Cisplatin is a chemotherapeutic agent that causes nephrotoxicity when it was administered for long periods. This study investigated the effect of ADMSCs in the attenuation of cisplatin induced AKI. Sprague-Dawley rats (180–220 g) (n=90) were divided into three groups, 30 rats each. Control group (rats were injected 1 ml/kg saline intraperitoneally. Cisplatin group (rats were injected a single dose of cisplatin (6 mg/kg I.P) without treatment. ADMSCs + CP group (rats were injected a single dose of cisplatin (6 mg/kg I.P) for 24 hours, followed by administration of ADMSCs (5×106) I.V). Ten rats were sacrificed on the days 3, 7 and 11, the kidney tissues and blood samples were obtained. Renal functions, oxidative stress parameters, molecular studies and histopathological studies were analyzed, as well as ADMSCs isolation and characterization was done.
Cisplatin injection caused disturbance in kidney function through increasing serum creatinine, blood urea nitrogen and MDA, and decreasing GSH activity. The amelioration in renal function appeared at day 3 with the use of ADMSCs. Injection of cisplatin induced tubular apoptosis and inflammation by increasing Caspase-3 and NFKB, in addition to tubular degenerations evaluated by pathological score, in contrast, ADMSCs group showed a significantly lowered inflammation and apoptosis at days 3, 7, 11. This study concluded that ADMSCs have reno-protective effects that can be explained by three possible mechanisms of action, targeting oxidative stress, targeting apoptosis and reducing inflammation through which it could improve cisplatin toxicity.