UCP2 overexpression also inhibited intracellular ROS production in the en face endothelium of aorta and mesenteric artery of DIO mice, whereas UCP2 deficiency enhanced ROS production.
Improved EDR in mesenteric arteries was inhibited by nitric oxide synthase inhibitor. injection restored both EDR and flow-mediated vasodilatation in DIO mice. Impairment of EDR and flow-mediated vasodilatation in aortae and mesenteric arteries from high-fat diet-induced obese mice (DIO) was exaggerated in UCP2KO DIO mice compared with wild-type DIO littermates, whereas AdUCP2 i.v. Source: Crossref Designable Micro/NanoStructured Smart Polymeric Materials. High-glucose exposure reduced EDR in mouse aortae, which was exaggerated in UCP2 knockout (KO) mice, whereas UCP2 overexpression by adenoviral infection (AdUCP2) restored the impaired EDR. Contributors: Guo-Yu Wen Xing-Long Zhou Xiao-Yu Tian Rui Xie Xiao-Jie Ju Zhuang Liu Yousef Faraj Wei Wang Liang-Yin Chu Show more detail.
ROS production is measured by CM-H(2)DCFDA and DHE fluorescence. Flow-mediated vasodilatation in 2(nd)-order mesenteric arteries was measured in pressure myograph. UCP2 protects against endothelial dysfunction induced by high-fat diet through inhibition of reactive oxygen species (ROS) production, and subsequent increase of nitric oxide bioavailability.Įndothelium-dependent relaxation (EDR) in aortae and mesenteric arteries in response to acetylcholine was measured in wire myograph. However, the role of UCP2 in endothelial dysfunction associated with diabetes and obesity is unclear. Instagram : doramii.mcFacebook : Doramii Music ChannelTiktok : Doramii.mcIf you enjoy this video Dont forget to turn on notification subscribe, like and sh. UCP2 also regulates insulin secretion and action. Previous studies indicate uncoupling protein-2 (UCP2) as an antioxidant defense against endothelial dysfunction in hypertension.
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