Effects of high glucose induced primary cardiomyocytes injury on necroptosis and the related mechanism / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 160-164, 2019.
Article
en Zh
| WPRIM
| ID: wpr-776541
Biblioteca responsable:
WPRO
ABSTRACT
OBJECTIVE@#To observe whether necroptosis was happened in high glucose (HG) - induced primary cardiomyocytes injury and to investigate the likely mechanism.@*METHODS@#The primary cultured cardiomyocytes were divided into 4 groups (n=9): control group (the cardiomyocytes were incubated with 5.5 mmol/L glucose for 48 h), HG group (the cardiomyocytes were incubated with 30 mmol/L glucose for 48 h), HG + necrostatin-1 (Nec-1) group (the cardiomyocytes was co-incubated with necroptosis inhibitor Nec-1 at 100 μmol/L and HG for 48 h) and hypertonic pressure group (HPG, the cardiomyocytes was co-incubated with 5.5 mmol/L glucose and 24.5 mmol/L mannitol for 48 h). Cell viability was measured by MTT method, reactive oxygen species (ROS) generation was measured by DHE staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were tested by ELISA method. The mRNA and protein expressions of necroptosis related genes receptor interacting serine/threonine protein kinase 1 (RIP1), RIP3, mixed lineage kinase domain-like protein (MLKL) were tested by quantitative real-time PCR and Western blot.@*RESULTS@#The results showed HG intervention decreased cardiomyocytes viability, increased ROS generation, up-regulated the levels of TNF-α, IL-6 and IL-1β, increased RIP1, RIP3, MLKL expressions at mRNA and protein levels. Nec-1 treatment attenuated HG-induced increased cardiomyocytes viability, reduced ROS generation, down-regulated the levels of TNF-α, IL-6 and IL-1β, decreased RIP1, RIP3, MLKL expressions at mRNA and protein levels.@*CONCLUSION@#Necroptosis was happened in high glucose-induced primary cardiomyocytes injury. Inhibition of necroptosis can reduce high glucose-induced cardiomyocytes damage, may be related to inhibition of oxidative stress and depression of inflammative factors releasing.
Texto completo:
1
Base de datos:
WPRIM
Asunto principal:
Patología
/
Células Cultivadas
/
Citocinas
/
Especies Reactivas de Oxígeno
/
Apoptosis
/
Estrés Oxidativo
/
Biología Celular
/
Miocitos Cardíacos
/
Glucosa
/
Metabolismo
Límite:
Humans
Idioma:
Zh
Revista:
Chinese Journal of Applied Physiology
Año:
2019
Tipo del documento:
Article