Comparative study of amlodipine vs. cilnidipine for the prevention of hepatic ischemia‐reperfusion injury in rat model

Abstract

Ca signaling plays crucial role in ischemia and reperfusion (I/R) injury. Although blockade of L-type Ca channels by amlodipine (AML) has been shown to suppress hepatic I/R injury in several animal models, information is still needed regarding the hepatoprotective effects of the dual L/N-type Ca channel blockers, cilnidipine (CIL). We examined the effect of pretreatment with AML or CIL (100 μg/kg i.p.) 45 min before induction of 60 min of liver ischemia followed by reperfusion, on oxidative stress markers, liver enzymes, serum tumor necrosis factor-α, interleukin-1β, apoptosis markers, and nuclear factor KB after 6 and 24 h of hepatic reperfusion. Both drugs significantly ameliorated biochemical and histological markers of hepatic I/R injury, but protection with CIL was more significant at the 6-h time point where protection with AML outlasted that of CIL. Both drugs offered significant protection against hepatic I/R damage, but the protection with CIL seemed more potent but of shorter duration than that observed with AML possibly due to the shorter half-life of CIL.

Protective effect of fenofibrate against ischemia‐/reperfusion‐induced cardiac arrhythmias in isolated rat hearts

“…A growing number of evidences have revealed that increased oxidative stress, upregulation of the inflammatory mediators tumor necrosis factor-a (TNFa) and interleukin 6 (IL-6), and downregulation of the anti-inflammatory cytokine IL-10 play pivotal role in cardiac arrest and I/R-induced cardiac damage [30][31][32][33]. Therefore, it is likely that the observed cardiac protective effect of fenofibrate in our study may have occurred via enhanced EETs production and subsequent suppression of the aforementioned pathological pathways in rat myocardial cells [34]. EETs function as EDHF and dilate coronary arteries [8,9,15], which is beneficial for cardiac function.…”