TY - JOUR
T1 - Curcumin attenuates vascular inflammation and cerebral vasospasm after subarachnoid hemorrhage in mice
AU - Wakade, Chandramohan
AU - King, Melanie D.
AU - Laird, Melissa D.
AU - Alleyne, Cargill H.
AU - Dhandapani, Krishnan M.
PY - 2009/1/1
Y1 - 2009/1/1
N2 - Cerebral vasospasm is a major cause of death and disability after subarachnoid hemorrhage (SAH); however, clinical therapies to limit the development of cerebral vasospasm are lacking. Although the causative factors underlying the development of cerebral vasospasm are poorly understood, oxidative stress contributes to disease progression. In the present study, curcumin (150 or 300 mg/kg) protected against the development of cerebral vasospasm and limited secondary cerebral infarction after SAH in mice. The protective effect of curcumin was associated with a significant attenuation of inflammatory gene expression and lipid peroxidation within the cerebral cortex and the middle cerebral artery. Despite the ability of curcumin to limit the development of cerebral vasospasm and secondary infarction, behavioral outcome was not improved, indicating a dissociation between cerebral vasospasm and neurologic outcome. Together, these data indicate a novel role for curcumin as a possible adjunct therapy after SAH, both to prevent the development of cerebral vasospasm and to reduce oxidative brain injury after secondary infarction.
AB - Cerebral vasospasm is a major cause of death and disability after subarachnoid hemorrhage (SAH); however, clinical therapies to limit the development of cerebral vasospasm are lacking. Although the causative factors underlying the development of cerebral vasospasm are poorly understood, oxidative stress contributes to disease progression. In the present study, curcumin (150 or 300 mg/kg) protected against the development of cerebral vasospasm and limited secondary cerebral infarction after SAH in mice. The protective effect of curcumin was associated with a significant attenuation of inflammatory gene expression and lipid peroxidation within the cerebral cortex and the middle cerebral artery. Despite the ability of curcumin to limit the development of cerebral vasospasm and secondary infarction, behavioral outcome was not improved, indicating a dissociation between cerebral vasospasm and neurologic outcome. Together, these data indicate a novel role for curcumin as a possible adjunct therapy after SAH, both to prevent the development of cerebral vasospasm and to reduce oxidative brain injury after secondary infarction.
UR - http://www.scopus.com/inward/record.url?scp=55249104098&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=55249104098&partnerID=8YFLogxK
U2 - 10.1089/ars.2008.2056
DO - 10.1089/ars.2008.2056
M3 - Article
C2 - 18752423
AN - SCOPUS:55249104098
SN - 1523-0864
VL - 11
SP - 35
EP - 45
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
IS - 1
ER -