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Toxicol Appl Pharmacol. 2018 May 1;346:28-36. doi: 10.1016/j.taap.2018.03.020. Epub 2018 Mar 21.

Curcumin plays neuroprotective roles against traumatic brain injury partly via Nrf2 signaling.

Author information

1
Department of Forensic Pathology, China Medical University School of Forensic Medicine, Shenyang 110122, China.
2
Department of Histology and Embryology, College of Basic Medical Sciences, China Medical University, Shenyang 110122, China.
3
Program of Environmental Toxicology, School of Public Health, China Medical Univeristy, Shenyang 110122, China.
4
Department of Forensic Pathology, China Medical University School of Forensic Medicine, Shenyang 110122, China. Electronic address: dwguan@cmu.edu.cn.
5
Department of Forensic Pathology, China Medical University School of Forensic Medicine, Shenyang 110122, China. Electronic address: rzhao@cmu.edu.cn.

Abstract

Traumatic brain injury (TBI), which leads to high mortality and morbidity, is a prominent public health problem worldwide with no effective treatment. Curcumin has been shown to be beneficial for neuroprotection in vivo and in vitro, but the underlying mechanism remains unclear. This study determined whether the neuroprotective role of curcumin in mouse TBI is dependent on the NF-E2-related factor (Nrf2) pathway. The Feeney weight-drop contusion model was used to mimic TBI. Curcumin was administered intraperitoneally 15 min after TBI induction, and brains were collected at 24 h after TBI. The levels of Nrf2 and its downstream genes (Hmox-1, Nqo1, Gclm, and Gclc) were detected by Western blot and qRT-PCR at 24 h after TBI. In addition, edema, oxidative damage, cell apoptosis and inflammatory reactions were evaluated in wild type (WT) and Nrf2-knockout (Nrf2-KO) mice to explore the role of Nrf2 signaling after curcumin treatment. In wild type mice, curcumin treatment resulted in reduced ipsilateral cortex injury, neutrophil infiltration, and microglia activation, improving neuron survival against TBI-induced apoptosis and degeneration. These effects were accompanied by increased expression and nuclear translocation of Nrf2, and enhanced expression of antioxidant enzymes. However, Nrf2 deletion attenuated the neuroprotective effects of curcumin in Nrf2-KO mice after TBI. These findings demonstrated that curcumin effects on TBI are associated with the activation the Nrf2 pathway, providing novel insights into the neuroprotective role of Nrf2 and the potential therapeutic use of curcumin for TBI.

KEYWORDS:

Antioxidant response; Apoptosis; Curcumin; Inflammation; NF-E2-related factor (Nrf2); Traumatic brain injury (TBI)

PMID:
29571711
DOI:
10.1016/j.taap.2018.03.020
[Indexed for MEDLINE]

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