Atorvastatin Protects against Ischemia-Reperfusion Injury in Fructose-Induced Insulin Resistant Rats

Abstract

Atorvastatin conferred significant protection against MI-RP injury and alleviated HFr induced IRS possibly by increasing NOS expression through Akt dependent pathway.

Atorvastatin protects obese mice against hepatic ischemia–reperfusion injury by Toll‐like receptor‐4 suppression and endothelial nitric oxide synthase activation

“…Only the latter has beneficial effects by causing vasodilatation of the hepatic microvasculature, opposing apoptosis of SEC, and suppressing thromboxane production 5,6 . Interestingly, while we observe little change in eNOS protein expression in livers from sham‐operated, atorvastatin‐treated mice, we acknowledge that this is in contradiction to other studies, where increments in eNOS are noted in myocardium and human umbilical vascular endothelial cells 35–39 . Thus, it is possible that statins de novo in liver‐derived cells have a different effect.…”

“…The increase in total eNOS in response to atorvastatin reflects the efficacy of statins to modulate NO production at the transcriptional level. [35][36][37][38][39] We also found that ATV also suppressed inducible NOS (iNOS) mRNA induction (not shown), which is under NF-kB regulatory control. The combined effect of iNOS suppression and eNOS induction/activation would be to diminish intracellular NO accumulation, with its unwanted effects on reactive nitrogen species generation and mitochondrial injury, at the same time promoting the endothelial cell secretion of NO.…”

“…Thus, in response to IRI, clear differences in eNOS and p‐eNOS expressions are observed. The increase in total eNOS in response to atorvastatin reflects the efficacy of statins to modulate NO production at the transcriptional level 35–39 . We also found that ATV also suppressed inducible NOS (iNOS) mRNA induction (not shown), which is under NF‐κB regulatory control.…”

“…5,6 Interestingly, while we observe little change in eNOS protein expression in livers from sham-operated, atorvastatin-treated mice, we acknowledge that this is in contradiction to other studies, where increments in eNOS are noted in myocardium and human umbilical vascular endothelial cells. [35][36][37][38][39] Thus, it is possible that statins de novo in liverderived cells have a different effect.…”

Low‐dose combination of alendronate and atorvastatin reduces ligature‐induced alveolar bone loss in rats

“…It has been shown that a nonchorinated BP, such as ALD, decreases MPO activity and reduces neutrophil influx into rat gingiva subjected to periodontitis . ATV has been shown to improve abnormalities in the free‐radical system and support the antioxidative defense mechanisms both in vitro and in vivo . Cadirci and colleagues have shown that a reduction of MPO levels after ATV therapy is accompanied by a concomitant decrease in the activity of the antioxidant enzyme, superoxide dismutase.…”