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Objective To observe glomerular mesangial cells (GMCs) proliferation induced by IgA1 and the association with the expression of apoptosis-related proteins-B cell lymphoma-2 (Bcl-2),cysteine aspartic acid protease-3 (Caspase-3),cysteine aspartic acid protease-9 (Caspase-9) and with mitofusin 2 (Mfn2) in rat GMCs,to study the possible mechanism of valsartan inhibiting rat GMCs proliferation,and to provide a new direction for the mechanism of GMCs proliferation and intervention research in IgA nephrology (IgAN).Methods GMCs stimulated with IgA1 were cultured in vitro to detect cellproliferation with the cell counting kit-8 cell activity assay (CCK8).GMCs were divided into three groups:CG,TG and VG.The GMCs proliferation level was detected by the CCK8,using real-time PCR to detect Mfn2 expression and Western blotting to detect protein levels of Mfn2,Bcl-2,Caspase-3,and Caspase-9.Results Rat GMCs proliferated significantly after stimulation with IgA1,and IgA1 could obviously stimulate high expression of Bcl-2 in GMCs and down regulate the expression of Mfn2,Caspase-3,and Caspase-9.Valsartan could inhibit the proliferation of GMCs induced by IgA1 significantly,downregulate the expression of Bcl-2,and upregulate the expression of Mfn2,Caspase-3,and Caspase-9.Conclusions These results showed that the mechanism of action of valsartan in the treatment of lgAN is inhibiting the proliferation of GMCs.This mechanism may be associated with the regulation of apoptosis-related proteins,such as Mfn2,Bcl-2,Caspase-3,and Caspase-9.These findings may provide a new direction for the mechanism of GMCs proliferation and intervention research in IgAN.
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Objective To observe the effect of Valsartan on a rat model of acute lung injury and the expression of transforming growth factor-β,TGF-β) ,Smad2/3, Smad7. Methods Twenty-four male adult Sprague-Dawley rats were random divided into three groups : The bleomycin (BLM) group, the control group, and the Valsartan group. Each group contained eight rats. The Valsartan group was treated with Valsartan everyday at a dose of 20 mg/kg after a single intratracheal instillation of bleomycin at a dose of 5mg/kg. BLM group was treated with saline instead of Valsartan after an instillation of bleomycin. The control group was treated with saline instead of Valsartan and bleomycin. Each group was killed at the 7th day after instillation. The lung tissues were harvested for H. E. stain, the immunohistochemistry was used to detect the expressions of TGF-β1, Smad2/3 ,and Smad7. Results The degree of alveolitis in the Valsartan group was ameliorated, compared with those in BLM group (P ＜0. 01). The expressions of TGF-β1 and Smad2/3 in lung tissue of the Valsartan group were significantly lower than that of BLM group(P ＜0. 01). The expressions of Smad7 in lung tissue of the Valsartan group were significantly higher than that of BLM group (0.23 ±0. 02 vs0. 36 ±0.03, P ＜0.01). Conclusions Valsartan could alleviate acute lung injury in rats, which probably be due to the expression decrease of TGF-β1 and Smad2/3 and the expression increase of Smad7 in lung tissues.
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lsartan could reduce the release of p-selectin.Conclusions Valsartan could relieve myocardial ischemia reperfusion injury of rat, which may be through reducing p-seleetin of plasma.
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Objectives The purpose of this study is to observe the effects of valsartan on hepapetic fibrosis. Methods Thirty male Sprague-Dawley rats were randomly divided into three groups: valsartan -prevetive group (A), modle group of hepatic fibrosis (B)and valsar-tan-treating group (C). The model of hepatic fibrosis in rats was induced by intraperitoneai injection of dimethylnitrosamine (DMN) for 4 weeks(2ml/kg everyday, three times a week). Valsartan (10mg/kg everyday) was given together with injection of DMN per intrngastric (Ig) in group A for 8 weeks. After stop injection of DMN, the S valsartan(10mg/kg, everyday)was given per Ig in group C for 4 weeks. After modeling, normal saline were given per Ig everyday in group B. At the end of eighth week, the histomorphylogic structure of the liver was ob-served with light microscope. Immunohistoebemical staining was used to evaluate the expression of a-SMA. Results In group B, there was a large necrotic area and a number of pesudolobes appeared in the liver tissue. In group A, there were normal hepatic cords. In the group C, there was fibrosis interval formation and portal area expansion and fibrotie intervals extending to the lobule. The quantitative analysis of Mas-son staining showed that the collagen quantities in group B was higher than that of other group(P<0.01). The collagen quantities in group A was lower than that of group C(P<0.05). The results of immanohistochemical staining showed that the expression of a-SMA in group B was strong positive, middle positive in group C, and weak positive in group A (P<0.05). Conclusion The valsartan has preventive and treatment effects on hepatic fibrosis in rats of hepatic fibrosis model induced by DMN, and the preventive effect of valsartan is better than its treatment effect. The valsartan can ameliorate the hver cirrhosis by partly suppressing the activation of HSC.