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1.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 36(10): 1241-1246, 2016 10.
Artigo em Chinês | MEDLINE | ID: mdl-30641014

RESUMO

Objective To observe the effects of Bushen Tiaojing Recipe (BTR) on the counts of survival preantral follicles and the bone morphogenetic protein receptor II (BMPR II )/activin receptor- like kinase 6-drosophila mothers against decapentaplegic proteins (ALK6-Smads) signal pathway in oocytes cultured in vitro, and to study its mechanism for improving the quality of oocytes. Methods Prean- tral follicles were mechanically isolated from 65 female 12-day old healthy Kunming mice, which were inoculated by normal rats' serum (as the control group) , high, medium, low dose BTR containing serums (as Shen-supplementing groups) , high dose BTR containing serum + K02288 (as the inhibitor group) , respectively. All were cultured by common method in vitro. On the 6th day the counts of survival preantral follicles were compared between each Shen-supplementing group and the control group respectively. mR- NA expressions of BMPR II, ALK6, Smad1 , Smad5, and Smad8 were detected by Real-time fluorescence quantitative PCR. The protein expressions of indices mentioned above and phospho-Smadl/5/8 (p- Smadl/5/8) were detected by cellular immunofluorescence test. Results Compared with the control group, the quantity of survival preantral follicles increased in the high dose BTR containing serum group; mRNA expressions of BMPR II, ALK6, Smad5, and Smad8 were elevated, protein expressions of indi- ces mentioned above and p-Smadl/5/8 were increased in the 3 Shen-supplementing groups (P <0. 05) ; mRNA and protein expressions of Smad1 were increased in high and medium dose BTR containing serum groups (P<0.05). Compared with the high dose BTR containing serum group, protein expressions of Smad1/5/8 were reduced in the inhibitor group (P <0.05). Conclusion BTR could elevate the quantity of survival preantral follicles cultured in vitroand improve the quality of oocytes, which might be possibly as- sociated to regulating the BMPR II/ALK6-Smads signal pathway in oocytes.


Assuntos
Receptores de Proteínas Morfogenéticas Ósseas Tipo II , Medicamentos de Ervas Chinesas , Oócitos , Animais , Receptores de Proteínas Morfogenéticas Ósseas Tipo I/efeitos dos fármacos , Receptores de Proteínas Morfogenéticas Ósseas Tipo I/metabolismo , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/efeitos dos fármacos , Receptores de Proteínas Morfogenéticas Ósseas Tipo II/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Feminino , Camundongos , Oócitos/efeitos dos fármacos , Oócitos/metabolismo , Folículo Ovariano , Ratos , Transdução de Sinais , Proteínas Smad/efeitos dos fármacos , Proteínas Smad/metabolismo
2.
J Oral Pathol Med ; 43(6): 464-70, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24484214

RESUMO

BACKGROUND: Oral submucous fibrosis (OSF) is a premalignant and fibrosing disease, which is closely associated with the habit of chewing areca nut. Panax notoginseng Buck F. H. Chen is an often used antifibrotic and antitumor agent. To treat areca nut-induced OSF, we have developed a chewable tablet, in which one of the major medicines is total Panax notoginseng saponins (PNS). In this study, we have investigated the antifibrotic effect and mechanism of PNS on areca nut-induced OSF in vitro. METHODS: Through human procollagen gene promoter luciferase reporter plasmid, hydroxyproline assay, gelatin zymography, qRT-PCR, ELISA, and Western blot, the influences of PNS on areca nut extract (ANE)-induced cell growth, collagen accumulation, procollagen gene transcription, MMP-2/-9 activity, MMP-1/-13 and TIMP-1/-2 expression, cytokine secretion, and the activation of PI3K/AKT, ERK/JNK/p38 MAPK, and TGFß/Smads pathways were detected. RESULTS: Panax notoginseng saponins could inhibit the ANE-induced abnormal growth and collagen accumulation of oral mucosal fibroblasts in a concentration-dependent manner. PNS (25 µg/ml) could significantly inhibit the ANE-induced expression of Col1A1 and Col3A1, augment the ANE-induced decrease of MMP-2/-9 activity, inhibit the ANE-induced increase of TIMP-1/-2 expression, and decrease the ANE-induced transcription and release of CTGF, TGFß1, IL-6, and TNFα. PNS (25 µg/ml) also significantly inhibited the ANE-induced activation of AKT and ERK/JNK/p38 MAPK pathways in oral mucosal fibroblasts and the ANE-induced activation of TGFß/smad pathway in HaCaT cells. CONCLUSION: Panax notoginseng saponins possess excellent anti-OSF activity, and its mechanism may be related to its ability to inhibit the ANE-induced activation of PI3K/AKT, ERK/JNK/p38 MAPK, and TGFß/smad pathways.


Assuntos
Areca/efeitos adversos , Mucosa Bucal/efeitos dos fármacos , Nozes/efeitos adversos , Fibrose Oral Submucosa/patologia , Panax notoginseng , Extratos Vegetais/farmacologia , Saponinas/farmacologia , Animais , Técnicas de Cultura de Células , Linhagem Celular , Colágeno Tipo I/efeitos dos fármacos , Cadeia alfa 1 do Colágeno Tipo I , Colágeno Tipo III/efeitos dos fármacos , Fator de Crescimento do Tecido Conjuntivo/efeitos dos fármacos , Fibroblastos/efeitos dos fármacos , Humanos , Hidroxiprolina/análise , Interleucina-6/análise , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Metaloproteinase 2 da Matriz/efeitos dos fármacos , Metaloproteinase 9 da Matriz/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos BALB C , Mucosa Bucal/citologia , Fibrose Oral Submucosa/etiologia , Fosfatidilinositol 3-Quinases/efeitos dos fármacos , Extratos Vegetais/efeitos adversos , Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos , Proteínas Smad/efeitos dos fármacos , Inibidor Tecidual de Metaloproteinase-1/efeitos dos fármacos , Inibidor Tecidual de Metaloproteinase-2/efeitos dos fármacos , Fator de Crescimento Transformador beta1/efeitos dos fármacos , Fator de Necrose Tumoral alfa/efeitos dos fármacos
3.
Phytomedicine ; 20(13): 1172-9, 2013 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-23856441

RESUMO

Recently, the TGF-ß1/Smad signaling pathway has been investigated in the pathogenesis of hepatofibrosis, and pharmacological treatment of liver fibrosis targeted this pathway to determine its contribution to the inhibition of fibrotic development. Importantly, ethnopharmacology-derived Pueraria lobata has been reported to effectively reverse the fibrotic process in the liver. In the present study, we performed dimethylnitrosamine (DMN)-induced liver fibrosis in rats to assess the benefits of puerarin (PR), which was isolated from Pueraria lobata (Willd.), on ECM-derived hepatocytes associated with the TGF-ß1/Smad pathway. Our results showed that the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), laminin (LN), type III precollagen (PCIII) and type IV collagen (CIV) were significantly reduced by PR treatment, while hepatic homogenates showed decreased levels of hydroxyproline (Hyp) and collagen I (Col I). Masson's trichrome staining indicated that the DMN-induced liver fibrosis was alleviated. In addition, the protein expression levels of transforming growth factor-ß l (TGF-ß l), smad2, smad3, α-SMA and TIMP-1 were downregulated specifically by PR treatment, whereas the protein expression levels of smad7 and MMP-1 were upregulated. Furthermore, we evaluated the PR-mediated inhibitory effect on TGF-ß1-treated proliferation and activation in a rat liver stellate cell line (HSC-T6). These data resulted in inhibition of the cell growth of HSC-T6 in a dose-dependent manner and a reduction in TßRI, smad2 and smad3 expressed proteins in the presence of PR on TGF-ß1-treated HSC-T6 cells, while smad7 levels were downregulated. Taken together, these findings identify a unique effect for PR-regulation of the TGF-ß1/Smad pathway in blocking fibrotic development and provide a promising strategy for hepatofibrosis treatment.


Assuntos
Regulação da Expressão Gênica/efeitos dos fármacos , Isoflavonas/uso terapêutico , Cirrose Hepática/tratamento farmacológico , Pueraria/química , Transdução de Sinais/efeitos dos fármacos , Fator de Crescimento Transformador beta1/efeitos dos fármacos , Animais , Linhagem Celular , Dimetilnitrosamina/farmacologia , Modelos Animais de Doenças , Regulação para Baixo , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Isoflavonas/isolamento & purificação , Isoflavonas/farmacologia , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Cirrose Hepática/induzido quimicamente , Cirrose Hepática/metabolismo , Masculino , Estrutura Molecular , Ratos , Ratos Sprague-Dawley , Proteínas Smad/efeitos dos fármacos , Proteínas Smad/metabolismo , Fator de Crescimento Transformador beta1/metabolismo
4.
J Asian Nat Prod Res ; 13(3): 215-24, 2011 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21409682

RESUMO

Oxymatrine (1), a component extracted from a traditional Chinese herb Sophora japonica (Sophora flavescens Ait.), has been demonstrated to have a variety of pharmacological actions. Abundant experimental evidence indicates that 1 may exert a protective effect on the cardiovascular system. This study was designed to explore the possible role of 1 against myocardial fibrosis induced by acute myocardial infarction (AMI) and its modulation on transforming growth factor beta 1 (TGF-ß(1))-Smads signaling pathways. Rats with AMI induced by ligation of left anterior descending branch were randomly assigned to receive 1 50 and 25 mg/kg intragastrically, and model group which were further compared with sham-operated group, and positive group treated with captopril. The effects of 4-week therapy with 1 starting 24 h after infarction had been investigated based on (1) hemodynamics, (2) tissue weights, (3) biochemical indicator (hydroxyproline contents in left ventricle), and (4) TGF-ß(1), TGF-ß(1) receptor (TßR(1)), Smad3, Smad4, Smad7, Col1, and Col3 expression by semi-quantitative reverse transcription PCR. Treatment with 1 significantly ameliorated hemodynamics, inhibited the expression of TßR(1) mRNA and Smad3 mRNA, and reduced the left ventricle weight/body weight. The results of this research indicated that 1 might protect against myocardial fibrosis and the mechanism may be involved in modulating TGF-ß(1)-Smads signal pathway.


Assuntos
Alcaloides/farmacologia , Infarto do Miocárdio/tratamento farmacológico , Quinolizinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Proteínas Smad/efeitos dos fármacos , Sophora/química , Fator de Crescimento Transformador beta1/metabolismo , Alcaloides/química , Animais , Medicina Tradicional Chinesa , Modelos Biológicos , Estrutura Molecular , Quinolizinas/química , RNA Mensageiro/análise , RNA Mensageiro/genética , Ratos , Proteínas Smad/genética , Fator de Crescimento Transformador beta1/efeitos dos fármacos , Fator de Crescimento Transformador beta1/genética
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