Effect of Quyu Chencuo Formula () on Renal Fibrosis in Obstructive Nephropathy Rats / 中国结合医学杂志

OBJECTIVE@#To observe the effect of Quyu Chencuo Formula (, QCF) on renal fibrosis in rats with obstructive nephropathy.@*METHODS@#Twenty-four rats were randomly divided into three groups, 4 for sham operation as the control group, 10 for unilateral ureteral obstruction (UUO) model group, and the rest 10 for QCF treating UUO model group. All rats were sacrificed under 3% pentobarbital (50 mg/kg) anesthesia on the 14th day after surgery, then the right kidney samples of rats were harvested for hematoxylin eosin (HE) staining and Masson staining to observe the renal pathological changes. Immunohistochemistry and Western blotting were used to examine the expression of transforming growth factor β1 (TGF-β1), and real-time polymerase chain reaction (RT-PCR) was employed to examine the expressions of TGF-β1, α-smooth muscle actin (α-SMA) and E-cadherin mRNA.@*RESULTS@#HE and Masson staining showed that the renal interstitial of the rats in the control group had no significant fibrotic lesion; in the model group, there were obvious interstitial fibrosis; for the QCF group, there were epithelial cell necrosis, infiltration of lymphocytes and mononuclear cells, aggravated interstitial fibrosis in varied degrees, but the pathological changes were less in the QCF group than in the model group. The immunohistochemistry and Western blotting results showed that the TGF-β1 expression was increased significantly in the model group, while decreased significantly in the QCF group (P<0.05); RT-PCR showed that the mRNA expression of α-SMA and TGF-β1 increased significantly in the model group, while both were significantly decreased in the QCF group compared with the model group (P<0.05). The mRNA expression of E-cadherin was decreased significantly in the model group, and it was significantly increased in the QCF group as compared with the model group (P<0.05).@*CONCLUSION@#QCF may improve renal fibrosis by regulating the expressions of TGF-β1, α-SMA and E-cadherin, and prevent the progress of kidney fibrosis.

Effect of astragaloside IV based on Toll/MyD88 dependent signaling pathway in treatment of renal fibrosis mice / 中草药

Objective To study the effect of astragaloside IV on renal fibrosis mice with unilateral ureteral obstruction (UUO) and discuss the mechanism. Methods Male C57BL/6 50 mice were divided into five groups randomly, such as Sham-operated group, model group and high-, medium-, and low-dose astragaloside IV groups. From the day of surgery, the mice in astragaloside IV groups (high-, medium- and low-dose) were treated by gavage of astragaloside IV for 2 weeks in doses of 50, 30, and 10 mg/(kg∙d) separately. The mice in Sham-operated group and model group were treated with saline instead of astragaloside IV. Serum creatinine and blood urea nitrogen were detected by chemical methods. Histopathological changes and collagen deposition of affected kidney were observed under optical microscope with HE and MASSON staining. The expression levels of Toll/MyD88 dependent signaling pathway related molecules (TLR4, TLR2, MyD88, TRAF6, NF-Kappa B, TNF-α, and IL-6) in affected kidney were measured by immunohistochemistry and Western blotting methods and observed from protein levels in each group. Results The degree of fibrosis and histopathological damage of affected kidney of mice in model group is the most obvious. And the expression levels of Toll/MyD88 dependent signaling pathway related molecules in affected kidney of mice in model group were the highest. With drug concentration increased in groups of astragaloside IV, in these groups, the injury of affected kidney had been obviously reduced, and the protein expression levels of Toll/MyD88 dependent signaling pathway related molecules (TLR4, TLR2, MyD88, TRAF6, and NF-Kappa B) were also in corresponding reduced, at the same time the expression of terminal inflammatory cytokines (TNF-alpha and IL-6) has been suppressed. Conclusion Astragaloside IV may improve renal interstitial fibrosis in mice after UUO by inhibiting the expression of Toll/MyD88 dependent signaling pathway and release of inflammatory cytokines (TNF-alpha and IL-6).