Nephrotoxic nephritis is a clinical condition with a high mortality rate. People with nephritis are susceptible to anemia. This may be due to the presence of sFas.. MSCs hold therapeutic potential in repairing tubular injury, ameliorating renal function deficits, and prolonging survival in acute renal injury. The aim of the present study was to investigate role of BM-derived MSCs cell therapy on mercuric chloride experimentally induced nephrotoxicity and their effect on sFas level in an in vivo albino rat animal model. 90 adult female albino rats were divided equally and randomly in to 3 groups. Group I -ve control group, Group II received an intramuscular injection of Mercuric chloride for 2 weeks (5 days/ week) (1 mg/kg body weight).Group III received an intramuscular injection of Mercuric chloride for 2 weeks (5 days/ week) (1 mg/kg body weight). After establishment of nephrotoxicity by kidney function test (KFT), single dose of labeled MSCs with GFP (Green Fluorescent Protein) injected in the tail vein at a dose of labeled MSCs 1× 106 cells After 2 weeks from 24 hours after last mercuric chloride dose injection, and 3 weeks from labeled MSCs injection. 15 rats from each group were suspected to Blood samples collection from infraorbital. Rats from each animal group were suspected for biochemical estimation of kidney function test (KFT); serum creatinine, Blood Urea Nitrogen (BUN) and complete blood count (CBC) then rats were sacrificed. Kidney were subjected to histopathologic examination by H&E and immunohistochemical examination by PCNA and sFas expression. MSCs suppressed serum urea and creatinine levels in HgCl2-treated rats with increased tissue regeneration and inhibition of tubular cell apoptosis, with decreased expression of PCNA and sFas and increased of the RBCs, Hct and Hb levels compared to the mercuric chloride group reflecting the improvement of anemia.