Vitamin E protects against polymorphonuclear leukocyte-dependent adhesion to endothelial cells

Abstract

We evaluated the effects of ␣-Toc on surface expression of CD11b/CD18 on polymorphonuclear leukocytes (PMN) stimulated with N-formylmethionyl-leucyl-phenylalanine (fMLP) and oxidized low-density lipoprotein (oxLDL). Incubation of PMN with fMLP (1 M) or oxLDL (100 g/mL) increased CD11b/CD18 expression; pretreatment with ␣-Toc reduced in a dose-dependent manner. PMN obtained from healthy adults ingesting 600 mg ␣-Toc per day for 10 days were similarly incubated with fMLP or oxLDL; the surface level of CD11b/CD18 was inversely correlated with serum ␣-Toc concentrations. Adherence of PMN to human umbilical vein endothelial cells was increased by fMLP or oxLDL stimulation but reduced by ␣-Toc pretreatment or anti-CD18 monoclonal antibodies. cAMP-dependent protein kinase (PKA) and protein kinase C (PKC) activity in PMN was also assayed. A PKC inhibitor, but not a PKA inhibitor, suppressed CD11b/CD18 up-regulation, and ␣-Toc slightly decreased fMLP-and oxLDL-induced activation of PKC. These results suggest that ␣-Toc may prevent inflammation by both reducing CD11b/ CD18 up-regulation and decreasing PMN-dependent adherence to EC. J. Leukoc. Biol. 65: 757-763; 1999.

Effect of Oral Vitamin E Administration on Acute Gastric Mucosal Lesion Progression in Rats Treated with Compound 48/80, a Mast Cell Degranulator

“…No doses of vitamin E administered to C48/80-untreated rats had any effect on Se-GSHpx activity in the gastric mucosa. [15][16][17][18][19][20] Administration of SOD plus CAT to C48/80-treated rats attenuated the decrease in gastric mucosal Se-GSHpx activity found at 3 h after the treatment, although the administration of SOD plus CAT to C48/80-untreated rats did not affect the gastric mucosal Se-GSHpx activity. Therefore, these findings suggest that orally administered vitamin E exerts a preventive effect on acute gastric mucosal lesion progression in rats treated with C48/80 by maintaining gastric mucosal SeGSHpx activity through its action to scavenge O 2 Ϫ and OH .…”

“…[16][17][18][19][20] Naito et al 22) have shown that vitamin E protects against ischemia-reperfusioninduced gastric mucosal injury under nitric oxide depletion in rats by inhibiting not only lipid peroxidation but also neutrophil infiltration in the gastric mucosal tissue. We have reported that neutrophil infiltration into gastric mucosal tissues contributes to not only the formation but also the progression of C48/80-induced acute gastric mucosal lesions in rats.…”

“…15) Vitamin E exerts an anti-inflammatory action by inhibiting the production O 2 Ϫ in activated neutrophils, adhesion of neutrophils to endothelial cells, and transendothelial migration of neutrophils. [16][17][18][19][20] Yoshikawa et al 21) reported that both a decrease in gastric mucosal vitamin E level and an increase in gastric mucosal lipid peroxidation occurred during the development of ischemia-reperfusion-induced gastric mucosal injury in rats and that the severity of ischemia-reperfusion-induced gastric mucosal injury was enhanced in vitamin E-deficient rats. Naito et al 22) have shown in nitric oxide-depleted rats that vitamin E plays an important role in protecting against ischemia-reperfusion-induced gastric mucosal injury, and have suggested that this gastroprotective effect of vitamin E is due to not only its antioxidant action but also its inhibitory action on neutrophil infiltration into the gastric mucosa.…”

Effects of Genistein on Oxidative Injury in Endothelial Cells

“…␣-Tocopherol is believed to have a cytoprotective effect, which is attributed to its ability to prevent leukocyte-endothelial interactions (27)(28)(29), and to act as a scavenger of highly reactive oxygen radicals in various pathophysiological processes (30,31). ␣-Tocopherol protects against apoptosis not only by scavenging reactive oxygen species, but also by inhibiting caspase activity, which means that its activity may exceed that of a mere antioxidant (22).…”

Vitamin E 80th Anniversary: A Double Life, Not Only Fighting Radicals

“…In monocytes and polymorphonuclea r leukocytes, ®-tocopherol decreases agonist-induced and LDL-induced adhesion to human endothelial cells both in vivo and in vitro (61)(62)(63), an event that depends on the inhibition of adhesion molecules expression (64)(65)(66). These events are relevant to the onset of in ammation as well as in the early stages of atherogenesis.…”