Endothelial cells covering the luminal surface of all blood vessels have a pivotal role in the control of vascular homeostasis mostly via the activation of protective mechanisms. These mechanisms include the endothelial formation of @entity842 (NO) in response to the activation of endothelial NO synthase, endothelium-dependent hyperpolarization involving endothelial SKCa and IKCa, which is subsequently transmitted to the underlying vascular smooth muscle via myoendothelial junctions, and in some blood vessels, also @entity4770 . These endothelial protective mechanisms will promote vasodilatation, inhibit platelet activation, and also prevent the expression of pro-atherothrombotic factors. In most types of @entity65 including type 1 and 2 @entity6 ( @entity2175 ), an @entity409 as indicated by blunted endothelium-dependent vasorelaxations and often also by the appearance of endothelium-dependent cyclooxygenase-mediated contractile responses is observed early in the development of the pathology and has been suggested to contribute to the development of both @entity455 in @entity2175 . The impaired endothelium-dependent relaxations in @entity2175 has indicated the involvement of reduced NO and endothelium-dependent hyperpolarization components and is associated with increased oxidative stress in the arterial wall involving @entity224 anion and @entity273 predominantly due to an up-regulation of @entity1110 oxidase and possibly also uncoupling of endothelial NO synthase. Investigations in experimental animals and @entity1 have also suggested that the angiotensin system contributes to the impaired endothelial function in @entity2175 . Several sources of @entity6398 (i.e., @entity6353 and plant extracts) have been shown to retard the induction of @entity409 in TD2 in part by preventing oxidative stress in the arterial wall most likely by normalizing the expression of @entity1110 oxidase, cyclooxygenase-1 and 2, eNOS uncoupling, and the angiotensin system. Both pre-clinical and clinical data will be presented and discussed. In addition, @entity6398 may possibly also improve the endothelial function by preventing the induction of endothelial senescence to high @entity413 and @entity2178 . Thus, @entity6398 by improving the @entity409 might help to retard the development of both macro- and @entity455 in @entity6 .

Role of @entity6398 in improving @entity409 in XXXX .

@entity2175 :: ('MESH:D003924', 'Disease') :: ['T2D'] @entity1 :: ('9606', 'Species') :: ['humans'] @entity455 :: ('MESH:D014652', 'Disease') :: ['macro-vascular and micro-vascular complications', 'micro-vascular complications'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetes'] @entity2178 :: ('183', 'Gene') :: ['angiotensin II'] @entity409 :: ('MESH:D008107', 'Disease') :: ['endothelial dysfunction'] @entity1110 :: ('MESH:D009249', 'Chemical') :: ['NADPH'] @entity4770 :: ('MESH:D011464', 'Chemical') :: ['prostacyclin'] @entity273 :: ('MESH:D006861', 'Chemical') :: ['hydrogen peroxide'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['nitric oxide'] @entity6353 :: ('3641', 'Species') :: ['cocoa'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose'] @entity6398 :: ('MESH:D059808', 'Chemical') :: ['polyphenols'] @entity224 :: ('MESH:D013481', 'Chemical') :: ['superoxide'] @entity65 :: ('MESH:D002318', 'Disease') :: ['cardiovascular diseases']
@entity6 :: (MESH:D003920,Disease) :: ['diabetes']
