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Neuroprotection by γ-Tocopherol in Lean and Obese Murine Models of Ischemic Stroke

Stock, Katie Lauren
http://rave.ohiolink.edu/etdc/view?acc_num=osu1557134813941474

Abstract Details

2019, Master of Science, Ohio State University, Human Ecology: Human Nutrition.
Background: Ischemic stroke results in brain injury in association with oxidative and nitrative stress. γ-Tocopherol (γ-T), a form of vitamin E, has antioxidative, anti-nitrative, and anti-inflammatory activities that may alleviate stroke-induced brain injury. Objectives/Hypothesis: The objective of this study was to investigate the neuroprotective benefits of prophylactic dietary γ-T supplementation in lean and obese mice subjected to ischemic stroke. It was hypothesized that obesity would exacerbate stroke severity, but that γ-T would protect against brain injury regardless of obesity status. Methods: Male C57BL/6J mice were fed a low-fat (LF) or high-fat (HF) diet supplemented with 0 or 500 mg γ-T/kg diet for 8-wks after which ischemic stroke was induced by 60-min occlusion of the middle cerebral artery. Brain lesion volume, was evaluated by 9.4T MRI at 48-h post-stroke. Locomotor functional tests were performed prior to and 48-h post-stroke to assess motor function loss. Concentrations of γ-T, α-tocopherol (α-T), and their metabolites (α-, γ-carboxyethyl hydrochroman (CEHC)) as well as the nitrated form of γ-T (nitro-γ-T) were measured by LC-MS in the serum, liver, and brain collected 48-h post-stroke. Immunohistochemical studies were conducted to measure cerebral expression of pro-inflammatory enzymes and biomarkers of oxidative/nitrative damage following stroke. Results: γ-T supplementation increased concentrations of γ-T in the circulation, liver tissue and brain tissue with HF-feeding potentiating this accumulation. Despite obesity and γ-T supplementation affecting α-T accumulation in the liver and circulation, neither treatment had an effect on α-T accumulation in the brain. α-CEHC, γ-CEHC, and nitro-γ-T were undetected in the brain. Contrary to the hypothesis, neither HF-feeding nor γ-T supplementation affected stroke-induced brain lesion volume or loss of motor function. γ-T supplementation, though, did reduce cerebral lipid peroxidation that was otherwise attenuated in HF mice. Conclusions: In conclusion, our work shows that γ-T supplementation in HF mice reduces cerebral lipid peroxidation following stroke in a γ-T dependent manner although, this does not result in improved stroke outcome as determined through stroke lesion volume and motor function loss.
Richard Bruno (Advisor)
Cameron Rink (Committee Member)
Tonya Orchard (Committee Member)
127 p.
Nutrition
Gamma-tocopherol, vitamin E, ischemic stroke

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Citations

  • Stock, K. L. (2019). Neuroprotection by γ-Tocopherol in Lean and Obese Murine Models of Ischemic Stroke [Master's thesis, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1557134813941474

    APA Style (7th edition)

  • Stock, Katie. Neuroprotection by γ-Tocopherol in Lean and Obese Murine Models of Ischemic Stroke. 2019. Ohio State University, Master's thesis. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1557134813941474.

    MLA Style (8th edition)

  • Stock, Katie. "Neuroprotection by γ-Tocopherol in Lean and Obese Murine Models of Ischemic Stroke." Master's thesis, Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1557134813941474

    Chicago Manual of Style (17th edition)

osu1557134813941474
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This open access ETD is published by The Ohio State University and OhioLINK.