Renoprotective effect of vinpocetine and cilostazol on glycerol induced renal injury in male rats

 Acute kidney injury (AKI) is characterized by a sudden loss of kidney function that is established by increased serum creatinine levels and decreased urinary output. AKI is one of a group of functional kidney conditions known as acute kidney disease and disorders (AKD), which can vary in severity and self-limiting to severe and chronic. Adminstrations of glycerol generate significant elevation in serum urea and creatinine that’s mean occurance of functional abnormalities in the kidney. Vinpocetine drug has many pharmacological targets with multiple action, phosphodiesterase inhibiters-1(PDE-1) inhibitor, a voltage-gated sodium channel, and Inhibitory kinase B (IKK) are 3 main molecule targets of vinpocetine. PDE1 has been implicated in the regulation of vasoconstriction, vascular and cardiac structure remodeling, and neuro-transmission. Cilostazol, a phosphodiesterase (PDE) III inhibitors, that widely used for many cases such as reduces direct vascular injury via different mechanism, such as vasodilation and antiplatelet action, anti-inflammation and platelet-leukocyte interaction minimisation, and inhibition of vascular proliferation via up-regulation of hepatocyte growth factors. In present study, we looked at the effect and mechanism of the drugs vinpocetine and cilostazol in an animal model of glycerol-induced AKI. Experiment done during the 14-day trial, rats were divided into five groups: the control group received 2ml/kg normal saline; the induction group received 10ml/kg intramuscular glycerol injection; the vinpocetine group received 5mg/kg via gavage for 14 days and on day 7 given glycerol IM, the cilostazol group received 50mg/kg for 14 days and on day 7 given glycerol IM, and the combination group received half dose vinpocetine (2.5mg/kg) and cilostazol (25mg/kg). We discovered that the induction group had higher levels of urea and creatinine, as well as increased inflammation and oxidative stress, and that their renal tissue showed morphological changes typical of AKI, whereas the combination groups reduced glycerol induce acute renal damage. This revealed that vinpocetine and cilostazol can reinforce renal rat protection by reducing serum urea and creatinine and improving histopathological changes.