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Deng W.,Renmin University of China | Deng W.,Hubei University | Fang Y.,Renmin University of China | Fang Y.,Hubei University | And 21 more authors.
Molecular Medicine Reports | Year: 2014

Cardiac remodeling is a major determinant of heart failure characterized by cardiac hypertrophy and fibrosis. Sanguinarine exerts widespread pharmacological effects, including antitumor and anti-inflammatory responses. In the present study, the effect of sanguinarine on cardiac hypertrophy, fibrosis and heart function was determined using the model induced by aortic banding (AB) in mice. AB surgery and sham surgery were performed on male wild-type C57 mice, aged 8-10 weeks, with or without administration of sanguinarine from one week after surgery for an additional seven weeks. Sanguinarine protected against the cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by the heart weight/body weight, lung weight/body weight and heart weight/tibia length ratios, echocardiographic and hemodynamic parameters, histological analysis, and the gene expression levels of hypertrophic and fibrotic markers. The inhibitory effect of sanguinarine on cardiac remodeling was mediated by inhibiting nuclear factor (NF)-κB signaling pathway activation. The findings indicated that sanguinarine protected against cardiac hypertrophy and fibrosis via inhibiting NF-κB activation. These findings may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure. Source


Deng W.,Wuhan University | Jiang D.,Wuhan University | Fang Y.,Wuhan University | Zhou H.,Wuhan University | And 8 more authors.
Journal of Molecular Histology | Year: 2013

Cardiac remodelling is a major determinant of heart failure (HF) and is characterised by cardiac hypertrophy, fibrosis, oxidative stress and myocytes apoptosis. Hesperetin, which belongs to the flavonoid subgroup of citrus flavonoids, is the main flavonoid in oranges and possesses multiple pharmacological properties. However, its role in cardiac remodelling remains unknown. We determined the effect of hesperetin on cardiac hypertrophy, fibrosis and heart function using an aortic banding (AB) mouse. Male, 8-10-week-old, wild-type C57 mice with or without oral hesperetin administration were subjected to AB or a sham operation. Our data demonstrated that hesperetin protected against cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by heart weigh/body weight, lung weight/body weight, heart weight/tibia length, echocardiographic and haemodynamic parameters, histological analysis, and gene expression of hypertrophic and fibrotic markers. Also, hesperetin attenuated oxidative stress and myocytes apoptosis induced by AB. The inhibitory effect of hesperetin on cardiac remodelling was mediated by blocking PKCα/βII-AKT, JNK and TGFβ1-Smad signalling pathways. In conclusion, we found that the orange flavonoid hesperetin protected against cardiac remodelling induced by pressure overload via inhibiting cardiac hypertrophy, fibrosis, oxidative stress and myocytes apoptosis. These findings suggest a potential therapeutic drug for cardiac remodelling and HF. © 2013 Springer Science+Business Media Dordrecht. Source


Wei L.,Renmin University of China | Wei L.,Hubei University | Deng W.,Renmin University of China | Deng W.,Hubei University | And 8 more authors.
Molecular Medicine Reports | Year: 2016

Hesperetin is a natural flavonoid, which has been reported to exert various biological activities and positive health effects on mammalian cells. The present study aimed to investigate the effects of hesperetin on the proliferation of primary cultured rat pulmonary artery smooth muscle cells (PASMCs), and to elucidate the possible underlying molecular mechanisms. The results of the present study indicated that hesperetin was able to inhibit the proliferation and DNA synthesis of platelet-derived growth factor-BB (PDGF-BB)-induced PASMCs in a dose- and time-dependent manner, without exerting cell cytotoxicity. In addition, hesperetin blocked the progression of the cell cycle from G0/G1 to S phase, which was correlated with the decreased mRNA expression levels of cyclin D1, cyclin E, cyclin-dependent kinase (CDK)2 and CDK4, and the increased mRNA expression levels of p27. Furthermore, the anti-proliferative effects of hesperetin were associated with suppression of the AKT/glycogen synthase kinase (GSK)3β and p38 signaling pathway, but were not associated with the extracellular signal-regulated kinases 1/2 and c-Jun N-terminal kinases signaling pathways. These results suggested that hesperetin may inhibit PDGFa-BB-induced PASMC proliferation via the AKT/GSK3β signaling pathway, and that it may possess therapeutic potential for the treatment of pulmonary vascular remodeling diseases. Source


Deng W.,Fudan University | Li J.,Fudan University | Yao P.,Fudan University | He F.,National Pharmaceutical Engineering Research Center | Huang C.,National Pharmaceutical Engineering Research Center
Macromolecular Bioscience | Year: 2010

In this report, we developed a simple and green process of simultaneous formation of doxorubicin-BSA-dextran nanoparticles in aqueous solution and high-effective encapsulation of doxorubicin. In the presence of BSA-dextran conjugates, which were produced by Maillard reaction, a binding of doxorubicin with BSA can suppress the self-aggregation of unprotonated doxorubicin. After a heat treatment, the gelation of BSA results in a formation of the nanoparticles and the doxorubicin was fixed inside the nanoparticles. The dextran shell makes the nanoparticles dispersible in solution. The nanoparticles have a spherical morphology and a hydrodynamic radius of about 90 nm. Importantly, the nanoparticles can significantly prolong the life of murine ascites hepatoma H22 tumor-bearing mice.Binding of doxorubicin with BSA can suppress the self-aggregation of unprotonated doxorubicin. After a heat treatment, the gelation of BSA results in a formation of doxorubicin-BSA-dextran nanoparticles and the doxorubicin was loaded inside the particles effectively. The dextran conjugated to the BSA through Maillard reaction stabilizes the nanoparticles in solution. The nanoparticles can significantly prolong the life of H22 tumor-bearing mice. Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Source


Cheng S.,Jiangxi University of Traditional Chinese Medicine | Zhao H.,Jiangxi University of Traditional Chinese Medicine | Zuo Z.,Jiangxi University of Traditional Chinese Medicine | Wang Y.,Fuzhou University | And 2 more authors.
Zhongguo Zhongyao Zazhi | Year: 2011

Objective: To observe effect of oral scorpio and scolopendra powder on T-cell subsets in peripheral blood and intestine from rats with collagen induced arthritis (CIA). Method: 60 rats were randomly divided into 6 groups: normal control group, model control group, low-dose scorpio and scolopendra group, middle-dose scorpio and scolopendra group, high-dose scorpio and scolopendra group, and type II collagen group. Rat's rheumatoid arthritis was induced by collagen II (C II). Level of T-cell subsets from peripheral blood and intestine was measured by flow cytometry. Result: CD4 + T cellular level was obviously increased (P < 0.05 or. P < 0.01) or kept increased tendency in peripheral blood and intestine from the model group compared with that of the normal group, while the ratio of CD4 +/CD8 + in intestine was obviously descent but the contrary in peripheral blood (P < 0.05 or P < 0.01). CD4 +, CD8 + T cellular level in intestine were obviously descent and the ratio of CD4 +/CD8 + increased in all treated groups when compared with in the model group (P < 0.05 or P < 0.01). However, CD4 + T cellular level and the ratio of CD4 +/CD8 + in peripheral blood were remarkablely decreased. Conclusion: The mechanism that scorpio and scolopendra could treat rat's rheumatoid arthritis may be regulating balance of T-lymphocyte subsets in peripheral blood and intestine. Source

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