Table 4 PKCδ inhibitors and their applications
From: PKCδ regulates the vascular biology in diabetic atherosclerosis
PKCδ inhibitor | Disease model | Pathophysiological processes |
|---|---|---|
Rottlerin | Atherosclerosis | Increases NO production, decreases ET-1 production in ECs [21, 131] |
Rottlerin | Atherosclerosis | |
Rottlerin | Atherosclerosis | attenuates the migration and adhesion of neutrophils [35] |
Rottlerin | Atherosclerosis | Inhibits NOX expression and ROS production in ECs [42] |
Rottlerin | Atherosclerosis | |
Rottlerin | Atherosclerosis | Alleviates migration and proliferation of VSMCs [66, 68, 70, 71] |
Rottlerin | Atherosclerosis | |
Rottlerin | Atherosclerosis | Suppresses IL-1β and iNOS expression, NO generation in monocytes [89, 95, 97] |
Rottlerin | Atherosclerosis | Inhibits SR-A and CD36 in macrophages [109] |
Rottlerin | Atherosclerosis | Regulates ABCA-1 and ABCG-1 expression in macrophages [111, 112] |
Rottlerin | Diabetic retinopathy | Reverses abnormally increased vascular permeability 30 |
Rottlerin | Inflammatory lung disorders | Reverses abnormally increased vascular permeability 33 |
δV1-1 | Sepsis-induced vascular damage | Reduces TNF-α-mediated ECs hyperpermeability [18] |
δV1-1 | Sepsis-induced vascular damage | Reduces neutrophils adhesion and migration [18] |
δV1-1 | Sepsis-induced lung injury | Attenuates inflammatory cell infiltration and endothelial ICAM-1 and VCAM-1 expression [15] |
δV1-1 | Inflammation-induced tissue damage | Inhibits neutrophils adhesion and migration [17] |
Polydatin | Atherosclerosis | Attenuates H2O2-induced oxidative stress in ECs [44] |
Curcuminoids | Atherosclerosis | Suppresses matrix invasion during PMA-induced THP-1 differentiation [104] |
Calcium dobesilate | Diabetic retinopathy | Reduces vascular leakage [132] |
Calcium dobesilate | Atherosclerosis | Attenuates monocyte-to-macrophage differentiation [106] |