Methyleugenol reduces cerebral ischemic injury by suppression of oxidative injury and inflammation

Abstract

The present study tested the cytoprotective effect of methyleugenol in an in vivo ischemia model (i.e. middle cerebral artery occlusion (MCAO) for 1.5 h and subsequent reperfusion for 24 h) and further investigated its mechanism of action in in vitro cerebral ischemic models. When applied shortly after reperfusion, methyleugenol largely reduced cerebral ischemic injury. Methyleugenol decreased the caspase-3 activation and death of cultured cerebral cortical neurons caused by oxygen-glucose deprivation (OGD) for 1 h and subsequent re-oxygenation for 24 h. Methyleugenol markedly reduced superoxide generation in the ischemic brain and decreased the intracellular oxidative stress caused by OGD/re-oxygenation. It was found that methyleugenol elevated the activities of superoxide dismutase and catalase. Further, methyleugenol inhibited the production of nitric oxide and decreased the protein expression of inducible nitric oxide synthase. Methyleugenol down-regulated the production of pro-inflammatory cytokines in the ischemic brain as well as in immunostimulated mixed glial cells. The results indicate that methyleugenol could be useful for the treatment of ischemia/inflammation-related diseases.

Methyl Eugenol: Its Occurrence, Distribution, and Role in Nature, Especially in Relation to Insect Behavior and Pollination

“…Recent research by Choi et al (2010) indicated that ME may have positive effects on human health as well. Based on their studies, ME may reduce cerebral ischemic injury through suppression of oxidative injury and inflammation (Choi et al 2010).…”

“…Based on their studies, ME may reduce cerebral ischemic injury through suppression of oxidative injury and inflammation (Choi et al 2010). The chemical also decreased activation of an enzyme, caspase-3, and the death of cultured cerebral cortical neurons through oxygen— glucose deprivation for one hour.…”

“…Additionally, it was shown that ME elevated the activities of superoxide dismutase and catalase, thereby markedly reducing superoxide generation in the ischemic brain and decreasing intracellular oxidative stress. Furthermore, ME also reduced the production of pro—inflammatory cytokines in the ischemic brain (Choi et al 2010). …”

Gastroprotective Activity of Methyleugenol from Peperomia hispidula on Ethanol-Induced Gastric Lesions in Rats

“…It is used as a flavoring agent in foods such as jellies, baked goods and ice cream and as a fragrance in soaps, lotions and perfumes. This compound is a central nervous system depressant with anesthetic, hypothermic, antianaphylaxis, antinociceptive, anti-inflammatory, myorelaxant and anticonvulsant properties (Abdo et al, 2001;Choi et al, 2010). This is the first report, to our knowledge, about the gastroprotective activity of methyleugenol on ethanol-induced gastric lesions.…”

Activation of p38-mitogen-activated protein kinase contributes to ischemia reperfusion in rat brain

“…Cerebral ischemia reperfusion and local cell debris have a strong cytotoxic effect in the brain parenchyma after middle cerebral artery occlusion (MCAO). The cytotoxic response occurs within minutes of the onset of cerebral ischemia and involves proinflammatory responses, oxidative stress, neurologic damage, and cell death (Choi et al, 2010). Inflammation leads to increased permeability of the BBB, and blood may be discharged from damaged vessels.…”