ABSTRACT
Objective To investigate the protective effects on the renal allografts from brain dead (BD) donor rats pretreated with bone marrow mesenchymal stem cells (MSCs).Method Three groups [normal transplant group (G1).BD transplant group (G2),and MSCs pretreated + BD transplant group (G3)] were set up.Male F344 rats served as donors and male Lewis rats as recipients.In G1,kidneys from F344 donor rats were implanted into Lewis recipients.In G2,kidneys from F344 BD donor rats were engrafted into Lewis recipients.In G3,after BD was established in F344 rats,MSCs were given intravenously to the rats.The kidneys harvested 6 h later were transplanted to Lewis recipients.Cyclosporine was intromuscularly given daily to the recipient rats for 10 days.Right kidneys were resected from recipients on day 10.Creatinine level was examined on day 14,21,28,and 35.Renal allografts harvested on day 35 were pathologically detected.The irnmunochemistry expression of interleukin (IL)-1β and tumor necrotic factor (TNF)-α in renal allograft tissue was tested.Result Serum creatinine levels in G2 were remarkably higher than those in G1 and G3 (P＜0.01) on day 14,21,28,and 35 postoperatively.The creatinine levels on the above mentioned time points had no statistically significant difference between G3 and G1 except on day 21.Postoperative pathological changes in G2 of both pronounced infiltration of mononuclear cells and tubular epithelia[inflammation were notably increased in renal allografts as compared with those in G1 and G3.There was no obvious difference between G1 and G3 in infiltrated mononuclear cells and tubular epithelial inflammation.Positive expression levels of both IL-1β and TNF-α in glomerular,tubular and interstitial epithelial cells were statistically enhanced in G2 as compared with those in G1 and G3 (H =7.210,P =0.027),while there was no statistically significant difference in the expression of both IL-1[β and TNF-α between G1 and G3.Conclusion Brain dead donor rats pretreated with bone marrow MSCs might reduce renal allograft injury via decreasing both inflammatory cell infiltration and IL-1β and TNF-α expression.