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ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
[Effects of sericine on TGF-beta1/Smad3 signal pathway of diabetic mephropathy rats kidney].
Chinese Journal of Applied Physiology 2011 Februrary
OBJECTIVE: To observe the effects of color silk cocoon extraction-sericine on transforming growth factor-beta1 (TGF-beta1) and Smad3 protein expression in kidney of diabetic nephropathy (DN) rats.
METHODS: 60 male SD rats were randomly divided into 5 groups (n = 12): normal control group, DN model group, sericine treatment group, metformin group and sericine prevention group. The rats in model group, sericine treatment group, metformin group and sericine prevention group were all established DN rats model by intraperitoneally injected streptozotocin (STZ). Blood glucose > or = 16.7 mmol/L was taken as standard to judge if the rats model were successfully established. After the rats model were successfully established, the rats in sericine treatment group were lavaged with sericine (2.4 g/(kg x d), 35 d). The rats in metformin group were lavaged with metformin (55.33 mg/(kg x d), 35 d). The rats in sericine prevention group were lavaged with the same dose sericine for 35 d before injecting STZ. The blood glucose and kidney weight/body weight of rats in each group were respectively detected. Immunohistochemical staining was used to observe the expression of TGF-beta1 and Western blot to detect the expression of Smad3 in kidney.
RESULTS: Compared with normal control rats: the blood glucose, kidney weight/body weight, TGF-beta1 and Smad3 expression in kidney of rats in model group increased obviously (P < 0.01). The blood glucose, TGF-beta1 and Smad3 expression in kidney of rats in sericin treatment group, sericin prevention group and metformin group were significantly lower than that of model group (P < 0.01). Moreover, there were no obvious differences between sericin treatment group, sericin prevention group and metformin group (P > 0.05). The kidney weight/body weight of rats in sericin treatment group, sericin prevention group and metformin group were significantly lower than that of model group (P < 0.01). Moreover, the kidney weight/body weight of rats in sericin treatment group and sericin prevention group were obviously lower than that of metformin group (P < 0.05).
CONCLUSION: Sericin can inhibit activation of TGF-beta1/Smad3 signal pathway in kidney of DN rats, lighten glomerulosclerosis and renal interstitial fibrosis, so has protective and preventive effects on kidney injury of DN rats. Moreover, the therapeutical and preventive effects of sericin on DN are similar with metformin.
METHODS: 60 male SD rats were randomly divided into 5 groups (n = 12): normal control group, DN model group, sericine treatment group, metformin group and sericine prevention group. The rats in model group, sericine treatment group, metformin group and sericine prevention group were all established DN rats model by intraperitoneally injected streptozotocin (STZ). Blood glucose > or = 16.7 mmol/L was taken as standard to judge if the rats model were successfully established. After the rats model were successfully established, the rats in sericine treatment group were lavaged with sericine (2.4 g/(kg x d), 35 d). The rats in metformin group were lavaged with metformin (55.33 mg/(kg x d), 35 d). The rats in sericine prevention group were lavaged with the same dose sericine for 35 d before injecting STZ. The blood glucose and kidney weight/body weight of rats in each group were respectively detected. Immunohistochemical staining was used to observe the expression of TGF-beta1 and Western blot to detect the expression of Smad3 in kidney.
RESULTS: Compared with normal control rats: the blood glucose, kidney weight/body weight, TGF-beta1 and Smad3 expression in kidney of rats in model group increased obviously (P < 0.01). The blood glucose, TGF-beta1 and Smad3 expression in kidney of rats in sericin treatment group, sericin prevention group and metformin group were significantly lower than that of model group (P < 0.01). Moreover, there were no obvious differences between sericin treatment group, sericin prevention group and metformin group (P > 0.05). The kidney weight/body weight of rats in sericin treatment group, sericin prevention group and metformin group were significantly lower than that of model group (P < 0.01). Moreover, the kidney weight/body weight of rats in sericin treatment group and sericin prevention group were obviously lower than that of metformin group (P < 0.05).
CONCLUSION: Sericin can inhibit activation of TGF-beta1/Smad3 signal pathway in kidney of DN rats, lighten glomerulosclerosis and renal interstitial fibrosis, so has protective and preventive effects on kidney injury of DN rats. Moreover, the therapeutical and preventive effects of sericin on DN are similar with metformin.
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