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Combination of carnosine and asiatic acid provided greater anti-inflammatory protection for HUVE cells and diabetic mice than individual treatments of carnosine or asiatic acid alone

The purpose of present HUVE cells and mice study was to investigate the combined effects of carnosine and asiatic acid (AA) against diabetic progression. In HUVE cells, high glucose decreased cell viability, reduced Bcl-2 mRNA expression and increased Bax mRNA expression. The co-treatment of 0.5 μM...

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Published in:Food and chemical toxicology 2019-04, Vol.126, p.192-198
Main Authors: Yan, Sheng-lei, Wang, Zhi-hong, Mong, Mei-chin, Yang, Ya-chen, Yin, Mei-chin
Format: Article
Language:English
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Summary:The purpose of present HUVE cells and mice study was to investigate the combined effects of carnosine and asiatic acid (AA) against diabetic progression. In HUVE cells, high glucose decreased cell viability, reduced Bcl-2 mRNA expression and increased Bax mRNA expression. The co-treatment of 0.5 μM carnosine plus 0.5 μM AA led to greater cell viability and Bcl-2 mRNA expression than 1 μM carnosine or 1 μM AA treatment alone. This combination more significantly decreased the production of DNA fragmentation, tumor necrosis factor (TNF)-alpha, reactive oxygen species (ROS), and nuclear factor kappa B binding activity than carnosine or AA treatment alone. In diabetic mice, the combination of 0.25% carnosine plus 0.25% AA in diet resulted in higher final body weight, and lower levels of plasma glucose and triglyceride than 0.5% carnosine or 0.5% AA treatment alone. Carnosine and AA combination caused more reduction in renal levels of leukin-6, TNF-alpha and ROS than carnosine or AA treatment alone. This combination also more significantly limited renal cyclooxygenase-2 activity and p-p38 phosphorylation than carnosine or AA treatment alone. These novel findings support that this combination is a more powerful remedy for diabetic control. Effects of carnosine (Car) and/or AA upon NF-κB p50/65 binding activity (OD value/mg protein). HUVE cells were pre-treated with 1 μM Car, 1 μM AA or 0.5 μM Car+0.5 μM AA for 24 h incubation at 37 °C. Then, cells were treated with DMEM containing high glucose (33 mM), and followed by incubating for another 24 h at 37 °C. Normal group had no Car, AA, or high glucose. Control group had no Car or AA, but with high glucose. Data are mean ± SD (n = 6). Values with different alphabet among bars are significantly different at P 
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2019.02.027