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1.
Arch Pharm Res ; 44(8): 1-12, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-25074038

RESUMO

This study investigates the hepatoprotective effects and the potential therapeutic mechanisms of loach (Misgurnus anguillicaudatus) lyophilized powder (MLP) on dimethylnitrosamine (DMN) induced liver fibrosis in rats. After treatment with MLP (50, 100, 200 mg/kg), alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (Alb), total protein (TP) and hydroxyproline (Hyp) levels were detected, to assess the destruction of hepatocytes and the extent of liver fibrosis. Matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), hyaluronic acid (HA), Laminin (LN), procollagen type-III (PC-III), collagen type-IV (C-IV), and transforming growth factor-ß1 (TGF-ß1) contents in serum were all tested using ELISA kits. Alpha-smooth muscle actin (α-SMA) and the tissue inhibitor of metalloproteinase-1 (TIMP-1) protein contents and distribution were evaluated using western blot and immunohistochemical analysis. MLP significantly decreased the serum concentrations of ALT, AST, Hyp, HA, LN, PC-III, C-IV, MMP-2, TIMP-1, α-SMA and TGF-ß1, while increasing the contents of Alb and MMP-9. No significant changes on TP serum concentrations were observed. These results suggest that MLP has anti-hepatic fibrosis effects and its mechanism may be associated with the attenuation of extracellular matrix (ECM) synthesis, the acceleration of ECM degradation, inhibition of hepatic stellate cells (HSCs) activation and TGF-ß1 expression.


Assuntos
Cipriniformes/metabolismo , Cirrose Hepática Experimental/prevenção & controle , Pós/farmacologia , Animais , Dimetilnitrosamina , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Matriz Extracelular/efeitos dos fármacos , Matriz Extracelular/metabolismo , Células Estreladas do Fígado/efeitos dos fármacos , Células Estreladas do Fígado/patologia , Hepatócitos/efeitos dos fármacos , Hepatócitos/patologia , Masculino , Pós/administração & dosagem , Pós/isolamento & purificação , Ratos , Ratos Wistar , Fator de Crescimento Transformador beta1/metabolismo
2.
World J Gastrointest Oncol ; 11(10): 909-924, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31662829

RESUMO

BACKGROUND: Circular RNAs (circRNAs) are a newly discovered class of endogenous non-coding RNAs that may have roles in cancer genesis and development. In the recent literature, dysregulated circRNAs have been extensively investigated in hepatocellular carcinoma (HCC). Whether or not circRNAs are of clinical value for the management of HCC has not been characterized. AIM: To meta-analyze the diagnostic and prognostic value of abnormally expressed circRNAs in HCC. METHODS: Eligible studies were sourced from PubMed, EMBASE, and CNKI online databases. Data on patients' clinical characteristics, including diagnostic efficacy and overall survival, were extracted. The diagnostic and prognostic parameters were respectively synthesized using the bivariate meta-analysis model and multivariate Cox hazard regression analysis based on Stata 12.0. The trim and fill method was adopted to assess the possible effects from publication bias. RESULTS: A total of 21 eligible studies were included. The pooled sensitivity, specificity, and area under the curve of abnormally expressed circRNAs in distinguishing HCC from non-cancer controls were 0.78 (95%CI: 0.69-0.85), 0.80 (95%CI: 0.74-0.86), and 0.86, respectively. Survival analyses showed that the down-regulated circRNA expression signature correlated perfectly with HCC survival [hazard ratio (HR) = 0.42, 95%CI: 0.19-0.91, P = 0.028; I 2 = 92.7%, P = 0.000], whereas the HCC cases with high circRNA levels had significantly poorer prognoses than those of patients with low circRNA levels (HR = 2.22, 95%CI: 1.50-3.30, P = 0.000; I 2 = 91%, P = 0.000). Moreover, abnormally expressed circRNAs were intimately associated with tumor size, differentiation grade, microvascular invasion, metastasis, TNM stage, and serum alpha fetal protein level in patients with HCC. Stratified analysis based on sample type, control source, and expression status also yielded robust results. CONCLUSION: Abnormally expressed circRNA signatures show immense potential as novel non-invasive biomarker(s) for HCC diagnosis and prognosis.

3.
Chem Commun (Camb) ; 54(30): 3712-3714, 2018 Apr 10.
Artigo em Inglês | MEDLINE | ID: mdl-29578228

RESUMO

A novel room temperature phosphorescent material has been developed by the use of luminescent organic rigid poly-imidazole moieties coordinating to a zinc phosphite framework, which shows excellent thermal and mechanical stability.

4.
Iran J Basic Med Sci ; 21(3): 318-324, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29511499

RESUMO

OBJECTIVES: To investigate the effect of miR-103 on the angiogenesis of ischemic stroke rats via targeting vascular endothelial growth factor (VEGF) at the molecular level. MATERIALS AND METHODS: Rat models had received the middle cerebral artery occlusion (MCAO) or sham operation before grouping, and cell models of oxygen-glucose deprivation (OGD) were performed. FITC-dextran, matrigel, and Trans-well assays were used to evaluate the vascular density, tube formation, and cell migration respectively. The expression levels of miR-103 and VEGF were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Dual-luciferase assay was used for analyzing the targeting relationship between miR-103 and VEGF. RESULTS: We found the reduced miR-103 in rats after MCAO. Down-regulating miR-103 with the miR-103 inhibitor enhanced VEGF, ameliorated the neurological scores, decreased infarct volume, and increased vascular density in rats after MCAO. Besides, in OGD human umbilical vein endothelial cells (HUVECs), inhibition of miR-103 could promote the increase of tube length and the migration of cells. Additionally, we found that miR-103 could directly target VEGF and thereby lead to the down-expression of VEGF. Meanwhile, si-VEGF could reverse the effect of miR-103 inhibitor on angiogenesis in rats subjected to MCAO. CONCLUSION: Inhibition of miR-103 could promote ischemic stroke angiogenesis and reduce infarction volume via enhancing VEGF, which provides a new target for the clinical treatment of ischemic stroke.

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