Abstract
Introduction: Cyclophosphamide (CPA) is an effective antineoplastic agent whose clinical utility is often limited by its potential to induce marked renal injury. This nephrotoxicity has been attributed to disrupted oxidative balance, exaggerated inflammatory signaling, activation of apoptotic pathways, and impairment of autophagic processes.
Objectives: This experimental study explored the possible reno-protective effects of chlorogenic acid (CGA) against CPA-induced nephrotoxicity.
Materials and Methods: In a rodent model of CPA-induced nephrotoxicity, CGA was administered orally at 2 dose levels for ten days, with a single CPA injection (150 mg/kg) given on the 4th day.
Results: In our study, CGA treatment dose-dependently attenuated CPA-induced elevations in renal damage biomarkers and reduced renal malondialdehyde levels in a dose-dependent manner and enhanced antioxidant defense systems in kidney tissue. In addition, CGA dose-dependently suppressed inflammatory mediators, including nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), and transforming growth factor beta 1 (TGF-β1). Moreover, it downregulated the apoptotic marker cleaved caspase-3 while upregulating the autophagy-related protein beclin-1 in a dose-dependent fashion. The reno-protective effects of CGA were further supported by histopathological studies.
Conclusion: All these findings suggest that CGA dose-dependently alleviates CPA-induced nephrotoxicity via suppression of redox imbalance, inflammation, apoptosis and promotion of autophagic activity.