Effects of bone marrow mesenchymal stem cells on the Bone metabolism of adriamycin induced nephritic rats
Related Articles |
Objective To investigate the effects of bone marrow mesenchymal stem cells (BMSCs) on the bone metabolism in adriamycin-induced nephritic rats. Methods generate adriamycin-induced nephritic rats(n=50), and randomly divide them into five groups as group A: the normal group, group B: the model group, group C: the hormone group, group D: nephritic rats with stem cells transplant, group E :nephritic rats with stem cells transplant + hormone treatment. The urine samples were collected on the day 7, 21 and 35 respectively after adriamycin injection, and urine protein levels were measured by automatic biochemistry analyzer. The serum protein levels of osteoprotegerin (OPG), nuclear factorκB receptor activating factor ligand(RANKL) were detected by ELISA. Using real-time quantitative PCR and Western blot to measure the expression of OPG and RANKL in tibia tissue. Results compared to the group A, on day7, urinary protein level of group B to E all showed significant increase (P <0.05); compared to group B, day 21 and 35 day, the urinary protein of the C, D and E decreased (P <0.05). The serum RANKL increased and the OPG decreased in group C compared to B group (P <0.05); in both group D and E, the serum OPG increased (P <0.05), the RANKL level were reduced (P <0.05) as compared to the C group; compared to D group, serum OPG in group E reduced, and the RANKL increased (P <0.05). Compared with the B group, the C group showed decreased level of protein and mRNA of OPG (P <0.05, P <0.01), however, the protein and mRNA of RANKL increased (P <0.01); compared to the C group, D and E group had an increased levels of both OPG protein and mRNA(P <0.05), and the RANKL protein and mRNA expression decreased (P <0.01). Compared with the D group, E group showed decreased level of the OPG protein and mRNA, and increased level of the RANKL protein (P <0.05, P <0.01). Conclusion BMSCs may promote osteoblast differentiation, and inhibit osteoclast genesis by OPG / RANKL / RANK pathway to limit the formation of prednisone-induced osteoporosis.