lignans and Brain-Edema

Intracerebral haemorrhage (ICH) induces inflammation, which can cause severe secondary injury. Recent evidence has suggested that magnolol (MG) has a protective effect against ischaemic stroke through the inhibition of inflammation. However, the anti-inflammatory effect of MG in intracerebral haemorrhage (ICH) remains unclear. Here, we report that the protective effect of MG in a rat model of ICH can be achieved by anti-inflammatory processes. We found that MG administration significantly reduced the brain water content, restored the blood-brain barrier (BBB) and subsequently attenuated neurological deficits via decreasing the activation of glial cells, decreasing the infiltration of neutrophils and reducing the production of pro-inflammation factors (IL-1β, TNF-α and MMP-9) in a rat model of ICH. These results suggest that MG reduced inflammatory injury and improved neurological outcomes in ICH model.

Topics: Animals; Anti-Inflammatory Agents; Astrocytes; Biphenyl Compounds; Blood-Brain Barrier; Brain; Brain Edema; Brain Ischemia; Cerebral Hemorrhage; Cytokines; Disease Models, Animal; Inflammation; Lignans; Male; Neuroglia; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Stroke

Topics: Animals; Apoptosis; Aquaporin 4; Blood-Brain Barrier; Brain Edema; Brain Injuries, Traumatic; Capillary Permeability; Caspase 3; Cell Line; Dioxoles; Disease Models, Animal; Endothelial Cells; Extracellular Signal-Regulated MAP Kinases; Lignans; Male; Mice, Inbred C57BL; Neuroprotective Agents; Occludin; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Time Factors; Zonula Occludens-1 Protein

This study was designed to investigate the effects of honokiol, a neuroprotective agent, on cerebral edema in cerebral ischemia reperfusion (IR) mice and its mechanism of anti-inflammation. Honokiol (0.7-70μg/kg) significantly reduced brain water contents and decreased the exudation of Evans blue dye from brain capillaries in cerebral IR mice. Honokiol (0.1-10μM) significantly reduced the p65 subunit level of NF-κB in the nucleus of primary culture-microglia. It (0.01-10μM) evidently reduced nitric oxide (NO) level in the microglia culture medium and in the microglia and astrocytes coculture medium. Honokiol (0.01-10μM) significantly decreased the level of TNF-α in the microglia medium or coculture cell medium. Honokiol (10μM) decreased the level of Regulated upon Activation Normal T-cell Expressed and Secreted (RANTES/CCL5) protein in medium of microglia or astrocytes. In conclusion, Honokiol has a potent anti-inflammatory effect in cerebral ischemia-reperfusion mice and this effect might be attributed to its inhibition ability on the NF-κB activation, consequently blocking the production of inflammatory factors including: NO, tumor necrosis factor-α (TNF-α) and RANTES/CCL5 in glial cells. These results provide evidence for the anti-inflammatory effect of honokiol for the potential treatment of ischemic stroke.

Topics: Animals; Anti-Inflammatory Agents; Astrocytes; Biphenyl Compounds; Brain Edema; Brain Ischemia; Capillary Permeability; Chemokine CCL5; Coculture Techniques; Cytokines; Drugs, Chinese Herbal; Female; Inflammation; Lignans; Male; Mice; Microglia; Neuroglia; NF-kappa B; Nitric Oxide; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Tumor Necrosis Factor-alpha