Objective: Stroke is one of the leading cause of death in Australia and worldwide which induces brain inflammation. Intravenous immunoglobulin (IVIg) is a new therapy, which has the ability to target multiple components of inflammation and has been shown to exert neuroprotection in experimental stroke models. Furthermore, our group has shown that increase in neuronal death following oxygen and glucose deprivation is significantly reduced by IVIg. However, the mechanism by which IVIg directly exerts this protective effect on neurons undergoing cell death remains unknown. This project investigates the direct neuroprotective mechanism of IVIg in stroke experimental models both in vitro and in vivo.
Methods: Trypan blue assay was used to quantify the number of cell death in neuronal culture treated with glucose free Locke’s buffer. Polymerase chain reaction (PCR) was performed to measure cytokine production at mRNA level and immunoblotting was performed to measure level of proteins. Immunohistochemistry was performed on murine brain tissue treated with IVIg after ischaemia reperfusion injury.
Results: The number of cell death was significantly decreased at higher concentration of IVIg compared to the control. Same pattern was also seen in the expression of cleaved caspase-3, p38 MAP kinase and phosphorylated JNK.
Conclusion: In light of the extensive clinical experience with IVIg for other indications, our data may justify prospect of using IVIG as an interventional therapy for stroke.