Intra-cerebral hemorrhage (ICH) is a particularly severe type of stroke accounting for 10–15 % of all strokes and is associated with a mortality rate of 30–50%. Neuroinflammation contributes to ICH-induced secondary brain injury and understanding the mechanisms causing neuroinflammation can be helpful to find new treatments of ICH. Recent studies demonstrated that toll like receptor 2 (TLR2) forms a heterodimer with TLR4 mediated ICH-induced inflammatory injury and the Hemoglobin released following an intracerebral bleed, triggers the formation of TLR2/TLR4 heterodimer through the myeloid differentiation primary response gene 88 (MyD88). Sparstolonin B (SsnB), a novel bioactive compound obtained from a Chinese herb Sparganium stoloniferum is believed as an anti-inflammatory compound that can suppress the inflammatory responses of macrophages to ligands for TLR2 and TLR4. SsnB has also been shown to block signaling pathways following TLR2 and TLR4 activation. It has been suggested that SsnB may be an antagonist to TLR2 and TLR4. But its effect on formation of the TLR2/TLR4 heterodimer remains still unclear. We hypothesize that SsnB would block TLR2/TLR4 heterodimer formation. So the administration of SsnB can interfere with the assembly of the TLR2/TLR4 heterodimer and may be a potential therapeutic approach in the treatment of ICH.

Ischemic stroke accounts for about 87 percent of all cases. It occurs as a result of an obstruction within a vessel of the brain and sudden loss of blood circulation to the corresponding area resulting in the loss of brain function. It is caused by thrombotic or embolic occlusion of an artery and is more common than hemorrhagic stroke. We know that most of the injuries after an acute ischemic stroke are due to thrombosis formation and the following neuroinflammation (thromboinflammation). So by blocking this pathway we can ameliorate the injuries and the infarct size and improve the brain function after an acute stroke. Platelet von willebrand factor (VWF) is a glycoprotein involved in hemostasis. It is released from the platelet alpha granules and binds to glycoprotein IIb/IIIa complex which forms a bridge between the sub endothelial surface and the platelet and promotes thrombosis formation. On the basis of this information, we hypothesize that we can alleviate the injuries of acute ischemic stroke by blocking the glycoprotein IIb/IIIa complex via a specific antagonist antibody and so preventing thrombosis formation. It can be a potential therapeutic approach in the treatment of acute ischemic stroke.