Effects of Renal Ischemic Postconditioning on Myocardial Ultrastructural Organization and Myocardial Expression of Bcl-2/Bax in Rabbits

Abstract

We investigated the cardioprotective effect of renal ischemic postconditioning (RI-PostC) and its mechanisms in a rabbit model. Rabbits underwent 60 min of left anterior descending coronary artery occlusion (LADO) and 6 h of reperfusion. The ischemia-reperfusion (IR) group underwent LADO and reperfusion only. In the RI-PostC group, the left renal artery underwent 3 cycles of occlusion for 30 seconds and release for 30 seconds, before the coronary artery was reperfused. In the RI-PostC + GF109203X group, the rabbits received 0.05 mg/kg GF109203X (protein kinase C inhibitor) intravenously for 10 min followed by RI-PostC. Light microscopy and electron microscopy demonstrated that the RI-PostC group showed less pronounced changes, a smaller infarct region, and less apoptosis than the other two groups. Bcl-2 and Bax protein expression did not differ between the IR and RI-PostC + GF109203X groups. However, in the RI-PostC group, Bcl-2 protein expression was significantly higher and Bax protein expression was significantly lower than in the other two groups (P < 0.05). Changes in heart rate and mean arterial pressure were also smaller in the RI-PostC group than in the other two groups. These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.

The protective effects of ischemic preconditioning on rats with renal ischemia-reperfusion injury and the effects on the expression of Bcl-2 and Bax

“…Renal blood flow needs to be blocked in renal transplantation, nephrolithotomy and surgical resection of renal tumors and other complex surgeries, and renal reperfusion after blood flow blocking can cause renal damage ( 10 ). Numerous studies have shown that ischemia-reperfusion injury may be related to the production of oxygen free radicals, adenine nucleotide metabolic disorders and cell apoptosis ( 11 ). Drugs (ulinastatin and propofol), low temperature, preconditioning and postconditioning can play a protective role in ischemia-reperfusion injury, and all these methods can be used to reduce ischemia-reperfusion injury to the kidneys ( 12 – 14 ).…”

Leptin and curcumin affect renal ischemia-reperfusion injury via modulation of P65 and Bax genes expression

“…Ischemia-reperfusion injury may be related to the synthesis of proinflammatory mediators, production of oxygen free radicals, and cell apoptosis [2]. The mechanisms that lead to the synthesis of proinflammatory and apoptotic mediators have been in-vestigated in recent years [3].…”