Title:Curcumin Alleviates Oxidative Stress, Neuroinflammation, and Promotes
Behavioral Recovery After Traumatic Brain Injury
Volume: 20
Issue: 1
Author(s): Bing Chen, Quan-xing Shi, Chuang Nie, Zhi-ping Zhao, Tao Wang, Qiang Zhou*Jianwen Gu*
Affiliation:
- Clinical laboratory, The Second Hospital of Anhui Medical University, Anhui, China
- Department of Neurosurgery,
People’s Liberation Army Strategic Support Force Medical Center, Beijing, China
Keywords:
Traumatic brain injury, curcumin, inflammation, oxidative stress, neuroprotective effect, cognitive dysfunction.
Abstract:
Background: Neuroinflammation and oxidative stress after traumatic brain injury (TBI)
can further lead to neuronal apoptosis, which plays a crucial role in the process of neuron death.
Curcumin, which is derived from the rhizome of the Curcuma longa plant, has multiple pharmacological
effects.
Objective: The objective of this study was to investigate whether curcumin treatment has neuroprotective
effects after TBI, and to elucidate the underlying mechanism.
Methods: A total of 124 mice were randomly divided into 4 groups: Sham group, TBI group,
TBI+Vehicle group, and TBI+Curcumin group. The TBI mice model used in this study was constructed
with TBI device induced by compressed gas, and 50 mg/kg curcumin was injected intraperitoneally
15 minutes after TBI. Then, the blood-brain barrier permeability, cerebral edema, oxidative
stress, inflammation, apoptosis-related protein, and behavioral tests of neurological function
were utilized to evaluate the protective effect of curcumin after TBI.
Results: Curcumin treatment markedly alleviated post-trauma cerebral edema and blood-brain
barrier integrity, and suppressed neuronal apoptosis, reduced mitochondrial injury and the expression
of apoptosis-related proteins. Moreover, curcumin also attenuates TBI-induced inflammatory
response and oxidative stress in brain tissue and improves cognitive dysfunction after TBI.
Conclusion: These data provide substantial evidence that curcumin has neuroprotective effects in
animal TBI models, possibly through the inhibition of inflammatory response and oxidative stress.