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Tetracycline antibiotics discovered in 1948 happen to be employed clinically for a lot more than half a century to treat bacterial infections (Dugger 1948; Mainoli and Piccinelli 1955). Compounds within the tetracycline group share a linear fused four-ring nucleus and act antimicrobially by blocking association of aminoacyl-tRNA with bacterial ribosomes to inhibit protein synthesis (Chopra and Roberts 2001). More recently, some tetracyclines were shown to possess therapeutic properties beyond their initial antimicrobial action. Minocycline mitigates harm from reperfusion injury inside the spinal cord, kidney, and liver (Kelly et al. 2004; Theruvath et al. 2008a; Wells et al. 2003). Doxycycline has shown related protective effects for myocardial infarction and cerebral ischemia (Castro et al. 2011; Pires et al. 2011). Chlorotetracycline and demeclocycline appear to inhibit reperfusion injury in neurons via suppression of an intracellular rise in Ca2+ and inhibition of calpains (Jiang et al. 2005). Reperfusion injury is related with morbidity and mortality following heart attack, stroke, diabetes, organ transplantation along with other clinical situations (Aronowski et al. 1997; King et al. 2000; Mustoe 2004; Yellon and Hausenloy 2007). Reperfusion injury happens soon after blood re-flows into an ischemic tissue. The surge of oxygen to oxygen-deprived tissues causes increased production of reactive oxygen species (ROS), leading to onset with the mitochondrial permeability transition (MPT). Opening of MPT pores that nonspecifically conduct low weight molecules up to 1500 Da causes the MPT and leads to mitochondrial depolarization, uncoupling of oxidative phosphorylation, higher amplitude mitochondrial swelling and outer membrane rupture (Di Lisa et al. 2003; Di Lisa et al. 2011; Lemasters et al. 2009). Such ruptured mitochondria release proapoptotic components like cytochrome c into the cytosol that activate caspases as well as other apoptotic events, culminating in cell death (Lemasters et al. 2002). Apoptosis requires ATP. When th.
