Trehalose protects the endothelium from cadmium-induced dysfunction.

The objective of the present study is to identify the possible regulatory role of trehalose (Tre) against cadmium chloride (CdCl )-induced endothelial cell dysfunction. To screen the dose-dependent effect of both Tre and CdCl , a methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was performed. Interestingly, MTT assay results have shown that co-incubation of Tre (1 mM) with CdCl significantly decreased the CdCl (5 µM) cytotoxicity. Nitric oxide (NO) measurement using Griess assay and 4-amino-5-methylamino-2',7'-difluorofluorescein fluorescence probe results have shown that CdCl decreases NO production in endothelial cells. Western blotting analysis results showed that CdCl decreases endothelial nitric oxide synthase (eNOS) and phospho endothelial nitric oxide synthase (peNOS) expression. The present study results have also observed that CdCl treatment increases reactive oxygen species (ROS) production. However, combination treatment (Tre + CdCl ) could restore the NO production in CdCl -treated cells. In addition, combination treatment could also restore eNOS and peNOS expression in endothelial cells. Moreover, Tre treatment was found to decrease CdCl -induced ROS production. Collectively, the present study results demonstrate that Tre possesses a significant protective action against CdCl -mediated endothelial dysfunction by increasing NO production, eNOS and peNOS expression, and by decreasing oxidative stress.