Evaluation the Kidney Protection Effect of Rosuvastatin against I\R injury in male rats. Assessment the Effect of Rosuvastatin on mTOR gene
DOI:
https://doi.org/10.52783/jns.v14.2580Keywords:
Rosuvastatin, RIRI, Bcl-2, BAX, mTORAbstract
Background: In certain situations, such as sepsis, myocardial infarction, ischaemic stroke, and acute kidney damage (AKI), ischaemia reperfusion injury (IRI) appears to be the main cause of morbidity and mortality. A decrease in the blood supply to the ischaemic organ during ischaemia results in hypoxia and a slowdown of the outflow of metabolic waste products, which allows the buildup of carbon dioxide (CO2) and other debris. Chronic severe ischaemia and hypoxia cause structural and functional changes in the microvascular system. When the ischaemic tissue is rapidly restored with fresh blood that is high in oxygen and nutrients, this causes damage and oedema and also causes the endothelial layer of capillaries to create reactive oxygen species (ROS), which intensifies the inflammatory process and the NFκB signalling pathway. Complement protein is secreted along with inflammatory or immune cells, such as lymphocytes, neutrophils, and macrophages, as well as inflammatory components like tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin-1β (IL-1β), and interferon gamma.
Objective: This animal work is done to investigate the effectiveness of Rosuvastatin in attenuating renal injury during ischemia reperfusion through modulation of mTOR expression 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. Rosuvastatin: Rats received an intraperitoneal injection of Rosuvastatin three days prior to RIRI.
Results: In comparison to the vehicle and control, the sham had significantly lower tissue levels of TNFα, IL-1β, F2 Isoprostane, BAX, and KIM-1; the results also showed that Rosuvastatin had significantly lower tissue levels of Bcl2 and mTOR, TNFα, IL-1β, BAX, and KIM-1; and the histopathology showed that Rosuvastatin could significantly reduce kidney damage.
Conclusion: The AR therapy group significantly reduced renal I/R damage in the adult male rats' bilateral renal I/R due to their pleiotropic effects, which include anti-inflammatory, anti-oxidant, and anti-apoptotic qualities, according to the study's overall findings.Additionally, by increasing the expression of the mTOR gene in ischaemic renal tissues, they prevented necrosis and apoptosis.
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