Apocynin ameliorates pressure overload-induced cardiac remodeling by inhibiting oxidative stress and apoptosis

Title:

Apocynin ameliorates pressure overload-induced cardiac remodeling by inhibiting oxidative stress and apoptosis

Creator:

Liu, J.-J., Lu, Y., Ping, N.-N., Li, X., Lin, Y.-X., and Li, C.-F.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:7041ac8c-ce0e-488b-9d2e-df0e19098c64
uuid:7041ac8c-ce0e-488b-9d2e-df0e19098c64

Subject:

apocynin, cardiac remodeling, angiotension II, NADPH oxidase, reactive oxygen species, and apoptosis

Type:

article, model:article, and TEXT

Description:

Oxidative stress plays an important role in pressure overloadinduced cardiac remodeling. The purpose of this study was to determine whether apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, attenuates pressure overload-induced cardiac remodeling in rats. After abdominal aorta constriction, the surviving rats were randomly divided into four groups: sham group, abdominal aorta constriction group, apocynin group, captopril group. Left ventricular pathological changes were studied using Masson’s trichrome staining. Metalloproteinase-2 (MMP-2) levels in the left ventricle were analyzed by western blot and gelatin zymography. Oxidative stress and apoptotic index were also examined in cardiomyocytes using dihydroethidium and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), respectively. Our results showed that abdominal aorta constriction significantly caused excess collagen deposition and cardiac insult. Treatment with apocynin significantly inhibited deposition of collagen and reduced the level of MMP-2. Furthermore, apocynin also decreased the NADPH oxidase activity, reactive oxygen species production and cardiomyocyte apoptotic index. Interestingly, apocynin only inhibited NADPH oxidase activity without affecting its expression or the level of angiotension II in the left ventricle. In conclusion, apocynin reduced collagen deposition, oxidative stress, and inhibited apoptosis, ultimately ameliorating cardiac remodeling by mechanisms that are independent of the renin-angiotensin system.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:5

Harvested from:

CDK

Metadata only:

false