Drug-induced activation of the nervous control of inflammation: A novel possibility for the treatment of hypoxic damage

作者：Bertolini Alfio^*

来源：European Journal of Pharmacology, 2012, 679(1-3): 1-8.

DOI：10.1016/j.ejphar.2012.01.004

• Ischemic disease
• Tissue hypoxia
• Ischemia-reperfusion
• Brain control of inflammation
• Cholinergic anti-inflammatory pathway
• Melanocortins
• alpha 7-Nicotinic receptor agonists
• Muscarinic receptor agonists
• Shock
• Stroke
• Myocardial infarction

Together with undernutrition and, on the opposite, overeating and obesity, sudden tissue hypoperfusion is the most important cause of mortality and disability worldwide. Tissue hypoperfusion/hypoxia rapidly triggers an unrestrained inflammatory cascade that is the main responsible for the severity of the eventual outcome. The brain plays a key role in inflammation, either through activation of the hypothalamic-pituitary-adrenal humoral response or through activation of the vagal %26quot;cholinergic anti-inflammatory pathway%26quot;. Both humoral and nervous brain responses to inflammation are under the regulatory control of melanocortins, which have moreover a direct anti-inflammatory effect on inflammatory cells. Abundant experimental and clinical evidence indicates that MC3/MC4 melanocortin receptor agonists and cholinergic receptor agonists (mainly at the alpha 7-nicotinic subtype) should by now be considered as completely innovative, effective drugs for the treatment of hypoxic conditions; melanocortin agonists being practically devoid of harmful side effects.

• 出版日期2012-3-15