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The Prophylactic Activity of Punica granatum L. mesocarp Protects Preadipocytes against Ribosylated BSA-Induced Toxicity.
Journal of the American College of Nutrition 2021 Februrary 20
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 (BSARIB )-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 BSARIB . Nuclear translocation of NFκB was assessed at 1 h and 24 h of BSARIB insult. Accumulation of oxidized proteins, activities of intrinsic antioxidant enzymes and IL-6 secretion were also determined after 24 h exposure to BSARIB .
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, BSARIB potentiated pro-apoptotic activity by inhibiting the nuclear translocation of NFκB. BSARIB 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 BSARIB . PME also counteracted the BSARIB -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 BSARIB -induced toxicity, oxidative stress and inflammation in preadipocytes.
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 BSARIB . Nuclear translocation of NFκB was assessed at 1 h and 24 h of BSARIB insult. Accumulation of oxidized proteins, activities of intrinsic antioxidant enzymes and IL-6 secretion were also determined after 24 h exposure to BSARIB .
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, BSARIB potentiated pro-apoptotic activity by inhibiting the nuclear translocation of NFκB. BSARIB 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 BSARIB . PME also counteracted the BSARIB -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 BSARIB -induced toxicity, oxidative stress and inflammation in preadipocytes.
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