Purpose: The organophosphate pesticide chlorpyrifos (CPF) can cause developmental , neurological deficiencies , and mitochondria-mediated oxidative stress responses. In this study, the effect of niosomal hesperidin (Nio+Hesp) on the polarization of M1-M2 liver macrophages and the amount of inflammatory cells secretion in the brain, liver, and ovary tissues of CPF induced mice (3 mg/kg for 4 weeks; Intraperitoneally) was investigated.
Methods: Fourty C57 mice were divided into CPF, Sham, CPF+Hesp, and CPF+Nio+Hesp groups and treated carried out orally for 30 days. The activity of superoxide dismutase (SOD) and malondialdehyde (MDA), tissue changes, inflammation, and apoptosis in brain, liver, and ovary tissues, the number of ovarian germ cells , and M1-M2 liver macrophage polarization were evaluated by examining the expression of CD163and CD68 genes.
Results: Nio+Hesp prescription caused an increase in SOD and a decrease in MDA. Nio+Hesp decreased the amount of cell apoptosis in the liver, also reduced the expression of CD163 and CD68genes. Although there was a significant difference between Hesperidin and Nio+Hesp in the increase of Graafian follicles, corpus luteum, and peri-antral follicles, no substantial difference was observed in primary follicles in the uterus. Both Nio+Hesp and Hesp alleviated CPF-induced hepatotoxicity, however, Nio+Hesp was superior to Hesp in downregulation of the CD163 and CD68genes expression.
Conclusion: The ameliorative effects of HSP and Nio+Hesp may be at least in part due to their antioxidant and anti-inflammatory properties. By attenuating, Nio+Hesp may have therapeutic applications for reversing CPF-induced toxicity as an appropriate antioxidant effects.