Atorvastatin restores arsenic-induced vascular dysfunction in rats: Modulation of nitric oxide signaling and inflammatory mediators

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dc.contributor.authorKesavan, Manickam
dc.contributor.authorSasindran Sarath, Thengumpallil
dc.contributor.authorKannan, Kandasamy
dc.contributor.authorSuresh, Subramaniyam
dc.contributor.authorGupta, Priyanka
dc.contributor.authorVijayakaran, Karunakaran
dc.contributor.authorSankar, Palanisamy
dc.contributor.authorKurade, Nitin Pandurang
dc.contributor.authorMishra, Santosh Kumar
dc.contributor.authorSarkar, Souvendra Nath
dc.contributor.authorTANUVAS
dc.date.accessioned2018-06-06T06:43:52Z
dc.date.available2018-06-06T06:43:52Z
dc.date.issued2014
dc.descriptionTNV_TAP_2014_280(107-116)en_US
dc.description.abstractWe evaluated whether atorvastatin, an extensively prescribed statin for reducing the risks of cardiovascular diseases, can reduce the risk of arsenic-induced vascular dysfunction and inflammation in rats and whether the modulation could be linked to improvement in vascular NO signaling. Rats were exposed to sodium arsenite (100 ppm)through drinkingwater for 90 consecutive days. Atorvastatin (10 mg/kgbw, orally)was administered once daily during the last 30 days of arsenic exposure. On the 91st day, blood was collected for measuring serum C-reactive protein. Thoracic aorta was isolated for assessing reactivity to phenylephrine, sodium nitroprusside and acetylcholine; evaluating eNOS and iNOS mRNA expression and measuring NO production,while abdominal aorta was used for ELISA of cytokines, chemokine and vascular cell adhesionmolecules. Histopathologywas done in aortic arches. Arsenic did not alter phenylephrine-elicited contraction. Atorvastatin inhibited Emax of phenylephrine, but it augmented the contractile response in aortic rings from arsenic-exposed animals. Sodium nitroprusside-induced relaxation was not altered with any treatment. However, arsenic reduced acetylcholineinduced relaxation and affected aortic eNOS at the levels of mRNA expression, protein concentration, phosphorylation and NO production. Further, it increased aortic iNOS mRNA expression, iNOS-derived NO synthesis, production of pro-inflammatory mediators (IL-1β, IL-6, MCP-1, VCAM, sICAM) and serum C-reactive protein and aortic vasculopathic lesions. Atorvastatin attenuated these arsenic-mediated functional, biochemical and structural alterations. Results show that atorvastatin has the potential to ameliorate arsenic-induced vascular dysfunction and inflammation by restoring endothelial function with improvement in NO signaling and attenuating production of pro-inflammatory mediators and cell adhesion molecules.en_US
dc.identifier.urihttp://krishikosh.egranth.ac.in/handle/1/5810049383
dc.keywordsArsenic Atorvastatin Vascular dysfunction Nitric oxide signaling Inflammatory mediators Raten_US
dc.language.isoenen_US
dc.pages107-116en_US
dc.publisherElsevieren_US
dc.subjectnullen_US
dc.titleAtorvastatin restores arsenic-induced vascular dysfunction in rats: Modulation of nitric oxide signaling and inflammatory mediatorsen_US
dc.title.alternativeToxicology and Applied Pharmacologyen_US
dc.typeArticleen_US
dc.volume280en_US
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