| Abstrakt: |
Background: Ischemia-reperfusion injury (IRI) occurs when the blood supply to tissue diminishes and subsequently restore. The basic pathophysiology involves reactive oxygen species, robust inflammation, and induction of cell death pathways terminated in organ dysfunction. Renal ischemia-reperfusion is a major cause of acute kidney injury (AKI) that occurs in clinical conditions implicates the challenge such as in transplantation surgery, renal artery stenosis, sepsis, cardiopulmonary bypass, and trauma. Objectives: This study was undertaken to investigate the potential protective effect of Vinpocetine (alkaloid extract of a periwinkle plant)on bilateral renal IRI in male rats, through study the effectiveness of Vinpocetine on renal function, it's possible role in modulation of the inflammatory cascade, and its anti-oxidant & anti apoptotic effect. Methods: A twenty-adult male Wistar albino rats, weights about (220-260 gm), aged 8-12 weeks, after two weeks of acclimatization, the rats were randomly divided into four groups (5 rats in each group) as follows: Sham group: rats underwent the same anesthetic and surgical procedure except clamping of the bilateral renal artery. Control group: rats subjected to the bilateral renal ischemia for 30 min by clamping renal pedicles and reperfusion for 2 hours. Vehicle group: rats received 10 % DMSO by I.P route before 30 min of induction of bilateral renal ischemia for 30 min by clamping of the pedicles and then 2 hours reperfusion. Vinpocetine pretreated group: rats pretreated with vinpocetine10 mg/kg I.P, 30 min before clamping of the renal pedicles and then underwent bilateral renal ischemia for 30 min and then reperfusion for 2 hours. At the end of the procedure, all rats were sacrificed and tissue and blood samples were collected. Samples subjected to various outcomes measurements including renal function test (serum urea and creatinine), renal level of inflammatory mediators (TNFα, IL-6), and total antioxidant capacity (TAC) were carried via the ELISA technique. Immunohistochemistry also was done to investigate proapoptotic protein (BAX) and antiapoptotic protein (BCL-2) and microscopical examinations were performed to determine the parenchyma injury. Results: The renal ischemia-reperfusion injury (RIRI) caused significant (p≤0.05) higher serum level of Urea& Creatinine and renal level of TNFα, IL-6, and BAX in control (+IR) and vehicle groups than those in the sham group. On the other hand, the renal level of TAC and Bcl-2 in both control and vehicle groups are significantly (p≤0.05) lower than those in the sham group. While pretreated vinpo group showed significantly (p≤0.05) lower serum level of urea S. Cr and lower renal level of TNFα, IL-6, and BAX in comparison to those in control and vehicle groups, besides the study, showed that the level of renal TAC and Bcl-2 in vinpo pretreated group significantly (p≤0.05) higher than that in control and vehicle groups. Histopathological findings of renal tissue in the vinpo pretreated group demonstrated significantly (p≤0.01) lower grade of architecture abnormality and severity of tubular damage when compared with control and vehicle groups. Conclusions: The present study found that Vinpocetine pretreatment attenuated renal IR injury in a rat model, mainly via improving renal function, oxidative modulating effects, suppressing inflammation, and decreasing cell apoptosis. [ABSTRACT FROM AUTHOR] |
