Pre- and Post-treatment with Cyclosporine a in a Rat Model of Transient Focal Cerebral Ischaemia with Multimodal MRI Screening

Abstract

We conclude that intracarotid cyclosporine A is effective in reducing infarct size when given prior to ischaemia, but not when administered at reperfusion.

Neuroprotective effects of gallic acid against hypoxia/reoxygenation-induced mitochondrial dysfunctions in vitro and cerebral ischemia/reperfusion injury in vivo

“…CsA is a specific MPTP inhibitor, which is thought to limit reperfusion injury by antagonizing MPTP opening and inhibiting mitochondrial (type II) apoptosis (Cho et al, 2013;Muramatsu et al, 2007). In the current study, we did not find any significant charge in ΔA 540 value between the CsA pretreatment group and the control group.…”

“…7A; B, n¼8, P40.05). Of note CsA is thought to be an inhibitor of the MPTP, and pretreatment with CsA 10 mg/kg decreases infarct volume after cerebral ischemia/reperfusion injury (Cho et al, 2013;Muramatsu et al, 2007). In the present study, compared to the MCAO group, an intravenous injection of CsA 10 mg/kg significantly reduced the total infarct volume (% of contralateral hemisphere) to 26.4273.03% ( Fig.…”

“…In response to opening of MPTP, MMP is dissipated and the death effector proteins such as Cytochrome C (Cyt C) are released from the inter-membrane space, which initiate mitochondrial (type II) apoptosis (Gómez-Crisóstomo et al, 2013). In addition, the neuroprotective effect of ischemic post-conditioning or treatment with cyclosporin A (CsA) in cerebral ischemia/reperfusion injury contributes to inhibition of MPTP opening (Cho et al, 2013;Siesjo et al, 1999;Sun et al, 2012). However, as an immunosuppressant drug, the serious adverse reaction of the immune system limits its clinical application (Rezzani, 2006).…”

Myocardial Conditioning

“…20,[25][26][27][28] Moreover, the endogenous protection afforded by postconditioning is not limited to heart and can be applied to treat global or regional ischemia-reperfusion injury in other organs or tissues. [29][30][31][32] Our current focus is, however, specifically on patients with ST-segment-elevation myocardial infarction (STEMI; ie, the population in which most of the clinical evidence has been obtained with respect to postconditioning).…”

Cyclosporine A, a Potential Therapy of Ischemic Reperfusion Injury. A Common History for Heart and Brain

“…CsA, apart from its immunosuppressive activity, inhibits PTP opening and reduces infarct size in animal models of cerebral ischemia [33][34][35][36][37][38][39][40][41][42][43][44] . The neuroprotective effect appears to depend on several factors, including the route of administration (intravenous (IV), intra-cerebral, ischemic preconditioning (IP) intra peritonea, intracarotid, subcutaneous, intracerebro ventricular), the dosage of CsA, the duration of ischemia, the timing of administration with respect to the onset of ischemia and of reperfusion, the nature of the ischemic model (transient middle cerebral artery occlusion (MCAO) or permanent MCAO, blood-brain barrier (BBB) permeability) and finally the association with other drugs.…”