Sodium valproate inhibited apoptosis in lethally scalded rat cardiomyocytes by regulating hypoxia-inducible factor-1α expression.
Pak J Pharm Sci
; 37(2(Special)): 423-428, 2024 Mar.
Article
in En
| MEDLINE
| ID: mdl-38822545
ABSTRACT
This study assessed the inhibitory effect of sodium valproate (VPA) on apoptosis of cardiomyocytes in lethally scalded rats. The model of a 50% total body surface area (TBSA) third-degree full-thickness scald was produced, 48 male SD rats were randomly divided into three groups (n = 16), the sham group and the scald group were given an intraperitoneal injection of 0.25ml of saline, the scald +VPA group was given an intraperitoneal injection of VPA (300 mg/kg) after scalded, Each group was subdivided into two subgroups (n=8) according to the two observation time points of 3h and 6h after scald. Apoptotic cardiomyocytes were observed, and myocardial tissue levels of nitric oxide (NO), cysteine protease-3 (caspase-3) activity, hypoxia-inducible factor-1α (HIF-1α), inducible nitric oxide synthase (iNOS), BCL2/adenovirus E1B interacting protein 3 (BNIP3) and caspase-3 protein were measured. Compared with sham scald group, severe scald elevated CK-MB, cardiomyocyte apoptosis rate, caspase-3 activity and protein levels, NO content, and HIF-1α signalling pathway proteins; whereas VPA decreased CK-MB, cardiomyocyte apoptosis rate and inhibited HIF-1α signalling pathway protein expression. In conclusion, these results suggested that VPA inhibited early cardiomyocyte apoptosis and attenuated myocardial injury in lethally scalded rats, which may be related to the regulation of the HIF-1α signalling pathway.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Burns
/
Valproic Acid
/
Apoptosis
/
Myocytes, Cardiac
/
Hypoxia-Inducible Factor 1, alpha Subunit
Limits:
Animals
Language:
En
Journal:
Pak J Pharm Sci
Journal subject:
FARMACIA
/
FARMACOLOGIA
/
QUIMICA
Year:
2024
Document type:
Article
Affiliation country:
China