[Protection and mechanisms of salvianolic-acid B on experimental renal interstitial fibrosis in rats].
Haiying Lu, Juan Zhou, Min Lü, Yumin Liu, Fei Wang, Min Lin, Yue Zhang
Abstract
Haiying Lu, Juan Zhou, Min Lü, Yumin Liu, Fei Wang, Min Lin, Yue Zhang
Abstract
OBJECTIVE: To investigate the effect and mechanism of salvianolic acid B (SA-B) on renal interstitial fibrosis in rats induced by unilateral ureteral obstruction (UUO). METHODS: 18 male SD rats were randomly divided into 3 groups, 6 in each group. After the models were established, the rats were treated with SA-B for 2 weeks. Then their renal pathology were examined by hight microscope and electron microscopy Protein expression levels of alpha-smooth muscle actin (alpha-SMA) and E-cadherin (E-cad) in the obstructed kidney were analyzed by Western blot and Biochemistry assay. RESULTS: Pathological examination of the kidney in model group showed tubules lumen widened and many inflammatory cells infiltrated, a part of renal tubule expanded and part of them atrophied. The tubular epithelial cells were karyorrhexis or karyolysis, some tubulars were atrophy. The protein expression of alpha-SMA were significantly up-regulated (P < 0.01) and E-cad were significantly down-regulated (P < 0.01) in the model group. After intervention with SA-B, the renal pathological status in the treatment group was significantly improved, the expression of alpha-SMA were significantly down-regulated (P < 0.05), but E-cad only a little up-regulated (P > 0.05). CONCLUSION: SA-B could antagonize renal interstitial fibrosis mainly by maintaining epithelial phenotype, inhibiting the protein of alpha-SMA which is the principal effect cells that are responsible for the progressive kidney fibrosis.
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OBJECTIVE: To investigate the effect and mechanism of salvianolic acid B (SA-B) on renal interstitial fibrosis in rats induced by unilateral ureteral obstruction (UUO). METHODS: 18 male SD rats were randomly divided into 3 groups, 6 in each group. After the models were established, the rats were treated with SA-B for 2 weeks. Then their renal pathology were examined by hight microscope and electron microscopy Protein expression levels of alpha-smooth muscle actin (alpha-SMA) and E-cadherin (E-cad) in the obstructed kidney were analyzed by Western blot and Biochemistry assay. RESULTS: Pathological examination of the kidney in model group showed tubules lumen widened and many inflammatory cells infiltrated, a part of renal tubule expanded and part of them atrophied. The tubular epithelial cells were karyorrhexis or karyolysis, some tubulars were atrophy. The protein expression of alpha-SMA were significantly up-regulated (P < 0.01) and E-cad were significantly down-regulated (P < 0.01) in the model group. After intervention with SA-B, the renal pathological status in the treatment group was significantly improved, the expression of alpha-SMA were significantly down-regulated (P < 0.05), but E-cad only a little up-regulated (P > 0.05). CONCLUSION: SA-B could antagonize renal interstitial fibrosis mainly by maintaining epithelial phenotype, inhibiting the protein of alpha-SMA which is the principal effect cells that are responsible for the progressive kidney fibrosis.
Key concepts: Kidney, Western blot, Medicine, Fibrosis, Pathology, Immunohistochemistry, SMA*, Pathological