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Trehalose protects the endothelium from cadmium-induced dysfunction.
Sarwareddy K Kumar1, Tarun Prakash1, Miralini Vetriselvan1
1Vascular Research Laboratory, School of Chemical and Biotechnology, SASTRA Deemed University, Thanjavur, India.
Cell Biology International
|December 29, 2020
Summary
Trehalose protects against cadmium chloride-induced endothelial dysfunction by restoring nitric oxide (NO) production and decreasing oxidative stress. This study highlights trehalose
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Cadmium chloride (CdCl2) induces endothelial cell dysfunction.
- Oxidative stress and reduced nitric oxide (NO) production are key features of CdCl2 toxicity.
- Endothelial nitric oxide synthase (eNOS) plays a critical role in regulating vascular function.
Purpose of the Study:
- To investigate the protective role of trehalose (Tre) against CdCl2-induced endothelial cell dysfunction.
- To elucidate the mechanisms underlying trehalose's protective effects.
Main Methods:
- Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay for cell viability.
- Griess assay and fluorescence probe for nitric oxide (NO) measurement.
- Western blotting for eNOS and phospho-eNOS (peNOS) expression.
- Reactive oxygen species (ROS) detection.
Main Results:
- CdCl2 significantly reduced endothelial cell viability and NO production.
- CdCl2 treatment decreased eNOS and peNOS expression and increased ROS production.
- Co-incubation with trehalose (Tre) mitigated CdCl2-induced cytotoxicity.
- Tre restored NO production, eNOS and peNOS expression, and reduced ROS levels in CdCl2-treated cells.
Conclusions:
- Trehalose exhibits significant protective effects against cadmium chloride-induced endothelial dysfunction.
- Trehalose ameliorates CdCl2 toxicity by enhancing NO bioavailability and reducing oxidative stress.
- Trehalose represents a potential therapeutic agent for mitigating cadmium-induced vascular damage.
