Neuroprotective effects of bilobalide on cerebral ischemia and reperfusion injury are associated with inhibition of pro-inflammatory mediator production and down-regulation of JNK1/2 and p38 MAPK activation

• DOI: 10.1186/s12974-014-0167-6
• Publication Date: 2014-09-25T15:18:55Z
• Authors: Mingjin Jiang; Jing Li; Qiuxian Peng; Yi Liu; Wei Liu; Chaohua Luo; Ju Peng; Junkui Li; Ken Kin Lam Yung; Zhixian Mo
• Keywords: Malondialdehyde

Mitogen-activated protein kinase (MAPK) signaling pathways are implicated in inflammatory and apoptotic processes of cerebral ischemia reperfusion (I/R) injury. Hence, MAPK represent a promising therapeutic target. Exploring the full potential inhibitors is useful strategy for ischemic stroke. Bilobalide, predominant sesquiterpene trilactone constituent Ginkgo biloba leaves, has been shown to exert powerful neuroprotective properties, which closely related both anti-inflammatory anti-apoptotic pathways. We investigated roles bilobalide models middle artery occlusion (MCAO/R) oxygen-glucose deprivation reoxygenation (OGD/R) I/R Moreover, we attempted confirm hypothesis that its protection effect via modulation pro-inflammatory mediators Male Sprague-Dawley rats were subjected MCAO 2 h followed by 24 h. Bilobalide was administered intraperitoneally 60 min before induction (MCAO). After reperfusion, neurological deficit scores, infarct volume, weight, brain edema assessed. Ischemic penumbrae cortex harvested determine superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide, TNF-Α, interleukin 1β (IL-1Β), p-ERK1/2, p-JNK1/2, p-p38 concentration. Similarly, influence on expression IL-1Β, also observed an OGD/R vitro model Pretreatment with (5, 10 mg/kg) significantly decreased edema, concentrations MDA, increased SOD activity. Furthermore, pretreatment down-regulated p-JNK1/2 expression, whereas they had no p-ERK1/2 penumbra. Supporting these observations vivo, (50, 100 μM) but did not change rat cortical neurons after These data indicate effects injury associated inhibition mediator production down-regulation JNK1/2 p38 activation.