OBJECTIVE: To inquire into the effects of angiotensin Ⅱ type 1 receptor antagonist (AT1RA) valsartan on apoptosis and the expression of apoptosis correlated protein Fas and FasL in the kidneys of rats with nephrotic glomerulosclerosis induced by adriamycin. METHODS: Thirty six SD rats were randomly divided into model group, treatment group and control group. The model was established by uninephrectomy and injection of adriamycin. In the treatment group, valsartan (20 mg/kg) was delivered daily by gavage for 12 weeks. The same amount of normal saline was delivered by gavage in the control and model groups. Apoptosis was examined by means of terminal deoxynucleotidyl transferase mediated d UTP nick end labeling (TUNEL). Glomerular apoptotic index (GAI) and renal tubule apoptotic index (TAI) were calculated. Immunohistochemistry was utilized to detect the expression of Fas and FasL. The morphological changes were observed under optic microscope and the glomerulosclerosis index (GSI) was determined. RESULTS: Compared with the control group, the GSI, GAI, TAI and the expression of Fas and FasL in model and treatment groups were stronger (P< 0.01 ). Compared with model group, they decreased in treatment group (P< 0.01 ). CONCLUSIONS: Valsartan may suppress the excessive apoptosis of kidney cells by lowering the expression of Fas and FasL so as to postpone the process of glomerulosclerosis."/>
Effects of Valsartan on Apoptosis and Expression of Fas and FasL in the Kidneys of Rats with Nephrotic Glomerulosclerosis Induced by Adriamycin
Abstract OBJECTIVE: To inquire into the effects of angiotensin Ⅱ type 1 receptor antagonist (AT1RA) valsartan on apoptosis and the expression of apoptosis correlated protein Fas and FasL in the kidneys of rats with nephrotic glomerulosclerosis induced by adriamycin. METHODS: Thirty six SD rats were randomly divided into model group, treatment group and control group. The model was established by uninephrectomy and injection of adriamycin. In the treatment group, valsartan (20 mg/kg) was delivered daily by gavage for 12 weeks. The same amount of normal saline was delivered by gavage in the control and model groups. Apoptosis was examined by means of terminal deoxynucleotidyl transferase mediated d UTP nick end labeling (TUNEL). Glomerular apoptotic index (GAI) and renal tubule apoptotic index (TAI) were calculated. Immunohistochemistry was utilized to detect the expression of Fas and FasL. The morphological changes were observed under optic microscope and the glomerulosclerosis index (GSI) was determined. RESULTS: Compared with the control group, the GSI, GAI, TAI and the expression of Fas and FasL in model and treatment groups were stronger (P< 0.01 ). Compared with model group, they decreased in treatment group (P< 0.01 ). CONCLUSIONS: Valsartan may suppress the excessive apoptosis of kidney cells by lowering the expression of Fas and FasL so as to postpone the process of glomerulosclerosis.
HAN Zi-Ming,XING Yan,WANG Hong-Wei et al. Effects of Valsartan on Apoptosis and Expression of Fas and FasL in the Kidneys of Rats with Nephrotic Glomerulosclerosis Induced by Adriamycin[J]. 中国当代儿科杂志, 2003, 5(4): 306-310.
HAN Zi-Ming,XING Yan,WANG Hong-Wei et al. Effects of Valsartan on Apoptosis and Expression of Fas and FasL in the Kidneys of Rats with Nephrotic Glomerulosclerosis Induced by Adriamycin[J]. CJCP, 2003, 5(4): 306-310.
