Since the discovery of the tetracycline in 1953, numerous natural andsemisynthelic tetracyclines have been reported with broad spectrum antibacterial activity .Doxycycline 1 and minocycline 2 are semisyn-thetic second...Since the discovery of the tetracycline in 1953, numerous natural andsemisynthelic tetracyclines have been reported with broad spectrum antibacterial activity .Doxycycline 1 and minocycline 2 are semisyn-thetic second-generation tetracyclines that exertanti-inflammatory effects. These effects appear completely separate and distinct fromtheirantimicrobial actio. Minocycline and doxycycline are absorbed rapidly and show higher brainpenetrability than other tetracyclines. During recent years, doxycycline and minocycline have shownto have neuroprotective effects in models of global and focal ischemia . The neuroprotective effectsare assumed to result from the inhibition of microglia activation. Furthermore, from an in vitrostudy, it was reported that minocycline induces neuroprotection against NMDA-induced neurotoxicityby inhibiting p38 MAP ki-nase activity in microglia . However, neuroprotective mechanisms andstructure-activity relationships of these compounds in neurons are unclear.展开更多
文摘Since the discovery of the tetracycline in 1953, numerous natural andsemisynthelic tetracyclines have been reported with broad spectrum antibacterial activity .Doxycycline 1 and minocycline 2 are semisyn-thetic second-generation tetracyclines that exertanti-inflammatory effects. These effects appear completely separate and distinct fromtheirantimicrobial actio. Minocycline and doxycycline are absorbed rapidly and show higher brainpenetrability than other tetracyclines. During recent years, doxycycline and minocycline have shownto have neuroprotective effects in models of global and focal ischemia . The neuroprotective effectsare assumed to result from the inhibition of microglia activation. Furthermore, from an in vitrostudy, it was reported that minocycline induces neuroprotection against NMDA-induced neurotoxicityby inhibiting p38 MAP ki-nase activity in microglia . However, neuroprotective mechanisms andstructure-activity relationships of these compounds in neurons are unclear.
