Neuroprotective effect of curcumin in an experimental rat model of subarachnoid hemorrhage.

Published

Journal Article

BACKGROUND: Subarachnoid hemorrhage (SAH) causes a high mortality rate and morbidity. It was suggested that oxidant stress plays an important role in neuronal injury after SAH. Therefore, we assessed the effect of curcumin on reducing cerebral vasospasm and neurologic injury in a SAH model in rat. METHODS: A double-hemorrhage model was used to induce SAH in rats. Groups of animals were treated with intraperitoneal injection of 20 mg/kg curcumin (curcumin group, n = 24) or dimethyl sulfoxide (vehicle group, n = 33), normal saline (SAH group, n = 34) or normal saline (sham group, n = 22), 3 h after SAH induction and daily for 6 days. Glutamate was measured before SAH induction and once daily for 7 days. Glutamate transporter-1, wall thickness and the perimeter of the basilar artery, neurologic scores, neuronal degeneration, malondialdehyde, superoxide dismutase, and catalase activities were assessed. RESULTS: Changes of glutamate levels were lower in the curcumin group versus the SAH and vehicle groups, especially on day 1 (56 folds attenuation vs. vehicle). Correspondingly, glutamate transporter-1 was preserved after SAH in curcumin-treated rats. In the hippocampus and the cortex, malondialdehyde was attenuated (30% and 50%, respectively). Superoxide dismutase (35% and 64%) and catalase (34% and 38%) activities were increased in the curcumin rats compared with the SAH rats. Mortality rate (relative risk: 0.59), wall thickness (30%) and perimeter (31%) of the basilar artery, neuron degeneration scores (39%), and neurologic scores (31%) were improved in curcumin-treated rats. CONCLUSIONS: Curcumin in multiple doses is effective against glutamate neurotoxicity and oxidative stress and improves the mortality rate in rats with SAH.

Full Text

Duke Authors

Cited Authors

  • Kuo, C-P; Lu, C-H; Wen, L-L; Cherng, C-H; Wong, C-S; Borel, CO; Ju, D-T; Chen, C-M; Wu, C-T

Published Date

  • December 2011

Published In

Volume / Issue

  • 115 / 6

Start / End Page

  • 1229 - 1238

PubMed ID

  • 21926905

Pubmed Central ID

  • 21926905

Electronic International Standard Serial Number (EISSN)

  • 1528-1175

Digital Object Identifier (DOI)

  • 10.1097/ALN.0b013e31823306f0

Language

  • eng

Conference Location

  • United States