Abstract:
:Many studies have reported that lutein may exert its biological activities, including anti‑inflammation, anti‑oxidase and anti‑apoptosis, through effects on reactive oxygen species (ROS). Thus, lutein may prevent the damaging activities of ROS in cells. The current study investigated the effect of lutein against severe traumatic brain injury (STBI) and examined the mechanism of this protective effect. Sprague‑Dawley rats were randomly divided into 5 groups: Control group, STBI model group, 40 mg/kg lutein‑treated group, 80 mg/kg lutein‑treated group and 160 mg/kg lutein‑treated group. In this study, lutein protects against STBI, suppressed, interleukin (IL)‑1β, IL‑6 and monocyte chemoattractant protein‑1 expression, reduced serum ROS levels, and reduced superoxide dismutase and glutathione peroxidase activities in STBI rats. Treatment with lutein effectively downregulated the expression of NF‑κB p65 and cyclooxygenase‑2, intercellular adhesion molecule (ICAM)‑1 protein, and upregulated nuclear factor erythroid 2 like 2 (Nrf‑2) and endothelin‑1 protein levels in STBI rats. These findings demonstrated that lutein protects against STBI, has anti‑inflammation and antioxidative effects and alters ICAM‑1/Nrf‑2 expression, which may be a novel therapeutic for STBI the clinic.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Tan D,Yu X,Chen M,Chen J,Xu Jdoi
10.3892/mmr.2017.7040subject
Has Abstractpub_date
2017-10-01 00:00:00pages
4235-4240issue
4eissn
1791-2997issn
1791-3004journal_volume
16pub_type
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