the reduced amount of infarct size and apoptotic cell death observed following in vivo therapy with minocycline was associated with a remarkable postischemic recovery of cardiac function. The cardioprotective effect has been checked at three levels: in vitro, using primary cultures of neonatal and adult cardiomyocytes, ex vivo, infusing minocycline to the isolated rat heart, and in vivo, injecting the animals with minocycline over an interval of 3 days. Regarding its antiapoptotic Erlotinib solubility mechanism of action, minocycline was shown to induce powerful inhibition of the activity level of effector caspases and many initiator, through the action of multiple elements. Besides the well-documented down-regulation of caspase 1 and 3, minocycline paid down the cardiac expression of caspase 1-2 in basal condition and stopped the postischemic up-regulation of all above caspases. Furthermore, minocycline effortlessly interfered with upstream and downstream mechanisms leading Mitochondrion to reactivation and secondary caspase activation, inducing paid off decompartmentalization of cytochrome c and Smac/DIABLO, together with increased rate of XIAP to Smac/DIABLO. These combined actions concur to regulate the functional activity of caspases at three different levels: promoting the inhibition of activated caspases, reducing the mitochondria mediated activation of caspase 9, and avoiding the reactivation of dormant caspases. Therefore, the results achieved with in vivo administration of minocycline effortlessly work to keep in check the level of caspase activity in the center, raising the idea of responsibility in ischemic/reperfused cardiac myocytes. Medical utilization of minocycline is not tied to the possible harmful effects of other conventional caspase inhibitors due to abrogation of normal homeostatic apoptosis in the human adult, since this action of caspase modulation isn’t dependent on a direct inhibition of caspase activity. Due to this, minocycline could be valuable in acute but also (-)-MK 801 in serious clinical settings, where it might provide important synergism with traditional cardioprotective agents in counteracting the incidence and the progression of myocyte cell loss. Forty CB6F1 adult male mice under-went unilateral distal middle cerebral artery occlusion and were imaged and sacrificed on 1, or 30 days after injury. Animals were given 2-2. 5 mg/kg minocycline i. p. Thirty minutes and 1-2 hours after then 2-2 and dMCAO. 5 mg/kg twice daily for 7 days. In each class, mice were injected with 5 to 10 mCi of 99mTc annexin V 2 hours before undergoing SPECT on days 1, 3 and 7, and 30. After imaging, brains were obtained for histology and evaluated for apoptosis using TUNEL mark and activated microglia using isolectin B4.