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1.
Chinese Pharmacological Bulletin ; (12): 842-847, 2022.
Artículo en Chino | WPRIM | ID: wpr-1014080

RESUMEN

Aim To investigate the inhibitory effect of kappa-opioid receptor(κ-OR)stimulation on extracellular signal-regulated kinase pathway on ET-1-induced cardiomyocyte hypertrophy in vitro cultured myocardial cells from neonatal rats.Methods Myocardial cells of neonatal rats were cultured in vitro.The hypertrophic myocytes were induced by ET-1(10 nmol·L-1)before κ-OR agonist U50488H(1 μmol·L-1)was administered.The antihypertrophic effect of κ-OR stimulation was observed in the presence of U0126(1μmol·L-1), Ro-31-8220(50 nmol·L-1)and PTX(5 mg·L-1).The cardiomyocytes volume was measured by computer photographalysis system.The relative expression of ERK1/2 was determined by Western blot.The morphological changes in cardiomyocytes were observed under an inverted phase contrast microscope.The expression of mRNA of atrial natriuretic peptide(ANP)was determined by RT-PCR.Results Compared with normal control group, ET-1 could induced cardiomyocyte hypertrophy.Compared with ET-1 model group, U50488H(1 μmol·L-1)could obviously inhibit ET-1-induced increase of the cardiomyocytes volume, expression of ANPmRNA and expression of ERK1/2, which was similar to U0126(1 μmol·L-1)and Ro-31-8220(50 nmol·L-1); however, the inhibitory effects of U50488H were partly lost when preincubated with U0126(1 μmol·L-1)and Ro-31-8220(50 nmol·L-1); the inhibitory effects of U50488H, U0126(1 μmol·L-1)and Ro-31-8220(50 nmol·L-1)were lost when preincubated with NOR-BNI.Conclusion The stimulation of kappa-opiod can inhibit myocardial hypertrophy induced by ET-1, which is possibly via attenuating ERK1/2.

2.
Journal of Forensic Medicine ; (6): 346-349, 2016.
Artículo en Chino | WPRIM | ID: wpr-984858

RESUMEN

OBJECTIVES@#To screen and collect the cases of unnatural death in custody and analyze the influences and forensic characteristics.@*METHODS@#Total 25 cases of unnatural death in detainees in custody form 2000 to 2015 were collected. Some forensic characteristics such as gender, age, yearly incidence, causes of death, manner of death were analyzed. The public security custodies were also compared with the prisons.@*RESULTS@#All dead involved were male, mostly were young and middle-aged adults. It showed that the number of cases tended to decrease year by year. The incidence of the injury cases were higher in public security custodies (64.7%) than that in the prisons (12.5%). However, there was a higher suicide rate in prisons (62.5%) than that in public security custodies (23.5%). The mainly cause of death were injury and asphyxia, there were also some cases died from intoxication and electricity.@*CONCLUSIONS@#The cases of unnatural death in custody expose some problems such as the imperfectness of law enforcement standardization, supervision loopholes and poor medical standards. A comprehensive and detailed autopsy has important implications for the identification of cause of death in custody.


Asunto(s)
Adulto , Humanos , Masculino , Persona de Mediana Edad , Asfixia , Autopsia , Causas de Muerte , Electricidad , Intoxicación , Prisiones , Suicidio
3.
Chinese Journal of Cardiology ; (12): 698-703, 2013.
Artículo en Chino | WPRIM | ID: wpr-261504

RESUMEN

<p><b>OBJECTIVE</b>To observe the impact of adenosine A1 receptor stimulation on extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathways on angiotensin II (AngII) stimulated cardiomyocytes of neonatal rats in vitro.</p><p><b>METHODS</b>Cardiomyocytes of neonatal rats were cultured in vitro. Cardiomyocytes hypertrophy was induced by AngII (0.1 µmol/L). The antihypertrophic effect of adenosine A1 receptor stimulation via adenosine A1 receptor agonist R-PIA (1 µmol/L) was observed in the presence or absence of ERK1/2 inhibitor 1, 4-Diamino-2, 3-dicyano-1, 4-bis(o-aminophenylmercapto) butadiene (U0126) 1 µmol/L, PKC inhibitor Ro-31-8220 (50 nmol/L), and pertussis toxin (PTX, 5 mg/L). The total protein content was assayed by the method of Lowry. The expression of mRNA of atrial natriuretic peptide (ANP) was determined by RT-PCR. [Ca(2+)]i was measured by confocal microscope using Fluo-3/AM as fluorescent indicator. The relative expression of ERK1/2 was determined by Western blot.</p><p><b>RESULTS</b>Compared with normal control group, AngII induced significant cardiomyocyte hypertrophy. Compared with AngII group, R-PIA significantly inhibited AngII-induced increase of the protein content, cardiomyocytes volume and expression of ERK1/2, calcium ion fluorescence intensity, similar as U0126 and Ro-31-8220. The inhibitory effects on AngII induced cardiomyocytes hypertrophy of R-PIA were lost when preincubated with PTX.</p><p><b>CONCLUSION</b>Adenosine A1 receptor can inhibit AngII induced cardiomyocyte hypertrophy through downregulating ERK signal pathways and reducing intracellular Ca(2+).</p>


Asunto(s)
Animales , Femenino , Masculino , Ratas , Agonistas del Receptor de Adenosina A1 , Farmacología , Angiotensina II , Farmacología , Calcio , Metabolismo , Cardiomegalia , Células Cultivadas , Sistema de Señalización de MAP Quinasas , Miocitos Cardíacos , Metabolismo , Patología , Ratas Sprague-Dawley , Receptor de Adenosina A1 , Metabolismo
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