Modulation Renal Expression of mTOR Gene via Calcitriol on RIRI in Rats

Background: It seems that IRI is primary factor causing morbidity and death in a number of conditions; including sepsis, MI, and AKI. The microvascular system undergoes structural and functional alterations as a result of ischaemia. Additionally, endothelial layer of capillaries produces ROS in response to the fast reperfusion of ischaemic tissues by blood, which exacerbates the NFκB pathway and inflammatory process. Several inflammatory components such as IL-1β, and TNF-α are released. Objective: This research is done to examine the effectiveness of Calcitriol in attenuating renal injury during IR through modulation mTOR gene. Method: 28 Wister Albino rats were randomly assigned to four equal groups, (N=7): Sham: Rats undergone laparotomy without ischemia. Control: Rats undergone laparotomy with bilateral RIRI for 30-minute following two hours of reperfusion. Vehicle: Rats given an intraperitoneal injection of DMSO three days before induction of RIRI. Calcitriol: Rats received an intraperitoneal injection of Calcitriol three days prior to RIRI. Results: TNFα, IL-1β, F2 Isoprostane, BAX, and KIM-1 tissue levels in sham were significantly lower than in vehicle and control. Additionally, the findings showed that compared to the vehicle and control, the Calcitriol had significantly decreased levels of KIM-1, TNFα, IL-1β, F2 Isoprostane, and BAX. It also showed that tissue content of Bcl2 and mTOR was significantly greater in Calcitriol compared to vehicle and control. The histopathology showed that Calcitriol could significantly lessen kidney damage in contrast to vehicle and control. Conclusion: This work concluded that Calcitriol significantly reduced RIRI damage in rats due to their pleiotropic effects.