Vitamin E in its natural form is also known as D-α-tocopherol; it exhibits antioxidative, anti-inflammatory, anti-atherosclerotic, anti-hyperlipidemic, and anti-diabetic activities. In keratinocytes, vitamin E decreased UVA-induced upregulation of IL-8 and AP-1 binding and decreased activity of NADPH oxidase and formation of malondialdehyde. When administered clinically, vitamin E decreases ROS, lipid oxidation, secretion of IL-1β, and endothelial cell-to-monocyte adhesion. Vitamin E is also protective against retinal edema in animal models of ischemia/reperfusion. Additionally, vitamin E inhibits intracellular adhesion molecule 1 (ICAM-1)-induced activation of PKC in endothelial cells. In vivo, this compound decreases serum triglycerides, VLDL, PPARγ and malondialdehyde levels and increases PPARα levels, improving insulin resistance. Vitamin E also inhibits PKC-DAG signaling and increases glomerular filtration rate (GFR) and decreases albuminuria, showing nephroprotective benefit in animal models of diabetic nephropathy.