315724.2020.1793701
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Objective It was aimed at comparing the glycating capacities of glucose and ribose in bovine serum albumin (BSA) and anti-glycation activity of pomegranate mesocarp extract (PME). The protective mechanism of PME against ribosylated BSA (BSA(RIB))-induced toxicity was also investigated. Methods BSA was incubated with glucose or ribose in the presence or absence of PME for 15 days. In preadipocytes pretreated with PME, cell viability, ROS production, lipid peroxidation and mitochondrial membrane potential were investigated following 1, 6, 12, 18 and 24 h exposure to BSA(RIB). Nuclear translocation of NF kappa B was assessed at 1 h and 24 h of BSA(RIB) insult. Accumulation of oxidized proteins, activities of intrinsic antioxidant enzymes and IL-6 secretion were also determined after 24 h exposure to BSA(RIB). Results Ribose was a harsher glycating agent as compared to glucose and PME showed strong anti-glycation activity by suppressing (P < 0.05) the increase in levels of fluorescent AGEs, Amadori products, protein carbonyl and advanced oxidation protein products (AOPP). In preadipocytes, BSA(RIB) potentiated pro-apoptotic activity by inhibiting the nuclear translocation of NF kappa B. BSA(RIB) induced a time dependent decrease in cell viability, which was significantly suppressed (P < 0.05) by PME. The extract also significantly reduced (P < 0.05) the time dependent increase in ROS level and associated lipid peroxidation as well as loss in mitochondrial membrane potential caused by BSA(RIB). PME also counteracted the BSA(RIB)-induced accumulation of oxidized proteins, decrease in intrinsic antioxidant activity and IL-6 over-secretion. Conclusions PME showed anti-glycation activity and afforded protection against BSA(RIB)-induced toxicity, oxidative stress and inflammation in preadipocytes.
引用
收藏
页码:502 / 516
页数:15
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