The Ameliorative Effects of Morin on Colistin‐Induced Kidney Injury in Ovariectomized Rats: Reduces Oxidative Stress, Inflammation Damage, Apoptosis, and Autophagic Death

Abstract

The aim of this study was to evaluate the potential protective effect of Morin (MOR) on Colistin (COL)-induced renal injury in rats biochemically and immunohistochemically. For this purpose, the rats were divided into five groups: Control, ovariectomy (OV), OV + MOR, OV + COL, and OV + COL + MOR. COL was administered intramuscularly at a total dose of 73 mg/kg, and MOR was administered orally at a dose of 100 mg/kg for 7 days. According to the findings obtained at the end of the study, it was determined that COL administration suppressed antioxidant markers such as glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and increased malondialdehyde (MDA) levels in the kidney tissue of rats. In addition, it was determined that OV + COL administration triggered the inflammatory response by increasing the levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin 1β (IL-1β). Caspase-3 immunoreactivity, an apoptosis marker, was detected at a moderate level in the COL. Beclin-1, an autophagy marker, was determined to show strong immunoreactivity in this group. COL + MOR treatment in rats was observed to increase the levels of enzymatic and nonenzymatic antioxidants and reduce the level of MDA. In addition, COL + MOR treatment was found to significantly attenuate COL-induced oxidative stress, inflammation, autophagy, and apoptosis processes in kidney tissue (p < 0.05). There were no differences in oxidative stress, apoptosis, inflammation, and autophagy parameters between the control, OV, and MOR groups. In conclusion, COL administration in rats caused significant damage to kidney tissue compared to the other groups, disrupting tissue integrity, but MOR treatment mitigated this damage.

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