Inflammatory reaction after brain damage and prospective therapy against damage impending cerebral infarction.
Cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The blood-borne invaders then accelerate the decomposition of brain cells by their toxic by-products, phagocytic action, and by the immune reaction. Recently accumulated data in our laboratories and other research facilities show that depleting the amount of circulating leukocytes or administering anti-inflammatory chemicals such as cytokine blocking agents, anti-adhesion molecule antibodies, and immunosuppressants effectively minimize the size of ischemia induced cerebral infarction. Based on the fact that leukocyte invasion of the affected brain tissue occurs 6 to 24 hours after onset of ischemia, administration of an anti-inflammatory therapy may widen the therapeutic window against stroke.
Matsuo
Y
Y
Developmental Research Laboratory, Shionogi & Co. Ltd., Osaka, Japan.
Yamasaki
Y
Y
Kogure
K
K
D000818:Animals; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy*; D002544:Cerebral Infarction / Q000517:prevention & control*; D006801:Humans; D009443:Neuritis / Q000209:etiology*; D018696:Neuroprotective Agents / Q000627:therapeutic use*
D018696:Neuroprotective Agents