Recent advances in the pharmacologic treatment of spinal cord injury

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

“…[4][5][6] Previous research has demonstrated that targeting the inflammatory response can improve nerve functional recovery in rat models of SCI. 7 Neuroinflammatory responses include maturation and secretion of proinflammatory cytokines interleukin (IL)-1β and IL-18, which induce cell death. 8 The maturation and secretion of pro-IL-1β and pro-IL-18 require the activation of proteolytic enzyme caspase-1, which is mediated by the activation of nucleotide-binding domain-like receptor protein 3 (NLRP3) and subsequently the recruitment of apoptosis-associated speck-like protein (ASC).…”

Combined and individual use of pancaspase inhibitor Q-VD-OPh and NMDA receptor antagonist Riluzole in experimental spinal cord injury

“…Riluzole is still being extensively used to treat ALS patients worldwide. [11,[46][47][48] In vitro studies have shown that riluzole protects motor neurons from the exitotoxic effects of glutamatic acid, which is secreted after cell death owing to anoxia. [11,49] In our study, statistically better resultsfor functional motor findings were obtained in Group 5 (Q-VD-OPh and riluzole) than in the trauma and riluzole only groups.…”

A study of methylprednisolone neuroprotection against acute injury to the rat spinal cord in vitro

“…The acute phase of SCI (due to the primary insult of mechanical, vascular or dysmetabolic nature) rapidly evolves into secondary damage, characterized by excitotoxicity caused by massive release of glutamate, in turn triggering a complex pathophysiological cascade generating toxic compounds (Dumont et al, 2001;Park et al, 2004;Rowland et al, 2008;Forder and Tymianski, 2009;Fatima et al, 2014). Thus, neuroprotection against secondary injury is a major therapeutic target (York et al, 2013;Cox et al, 2014) to preserve the spinal gray (Lipton, 2006;Sa´mano et al, 2012) and white matter containing the long-fiber tracts (Kanellopoulos et al, 2000;Lee et al, 2008;Margaryan et al, 2010;Sun et al, 2010;Cox et al, 2014). Large-scale clinical trials proposed the early i.v.…”