MK 801 and dexamethasone reduce both tumor necrosis factor levels and infarct volume after focal cerebral ischemia in the rat brain
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Cited by (71)
Time dependent neuroprotection of dexamethasone in experimental focal cerebral ischemia: The involvement of NF-κB pathways
2018, Brain ResearchCitation Excerpt :For example, de Courten-Myers et al. (1994) indicate that administering methylprednisolone at high doses early (starting 30 min after occlusion) after onset of ischemia significantly reduces tissue injury in cats that survive 4 days of temporary middle cerebral artery occlusion. In the study of Bertorelli et al. (1998), dexamethasone was given 10 min after MCAO, and at the high dose of 3 mg/kg i.p., reduced TNF production in the ipsilateral cortex and reduce brain edema, decreased infarct size by 50%. Corticosteroids therapy in most of the study reported negative results were later than two hours (de la Torre and Surgeon, 1976; Koide et al., 1986; Norris and Hachinski, 1986).
Corticosteroids and perinatal hypoxic-ischemic brain injury
2018, Drug Discovery TodayRole of microglia in ischemic focal stroke and recovery: focus on Toll-like receptors
2017, Progress in Neuro-Psychopharmacology and Biological PsychiatryContext-Dependent GluN2B-Selective Inhibitors of NMDA Receptor Function Are Neuroprotective with Minimal Side Effects
2015, NeuronCitation Excerpt :Of these four behaviors (locomotor activity, rotorod, PCP discrimination, and lever pressing), we identified only one in which 93-31 caused significant effects at doses of 30 mg/kg or higher. From the ED50 for neuroprotection (<1 mg/kg) we calculate a TR for neuroprotection in rodents following IP administration of >30 for the pH-sensitive 93-31 GluN2B inhibitor, a value considerably higher than that estimated for neuroprotection in the literature for ifenprodil and dizolcilpine (TR ≤ 1; Hatfield et al., 1992; Bertorelli et al., 1998; Dawson et al., 2001; Xiao et al., 2004) and CP-101,606 (TR ∼4; Yang et al., 2003, Nicholson et al., 2007). Two important findings emerge from this study.
Dexamethasone-induced neuroprotection in hypoxic-ischemic brain injury in newborn rats is partly mediated via Akt activation
2014, Brain ResearchCitation Excerpt :So, we suggest that corticosteroids may induce pharmacological preconditioning. Pretreatment with Dex is neuroprotective in neonatal rats (Barks et al., 1991; Dardzinski et al., 2000; Felszeghy et al., 2004; Tuor et al., 1993) and in the adult rat and mice (Bertorelli et al., 1998; Limbourg et al., 2002). Pretreatment with Dex has shown very strong neuroprotection, from 90% to 100% of brain damage in the present study and in other reports (Feng et al., 2011; Liu et al., 1995; Tuor and Del Bigio, 1996).
Dexamethasone exacerbates cerebral edema and brain injury following lithium-pilocarpine induced status epilepticus
2014, Neurobiology of DiseaseCitation Excerpt :Following status epilepticus, rats were randomly assigned to one of two groups: SE-DEX10 rats (n = 13) received dexamethasone sodium phosphate (10 mg/kg, equivalent to 7.6 mg/kg dexamethasone) immediately following status epilepticus and at 24 h (10 mg/kg) following SE. This dose is comparable to doses that have shown or attempted to demonstrate efficacy in other rat models of brain edema (Altman et al., 1984; Bertorelli et al., 1998; Mima and Shigeno, 2000; Shapira et al., 1988; Tran et al., 2010). SE rats (n = 15) received saline injections in place of dexamethasone.