Conclusion
This study revealed that RA's positive effects on folic acid-induced renal injury might result from the involvement of the FoxO3/NFκB pathway, thereby suppressing inflammation and apoptosis.
Methods
Thirty-six male C57/BL6 mice were randomly divided into six groups (N=6): Control (received normal saline), NaHCO3 (received NaHCO3 as folic acid solvent), FA (received folic acid (FA)(IP) to induce renal injury), RA (received 100 mg/kg RA), RA50-FA (received 50 mg/kg RA solution after folic acid injection), and RA100-FA (received 100 mg/kg RA after folic acid injection). For ten days, the treatment groups received RA by gavage. The effects of RA were assessed using H & E staining, biochemical tests, western blotting, and ELISA in the kidney tissues of the mice. Real-time RT-PCR was also performed to evaluate the expression changes of renal genes.
Results
Our data showed that treatment by RA led to the over-expression of FoxO3 (P<0.05) and decrease in NFκB levels (P<0.01 and P<0.05) and expression of TNFα (P<0.05) and IL6 (P<0.001 and P<0.01). Other evaluations showed a decrease in p53 (P<0.01 and P<0.001), Bax/Bcl-2 ratio expression (P<0.01 and P<0.05), and Caspase-3 level (P<0.01 and P<0.05) compared to the folic acid group. Histological and biochemical results also confirmed the attenuation of tissue damage.