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1.
Biomed Res Int ; 2017: 3754942, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28164119

RESUMEN

Background and Objective. It has been reported that sodium ferulate (SF) has hematopoietic function against anemia and immune regulation, inflammatory reaction inhibition, inhibition of tumor cell proliferation, cardiovascular and cerebrovascular protection, and other functions. Thus, this study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways. Methods. Seventy-two male C57BL/6J mice were selected and divided into 6 groups: control group, PBS group, model group (AngII), model + low-dose SF group (AngII + 10 mg/kg SF), model + high-dose SF group (AngII + 40 mg/kg SF), and model + high-dose SF + agonist group (AngII + 40 mg/kg SCU + 10 mg/kg TBHQ). After 7 d/14 d/28 days of treatments, the changes of blood pressure and heart rates of mice were compared. The morphology of myocardial tissue and the apoptosis rate of myocardial cells were observed. The mRNA and protein expressions of atrial natriuretic peptide (ANP), transforming growth factor-ß (TGF-ß), collagen III (Col III), and MAPK/ERK and JNK pathway-related proteins were detected after 28 days of treatments. Results. SF improved the mice's cardiac abnormality and decreased the apoptosis rate of myocardial cells in a time- and dose-dependent manner (all P < 0.05). MAPK/ERK pathway activator inhibited the protective effect of SF in myocardial tissue of mice (P < 0.05). SF could inhibit the expression of p-ERK, p-p38MAPK, and p-JNK and regulate the expressions of ANP, TGF-ß, and Col III (all P < 0.05). Conclusion. Our findings provide evidence that SF could protect against AngII-induced cardiac hypertrophy in mice by downregulating the MAPK/ERK and JNK pathways.


Asunto(s)
Cardiomegalia/tratamiento farmacológico , Cardiomegalia/enzimología , Cardiotónicos/uso terapéutico , Ácidos Cumáricos/uso terapéutico , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Sistema de Señalización de MAP Quinasas , Angiotensina II , Animales , Apoptosis/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Cardiomegalia/diagnóstico por imagen , Cardiomegalia/fisiopatología , Cardiotónicos/farmacología , Ácidos Cumáricos/farmacología , Diástole/efectos de los fármacos , Activación Enzimática/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Masculino , Ratones Endogámicos C57BL , Miocardio/patología , ARN Mensajero/genética , ARN Mensajero/metabolismo , Sístole/efectos de los fármacos
2.
China Pharmacy ; (12): 119-121, 2017.
Artículo en Chino | WPRIM (Pacífico Occidental) | ID: wpr-507831

RESUMEN

OBJECTIVE:To study the effects of particle size of ticagrelor crude drug on in vitro dissolution behavior of Ticagre-lor tablets. METHODS:Ticagrelor crude drug and different particle size of ticagrelor powder A,B,C,D,E after smashing for dif-ferent time(15,30,40,60 s)were used to prepare the tablet by wet granulation method. Accumulative in vitro dissolution rate of prepared tablets within 60 min were determined by UV spectrophotometry at 300 nm(using 0.2% tween as medium,paddle meth-od). Using original tablet as reference preparation,the similarity factor(f2)method was used to compare the similarity of dissolu-tion behavior between 5 prepared tablets and original tablet. RESULTS:d(0.9)of powder A,B,C,D,E were 69.181,40.778, 24.805,12.611,3.083 μm,respectively. The corresponding f2 were 27.77,36.79,50.06,67.68,79.99. CONCLUSIONS:The par-ticle size of ticagrelor crude drug is much smaller,and the dissolution behavior of prepared tablet is closer to that of original tablet. The in vitro dissolution rate of Ticagrelor tablets is improved remarkably by micronization technology. In order to produce Ticagre-lor tablets with the same bioavailability as original tablet,particle size of ticagrelor crude drug powder should be controlled with d(0.9)≤20μm.

3.
Artículo en Chino | WPRIM (Pacífico Occidental) | ID: wpr-815299

RESUMEN

OBJECTIVE@#To isolate the collagen phagocytic subpopulation of fibroblast (CPSF) and non-collagen phagocytic subpopulation of fibroblast (nCPSF) and to identify their differentially expressed genes.
@*METHODS@#The CPSF and nCPSF was isolated by using collagen-fluorescein-isothiocynate-latex bead (COL-FITC-LB) phagocytosis technique and FCM sorting method. Microarray analysis was used to screen the differentially expressed genes, which were verified by real-time PCR. 
@*RESULTS@#CPSF and nCPSF was successfully isolated. Seventeen differentially expressed genes were identified. Compared with nCPSF, the expression of 12 or 5 genes was up-regulated or down-regulated in CPSF. Three of the 12 up-regulated genes were urokinase plasminogen activator receptor-associated protein (uPARAP), cytochrome b-245, beta polypeptide (CYBB) and Hook homolog 1 (HOOK1), which were confirmed by real-time PCR. uPARAP mRNA expression level in CPSF was 2788 times of that in nCPSF. CYBB mRNA expression in CPSF was only 0.85 times of that in nCPSF. HOOK1 mRNA expression in CPSF was 1.96 times of that in nCPSF (P<0.05). 
@*CONCLUSION@#A novel method is successfully established to isolate CPSF and nCPSF. uPARAP is the main differentially expressed gene in CPSF and nCPSF, which is obviously involved in the fibroblast collagen phagocytosis. It might be a potential biomarker for treatment of collagen diseases.


Asunto(s)
Humanos , Colágeno , Genética , Regulación hacia Abajo , Fibroblastos , Biología Celular , Análisis por Micromatrices , Fagocitosis , Regulación hacia Arriba
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