https://www.selleckchem.com/products/tpca-1.html
Background Pathophysiology of aneurysmal subarachnoid hemorrhage (aSAH) is highly complex. Bleeding from ruptured aneurysm causes increase in intracranial pressure that disrupts blood-brain barrier leading to infiltration of peripheral immune cells. Interactions between the infiltrated leukocytes and the resident brain cells in the injured tissue mainly determine the delayed tissue damage. Recruitment of leukocytes in the injured brain is mainly mediated by the chemokines. Chemokine C-C motif ligand 5 (CCL5) is a potent pro-inflammatory
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