Animal models of focal ischaemia induced by middle cerebral artery occlusion 
(MCAO) provide most evidence for cellular inflammatory responses in stroke. 
Permanent MCAO results in a modest neutrophil infiltration at 24 h after 
ischaemia, predominantly around arterial vessels at the margins of infarction, 
whereas MCAO with subsequent reperfusion is associated with substantial 
infiltration by neutrophils throughout the entire infarct. Several studies show 
that C-reactive protein (CRP), an inflammatory marker, is associated with stroke 
outcomes and future vascular events. Several drugs, especially 
hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), have been 
demonstrated to reduce hsCRP levels independently of their effects on plasma 
cholesterol. Various cytokines were shown to be expressed in the injured brain. 
Recent investigations demonstrated that mRNAs of above cytokines were induced in 
the ischemic rat brain. TNF-alpha is a pleiotropic cytokine that mediates key 
roles in many physiological and pathological cellular processes including acute 
and chronic inflammation, programmed cell death or apoptosis, anti-tumor 
responses, and infection. Pharmaceutical industry to search a small molecule TNF 
inhibitor have taken multiple strategies. Significant protection after in vivo 
oral use of SB-239063 from brain injury and neurological deficits was observed 
in one study. In the same study significant protection from brain injury and 
neurological deficits was also demonstrated due to i.v post-stroke treatment 
with the same compound. Leukocyte-endothelial adhesion process consists of 
several steps, beginning with rolling of the leukocyte on the endothelial 
surface until it has slowed down to such a degree that it sticks to the 
endothelium. Treatment with a murine anti-ICAM-1 antibody (enlimomab) has been 
investigated in patients with acute ischemic stroke in the Enlimomab Acute 
Stroke Trial (EAST). Unfortunately, the case fatality rate in this trial was 
significantly higher in the enlimomab patient group than in the placebo group. 
Furthermore, experimental data have shown that focal cerebral ischemia induces a 
time-dependent activation of granulocytes, lymphocytes, and macrophages. 
Dissipation of ATP by CD39 reduced P2X7 receptor stimulation and thereby 
suppressed baseline leukocyte alphaMbeta2-integrin expression. As 
alphaMbeta2-integrin blockade reversed the postischemic, inflammatory phenotype 
of Cd39-/- mice, these data suggest that phosphohydrolytic activity on the 
leukocyte surface suppresses cell-cell interactions that would otherwise promote 
thrombosis or inflammation.