Effect of Fluvastatin on the Activity of the Extracellular Signal-regulated Kinase in the Renal Cortex of Diabetic Rats
Rui-Li Jin
Abstract
Rui-Li Jin
Abstract
Objective:To investigate the effect of fluvastatin on the activity of the extracellular signal-regulated kinase(ERK1/2)in renal cortex in diabetic rats.Methods:These rats were randomly divided into 3 groups: control rats (Group NC), diabetic rats(Group DC) and diabetic rats treated with fluvastatin(Group DF).The following studies were performed in each group in 2 weeks and 6 weeks after the treatment with fluvastatin. All of the items such as serum lipids consisting of total cholesterol(TC),triglyceride(T),low-density lipoprotein(LDL),blood glucose(BG),urine albumin effusion rate(UAER),and kidney hypertrophy index were measured.The level of phospho-ERK1/2 and TGF-β 1 in the renal cortex were examined by western blot.Immunohistochemical technique was used to estimate the expression of type Ⅳcollagen. The renal tissue of diabetic rats was observed with light microscope after periodic acid-Schiff(PAS) staining and transmission electron microscope.Results:In 2 or 6 weeks,serum cholesterol(TC),triglyceride (TG),low-density lipoprotein (LDL),kidney hypertrophy index,urine albumin effusion rate(UAER),collagen type Ⅳ,pERK1/2 and TGF-β1 in diabetic rats of fluvastatin treated group were significantly lower than diabetic untreated rats(P 0.05),but higher than Group NC(P 0.01).Renal pathological changes in Group DF were improved obviously in 6 weeks.Conclusion:Fluvastatin can down-regulate the activity of signal transduction pathway-ERK1/2,inhibit the overproduction of TGF-β 1,decrease the expression of type Ⅳcollagen,improve the renal pathological changes,inhibit and delay the glomerular sclerosis.
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Objective:To investigate the effect of fluvastatin on the activity of the extracellular signal-regulated kinase(ERK1/2)in renal cortex in diabetic rats.Methods:These rats were randomly divided into 3 groups: control rats (Group NC), diabetic rats(Group DC) and diabetic rats treated with fluvastatin(Group DF).The following studies were performed in each group in 2 weeks and 6 weeks after the treatment with fluvastatin. All of the items such as serum lipids consisting of total cholesterol(TC),triglyceride(T),low-density lipoprotein(LDL),blood glucose(BG),urine albumin effusion rate(UAER),and kidney hypertrophy index were measured.The level of phospho-ERK1/2 and TGF-β 1 in the renal cortex were examined by western blot.Immunohistochemical technique was used to estimate the expression of type Ⅳcollagen. The renal tissue of diabetic rats was observed with light microscope after periodic acid-Schiff(PAS) staining and transmission electron microscope.Results:In 2 or 6 weeks,serum cholesterol(TC),triglyceride (TG),low-density lipoprotein (LDL),kidney hypertrophy index,urine albumin effusion rate(UAER),collagen type Ⅳ,pERK1/2 and TGF-β1 in diabetic rats of fluvastatin treated group were significantly lower than diabetic untreated rats(P 0.05),but higher than Group NC(P 0.01).Renal pathological changes in Group DF were improved obviously in 6 weeks.Conclusion:Fluvastatin can down-regulate the activity of signal transduction pathway-ERK1/2,inhibit the overproduction of TGF-β 1,decrease the expression of type Ⅳcollagen,improve the renal pathological changes,inhibit and delay the glomerular sclerosis.
Key concepts: Endocrinology, Internal medicine, Fluvastatin, Renal cortex, Renal Hypertrophy, Kidney, Medicine, Diabetes mellitus