GSK-3β inhibition induces cardioprotection via attenuating activation of NLRP3 inflammasome after acute myocardial infarction in rats
- Author:
Shu-Hui WANG
1
;
Li-Na XU
;
Cheng CHANG
;
Yu YAO
;
Sheng-Na HAN
;
Li-Rong ZHANG
Author Information
1. Department of Pharmacology
- Keywords:
acute myocardial infarction;
glycogen synthase 3β;
NLRP3 inflammasome;
ASC;
IL-1β
- From:
Chinese Journal of Pharmacology and Toxicology
2018;32(4):270-270
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To observe the effects of glycogen synthase 3β (GSK-3β) in the regula-tion of NLRP3 inflammasome activation after acute myocardial infarction (MI) in Sprague Dawley(SD) rats. METHODS Ligation of the left anterior descending (LAD) in SD rats was used to establish an acute myocardial infarction model. SD rats were randomly divided into 3 groups (n=10, each group):sham group,MI group,and MI+SB group:the GSK-3β inhibitor(SB216763)was given 1 h by intrave-nous injection(0.6 mg·kg-1·d-1)before surgery.The serum and heart tissue were collected to measure lactate dehydrogenase (LDH) and IL-1β content and mRNA and protein levels of NLRP3, ASC, Cas-pase-1,IL-1β and GSK-3β after 2 days and 7 days operation,respectively.RESULTS The serum levels of LDH and IL-1β in the MI group were significantly higher than those in the sham group(P<0.01),and the MI+SB group was obviously lower than the MI group(P<0.01).In addition,mRNA and protein levels of NNLRP3, ASC, Caspase-1, IL-1β and GSK-3β expressions in MI group were clearly increased (P<0.01) compared with those in sham group.These indicators were significantly decreased in SB+MI group (P<0.01). Interestingly, the indicators were all higher at 7 days than 2 days. CONCLUSION GSK-3β inhibition induces cardioprotection via attenuating the activation of NLRP3 inflammasome after the acute myocardial infarction in rats.
