Matsumoto Takayuki, Watanabe Shun, Kawamura Ryusuke, Taguchi Kumiko, Kobayashi Tsuneo
Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo 142-8501, Japan.
Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo 142-8501, Japan.
Life Sci. 2014 Nov 24;118(2):200-5. doi: 10.1016/j.lfs.2013.11.016. Epub 2013 Dec 1.
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 (43 weeks old) were treated with EGCG (200 mg/kg/day for 2 months, 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 gp91(phox) [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.
越来越多的证据表明，表没食子儿茶素没食子酸酯（EGCG），一种从绿茶中分离出的主要儿茶素，具有多种有益作用，如抗氧化和抗炎活性。然而，EGCG治疗是否能抑制2型糖尿病大鼠颈动脉中内皮素-1（ET-1）诱导的收缩尚不清楚，尤其是在疾病的慢性阶段。我们假设长期用EGCG治疗会减弱2型糖尿病动脉中ET-1诱导的收缩。
用EGCG（200mg/kg/天，口服，持续2个月）处理大冢长- Evans德岛肥胖（OLETF）大鼠（43周龄），并测量EGCG处理和未处理的OLETF大鼠以及对照大冢长- Evans德岛（LETO）大鼠的颈总动脉（CA）对ET-1、去氧肾上腺素（PE）、乙酰胆碱（ACh）和硝普钠（SNP）的反应性。
在OLETF大鼠中，与未处理组相比，EGCG减弱了CA对ET-1的反应性。然而，EGCG并未改变OLETF大鼠CA中PE诱导的收缩。在内皮剥脱的动脉中，EGCG对OLETF组或LETO组的ET-1诱导的收缩均无影响。EGCG处理使OLETF组CA中ACh诱导的舒张增加。两组中EGCG处理均未改变CA中ET受体、内皮型一氧化氮合酶、超氧化物歧化酶和gp91（phox）[一种NAD（P）H氧化酶成分]的表达。
我们的数据表明，在此处研究的时间范围内，EGCG减弱了2型糖尿病大鼠CA中ET-1诱导的收缩，其机制之一可能涉及使内皮功能正常化。
