Epigallocatechin gallate attenuates ET-1-induced contraction in carotid artery from type 2 diabetic OLETF rat at chronic stage of disease

• Published in: Life sciences (1973) Vol. 118; no. 2; pp. 200 - 205
• Main Authors: Matsumoto, Takayuki, Watanabe, Shun, Kawamura, Ryusuke, Taguchi, Kumiko, Kobayashi, Tsuneo
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 24.11.2014
• Subjects: Acetylcholine - pharmacology; Animals; Carotid Arteries - drug effects; Carotid Arteries - physiopathology; Carotid artery; Catechin - analogs & derivatives; Catechin - pharmacology; Catechin - therapeutic use; Chronic Disease; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - physiopathology; EGCG; Endothelin-1; ET-1; In Vitro Techniques; Male; NADPH Oxidases - metabolism; Nitric Oxide Synthase Type III - metabolism; Nitroprusside - pharmacology; Phenylephrine; Rats, Inbred OLETF; Receptors, Endothelin - metabolism; Superoxide Dismutase - metabolism; Type 2 diabetes; Vasoconstriction; Vasoconstriction - drug effects; Vasodilation - drug effects; Type 2 diabetes; ET-1; Carotid artery; EGCG; Vasoconstriction
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2013.11.016

There is a growing body of evidence suggesting that epigallocatechin gallate (EGCG), a major catechin isolated from green tea, has several beneficial effects, such as anti-oxidant and anti-inflammatory activities. However, whether treatment with EGCG can suppress the endothelin-1 (ET-1)-induced contraction in carotid arteries from type 2 diabetic rats is unknown, especially at the chronic stage of the disease. We hypothesized that long-term treatment with EGCG would attenuate ET-1-induced contractions in type 2 diabetic arteries. Otsuka Long–Evans Tokushima fatty (OLETF) rats (43weeks old) were treated with EGCG (200mg/kg/day for 2months, p.o.), and the responsiveness to ET-1, phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) was measured in common carotid artery (CA) from EGCG-treated and -untreated OLETF rats and control Long–Evans Tokushima Otsuka (LETO) rats. In OLETF rats, EGCG attenuated responsiveness to ET-1 in CA compared to untreated groups. However, EGCG did not alter PE-induced contractions in CA from OLETF rats. In endothelium-denuded arteries, EGCG did not affect ET-1-induced contractions in either the OLETF or LETO group. Acetylcholine-induced relaxation was increased by EGCG treatment in CA from the OLETF group. The expressions of ET receptors, endothelial nitric oxide synthase, superoxide dismutases, and gp91phox [an NAD(P)H oxidase component] in CA were not altered by EGCG treatment in either group. Our data suggest that, within the timescale investigated here, EGCG attenuates ET-1-induced contractions in CA from type 2 diabetic rats, and one of the mechanisms may involve normalizing endothelial function. [Display omitted]