Reduction of lipoxidative load by secretory phospholipase A2 inhibition protects against neurovascular injury following experimental stroke in rat

Abstract

Background: In animal models, ischemia reperfusion (IR) injury triggers membrane lipid degradation and accumulation of lipoxidative exacerbations in neurovascular unit, leading to blood brain barrier (BBB) damage and neurologic deficits. In this study, we investigated whether impeding membrane lipid breakdown by inhibiting secretory phospholipase A2 (sPLA2) activity reduces BBB leakage, leading to neuroprotection and functional recovery.

TTC staining of damaged brain areas after MCA occlusion in the rat does not constrict quantitative gene and protein analyses

“…The literature revealed that results of gene expression analysis in experimental stroke are sometimes difficult to construe. Some reports completely lack information about the origin of the investigated tissue (Liu et al, 2009;Zhang et al, 2009); in other cases the entire cortices were used for analysis (Hoda et al, 2009;Huang et al, 2009).…”

Low Molecular Weight Phospholipases A2 in Mammalian Brain and Neural Cells: Roles in Functions and Dysfunctions

“…Confocal microscopy revealed that GIIA was mainly localized in astrocytes but not in microglia. Further support to the involvement of a sPLA 2 in brain ischemic injury was derived from the observations that inhibitors of this type of enzymes exert a neuroprotective effect [118][119][120].…”

Age-associated neurodegeneration and oxidative damage to lipids, proteins and DNA

“…However, most of the enzymes in the family of phospholipase A2 are rather generators of oxidative stress and lipid peroxidation during prostaglandin synthesis from ArAc, a products of PLA2 reaction than repair of lipid peroxidation (Adibhatla and Hatcher, 2008b). Thus, inhibitors of secretory phospholipase A2 emerged as a potential tool to decrease inflammation and associated lipid peroxidation in addition to well-known inhibitors of cyclooxygenase 2 (COX2) (Hoda et al, 2009).…”