Biochemical and Immunohistochemical Evaluation of the Effects of Zingerone Against Colistin-Induced Lung Injury in Ovariectomized Rats

The objective of this study was to conduct a biochemical and immunohistochemical assessment of the potential effects of zingerone (ZNG) on colistin (COL)-induced pulmonary injury in rats. To achieve this, a total of 35 female rats were utilized, of which 28 underwent ovariectomy (OV). The experimental groups were as follows: Control group received only saline intramuscularly without OV; OV group underwent OV and received saline intramuscularly; OV + ZNG group received 50 mg/kg ZNG via oral gavage; OV + COL group received a total of 73 mg/kg COL intramuscularly; OV + COL + ZNG group received a COL intramuscularly administration. Subsequently, ZNG was administered by oral gavage for a duration of 7 days. The results obtained at the conclusion of the study indicated that COL administration led to a suppression of antioxidant markers, including glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), while it elevated malondialdehyde (MDA) levels in the lung tissue of rats. Furthermore, COL administration induced inflammation by increasing the levels of interleukin 1β (IL-1β), nuclear factor kappa B (NF-κB), and tumor necrosis factor-alpha (TNF-α). Immunohistochemical analysis of Beclin-1, and Caspase-3 were found to be more pronounced in the OV + COL group compared to the other groups. ZNG treatment resulted in an increase in both nonenzymatic and enzymatic antioxidant levels and a reduction in MDA levels in rats. Furthermore, ZNG mitigated COL-induced inflammation, oxidative stress, autophagy, and apoptosis in lung tissue. No significant differences were observed in oxidative stress, inflammation, apoptosis, and autophagy parameters among the control, OV, and OV + ZNG groups. In conclusion, it was determined that COL administration in rats led to lung tissue damage and compromised tissue integrity, while ZNG treatment ameliorated the damage induced by COL. © 2025 Wiley Periodicals LLC.