* Instructor, Department of Anesthesiology, National Defense Medical Center and Tri-Service General Hospital, Taipei, Taiwan, Republic of China, and Visiting Research Scholar, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina. † Assistant Professor and Attending Physician, Department of Anesthesiology, National Defense Medical Center and Tri-Service General Hospital. ‡ Assistant Professor, Department of Clinical Laboratory, En Chu Kong Hospital, Taipei, Taiwan, Republic of China. § Associate Professor and Director, Department of Anesthesiology, National Defense Medical Center and Tri-Service General Hospital. # Professor and Chairman, Department of Anesthesiology, Cathay General Hospital, Taipei, Taiwan, Republic of China. ‖ Professor, Department of Anesthesiology, Duke University Medical Center. ** Assistant Professor and Attending Physician, Department of Neurosurgery, National Defense Medical Center and Tri-Service General Hospital. †† Research Assistant, Department of Anesthesiology, National Defense Medical Center and Tri-Service General Hospital. ‡‡ Associate Professor and Attending Physician, Department of Anesthesiology, National Defense Medical Center and Tri-Service General Hosptial.
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.
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.
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.
Curcumin in multiple doses is effective against glutamate neurotoxicity and oxidative stress and improves the mortality rate in rats with SAH.
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