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Hydrogen sulfide inhibits adenosine triphosphate-induced activation and IL-1βreleases in rat microglia / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 1408-1412, 2016.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-495877
Biblioteca responsável: WPRO
ABSTRACT

AIM:

To investigate the effects of sodium hydrosulfide ( NaHS ) , a donor of hydrogen sulfide ( H2 S) , on the membrane permeability , intracellular Ca 2+concentration ( [ Ca2+] i ) and the release of IL-1βinduced by a-denosine triphosphate (ATP) in rat microglia, and to explore the effect of H2S on ATP-P2X purinergic signaling pathway and the molecular mechanism of its neuroprotective effect .

METHODS:

Rat microglia in logarithmic growth phase were used in the study.The [Ca2+]i was detected by Fura-2/AM staining.Fluorescent dye YO-PRO-1 was used to observe the membrane permeability.Interleukin-1β(IL-1β) was measured by rat IL-1βELISA kits.

RESULTS:

The YO-PRO-1 flu-orescence intensity was obviously elevated by ATP induction in a dose -dependent manner in the rat microglia , but this effect was counteracted by NaHS pretreatment (P<0.05).[Ca2+]i rapidly increased and then decreased slowly , forming a sta-ble platform for a long time when rat microglia were treated with ATP .Ca2+spike activity induced by ATP had no change , but the platform disappeared (P<0.05) after NaHS pretreatment.The ATP and LPS together facilitated the release of IL-1β, but the phenomenon was inhibited by NaHS (P<0.05).

CONCLUSION:

Hydrogen sulfide may decrease the mem-brane permeability , calcium inflow and IL-1βrelease in rat microglia activated by high dose of ATP .The cytoprotection of hydrogen sulfide may be mediated by purinergic signaling pathway .

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2016 Tipo de documento: Artigo
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