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Smad AND Silibinin

Dongmei Qin, Yaru Nie, Zhiping Wen
OBJECTIVES: To clarify the protective effects of Cichorium glandulosum (CG) extracts on thioacetamide (TAA)-induced rat hepatic fibrosis. MATERIALS AND METHODS: The dry roots of CG were smashed and percolated with 95% ethanol, and the residual was prepared into petroleum ether extract (CG-V), ethyl acetate extract (CG-VI) and n-butyl alcohol extract (CG-VII). Thirty-six Wistar rats were randomly divided into a normal group, a model group, a CG-V group (15 mg/kg), a CG-VI group (3 mg/kg), a CG-VII group (6 mg/kg) and a positive drug group (silibinin capsule, 8 mg/kg)...
November 2014: Iranian Journal of Basic Medical Sciences
Yi-Hao Chen, Chang-Min Liang, Ching-Long Chen, Jiann-Torng Chen, Yun-Hsiang Chang, Da-Wen Lu, Ke-Hung Chien, Ming-Cheng Tai
PURPOSE: To investigate the effect of silibinin in myofibroblast transdifferentiation and in animal trabeculectomy models. METHODS: The effect of silibinin on the expression of α-smooth muscle actin (α-SMA) and vimentin in response to transforming growth factor-β1 (TGF-β1) was determined in human tenon fibroblasts (HTFs). Cell migration and collagen contraction arrays were used to demonstrate the functionality of silibinin-modulated HTFs. ELISA analysis was used to determine the effect of silibinin on the release of type 1 collagen and connective tissue growth factor (CTGF)...
November 2013: Acta Ophthalmologica
Jae-We Cho, Kwon-Jun Il, Kyu-Suk Lee
The inhibition of the Smad2/3 pathway is a key step involved in the downregulation of type I collagen synthesis, thus preventing keloid formation in tissue. In this study, we investigated the effect of silibinin on the proliferation of human skin fibroblasts (HSFs), as well as its effect on the expression of type I collagen, matrix metalloproteinase (MMP)-1, Smad2 and Smad3. Our results showed that the proliferation rates of the fibroblasts were not markedly decreased in a dose- and time-dependent manner following treatment with silibinin...
May 2013: International Journal of Molecular Medicine
Wen Ai, Yan Zhang, Qi-Zhu Tang, Ling Yan, Zhou-Yan Bian, Chen Liu, He Huang, Xue Bai, Lu Yin, Hongliang Li
Cardiac hypertrophy is a major determinant of heart failure. The epidermal growth factor receptor (EGFR) plays an important role in cardiac hypertrophy. Since silibinin suppresses EGFR in vitro and in vivo, we hypothesized that silibinin would attenuate cardiac hypertrophy through disrupting EGFR signaling. In this study, we examined this hypothesis using neonatal cardiac myocytes and fibroblasts induced by angiotensin II (Ang II) and animal model by aortic banding (AB) mice. Our data revealed that silibinin obviously blocked cardiac hypertrophic responses induced by pressure overload...
August 1, 2010: Journal of Cellular Biochemistry
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