ABSTRACT
Diabetic nephropathy (DN) is a common and serious clinical complication of diabetes and presently there are no effective ways to prevent its occurrence and progression. Recent studies show that pentoxifylline (PTX) can improve renal hemodynamics, reduce urinary protein excretion, and alleviate or delay renal failure in DN patients. In this study, we focused on the anti-oxidative stress effect of PTX on alleviating renal damages of DN using rat models. DN rats were established with injection of streptozotocin. Blood glucose, urinary protein excretion, serum cystatin C, renal biopsy, superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and renal homogenate and renal nitrotyrosine levels were analyzed before and 12 weeks after the treatment of PTX. Before treatment, all the DN rats had elevated blood glucose, increased urinary protein excretion and elevated serum cystatin C. Morphologically, DN rats exhibited renal tissue damages, including swelling and fusions of foot processes of podocytes under electron microscope. Masson staining revealed blue collagen deposition in glomeruli and renal interstitium. With treatment of PTX, symptoms and renal pathological changes of DN rats were alleviated. Furthermore, the MDA levels were increased and the SOD levels were decreased in the serum and kidneys of DN rats, and these changes were reversed by PTX. The expression of nitrotyrosine was up-regulated in DN rat model and down-regulated by PTX, indicating that PTX was able to inhibit oxidative reactions in DN rats. PTX could alleviate renal damage in DN, which may be attributable to its anti-oxidative stress activity.
Subject(s)
Animals , Rats , Biomarkers , Diabetes Mellitus, Experimental , Drug Therapy , Pathology , Diabetic Nephropathies , Drug Therapy , Metabolism , Pathology , Gene Expression Regulation , Kidney , Metabolism , Pathology , Malondialdehyde , Blood , Oxidative Stress , Pentoxifylline , Pharmacology , Streptozocin , Superoxide Dismutase , Metabolism , Tyrosine , MetabolismABSTRACT
Diabetic nephropathy (DN) is a common and serious clinical complication of diabetes and presently there are no effective ways to prevent its occurrence and progression. Recent studies show that pentoxifylline (PTX) can improve renal hemodynamics, reduce urinary protein excretion, and alleviate or delay renal failure in DN patients. In this study, we focused on the anti-oxidative stress effect of PTX on alleviating renal damages of DN using rat models. DN rats were established with injection of streptozotocin. Blood glucose, urinary protein excretion, serum cystatin C, renal biopsy, superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and renal homogenate and renal nitrotyrosine levels were analyzed before and 12 weeks after the treatment of PTX. Before treatment, all the DN rats had elevated blood glucose, increased urinary protein excretion and elevated serum cystatin C. Morphologically, DN rats exhibited renal tissue damages, including swelling and fusions of foot processes of podocytes under electron microscope. Masson staining revealed blue collagen deposition in glomeruli and renal interstitium. With treatment of PTX, symptoms and renal pathological changes of DN rats were alleviated. Furthermore, the MDA levels were increased and the SOD levels were decreased in the serum and kidneys of DN rats, and these changes were reversed by PTX. The expression of nitrotyrosine was up-regulated in DN rat model and down-regulated by PTX, indicating that PTX was able to inhibit oxidative reactions in DN rats. PTX could alleviate renal damage in DN, which may be attributable to its anti-oxidative stress activity.
ABSTRACT
Objective: To investigate whether transplantation of mesenchymal stem cells(MSCs) through renal arteries can protect kidney from acute tubular necrosis(ATN), so as to lay a foundation for MSC transplantation in treatment of ATN. Methods: Five-week-old nude mice were randomly divided into three groups: normal control group (n = 10), acute tubular necrosis(ATN) model group without(n = 10) and with MSCs treatment group(n = 11). ATN nude mice were induced with 50% glycerin. MSCs labeled with enhanced green fluorescent proteins(EGFP) were injected into kidney through renal arteries. Serum creatinine was determined in all groups and pathological changes of renal tissues were detected using H-E staining. The amount and distribution of the EGFP-marked MSCs in renal tissues were determined with fluorescence microscope. Results: Degeneration and exfoliation of renal tubular epithelial cells, and even renal tubular tamponade with cast-off cells were observed in the ATN group; these pathological changes were mainly located at renal cortex and juncture of renal cortex and medulla. The damages were greatly alleviated in the ATN + MSCs transplantation group, with no swelling of epithelial cells, nuclear condensation or edema. Fourteen days after MSCs transplantation, EGFP positive cells were increased in renal tubules of recipient mice. Conclusion: The MSCs transplantation via renal artery can locate in renal tubular epithelium, and promote the repair of injured renal tubular epithelial cells.
ABSTRACT
Aim The effect of tetrandrine on TGF-?1 mRNA expression in glomerulosclerosis rat was observed. Methods The rats were randomly divided into four groups, such as the normal control group (sham operative rat), glomerulosclerosis model group,tetrandrine group and amlodipine group. The expression of TGF-?1 mRNA was analyzed by Northern blot hybridization. Results The expressions of TGF-?1 mRNA in two treating groups were much lower than untreated model group. There were no difference between these two treating groups. Conclusion Tetrandrine can decrease the expression of TGF-?1 mRNA in glomerulosclerosis rat induced by unilateral renctomy plus adriamycin.