Verbenone prevents cyclophosphamide-induced oxidative stress, inflammation, fibrosis, and cellular changes in the kidneys of Swiss albino mice by targeting NF-ĸB/TGF-β signaling pathways.

OBJECTIVES

Verbenone was assessed for its protective effect in cyclophosphamide-induced nephrotoxicity in Swiss albino mice.

MATERIALS AND METHODS

Mice were divided into six groups (n = 6). Vehicle Control, CP 200, VRB 200 + CP, VRB 300 + CP, FF 80 + CP, and VRB 300 . VRB and FF were given orally for 14 days, while CP was given intraperitoneally only on the seventh day. Mice were sacrificed on the 15 day, and various parameters were examined to ascertain the injury, inflammation, fibrosis, and histological variations in the kidney.

RESULTS

Our results revealed that malondialdehyde, TNF-α, interleukin-6, and IL-1β levels were increased by 248%, 128.5%, 170.68%, and 252%, respectively, and IL-10, catalase, glutathione, and SOD were decreased by 75.75%, 73.58%, 77%, and 81%, respectively in the CP treated group as compared to the control. VRB 300 and FF 80, however, reversed these parameters to normal. In the case of the test drug (VRB 300), the level of malondialdehyde, TNF-α, interleukin-6, and IL-1β levels were considerably decreased by 48%, 41%, 44.5%, and 22.7%, respectively. The levels of IL-10, catalase, glutathione, and SOD were increased by 169%, 228.5%, 208%, and 237%, respectively, as compared to the CP group. VRB 300 and FF 80 also caused a drop in serum creatinine, Uric acid, BUN, and urea levels when compared with the CP group. It reversed fibrosis and cellular architecture to normal, as established by histopathology and immunohistochemistry.

CONCLUSION

The data confirmed that verbenone significantly plays a role in protection against cyclophosphamide-induced renal damage.