4.7 Article

Neuroprotection against cerebral ischemia/reperfusion by dietary phytochemical extracts from Tibetan turnip (Brassica rapa L.)

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 265, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113410

Keywords

Brassica rapa L.; PI3K/AkT/mTOR; Neuroprotection; Cerebral ischemia/reperfusion

Funding

  1. National Key Research and Development Program of China [2017YFC1601704]
  2. National Natural Science Foundation of China [21603087]
  3. Science and Technology Support Plan of Jiangsu Province [BE2018316]
  4. National First-class Discipline Program of Food Science and Technology [JUFSTR2018030]

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The study aimed to investigate the neuroprotective effect of the aqueous extract of turnip on cerebral ischemia/reperfusion. The results showed that the extract can reduce cerebral infarct volume, improve behavioral deficits in MCAO/R mice, and exhibit antioxidant effects in HT-22 cells, while enhancing cell survival by activating the PI3K/Akt/mTOR pathway in OGD/R-injured cells.
Ethnopharmacological relevance: The Tibetan turnip (Brassica rapa L.) has a wide array of medicine properties including heat-clearing, detoxifying and anti-hypoxia as listed in the famous centuries-old Tibetan medicine classic The Four Medical Tantras. Evidence-based medicine also indicated the anti-hypoxic effect of turnips, suggesting a potential link to neuroprotective effect on ischemic stroke. This thereby enables turnips to serve as a novel nontoxic agent in related treatment. Aim of the study: This study aimed to investigate the neuroprotective effect and elucidate the mechanism of aqueous extract of turnip (AET) on cerebral ischemia/reperfusion. Materials and methods: The experimental models of cerebral ischemia included transient middle cerebral artery occlusion/reperfusion (MCAO) in C57BL/6J mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in HT-22 cells. Long-term effect of AET on infarct volume was evaluated by microtubule-associated protein 2 (MAP2) immunofluorescence 28 days after MCAO, and on neurofunctional outcomes determined by rotarod, grid walking, and cylinder tests in the meantime. Efficacy of AET was determined by the cell viability, the release of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) in neurons. The underlying mechanism of AET rescued OGD/R cells were characterized by PI3K, Akt and mTOR expressions, which were further used to validate AET's role in the pathway. Results: AET can reduce cerebral infarct volume and ameliorate behavioral deficits of MCAO/R mice dose-dependently. In vitro experiment further demonstrated that suitable concentrations of AET inhibited ROS, LDH production and restored mitochondrial expression induced by OGD/R. AET pretreatment can reverse the OGD/R-induced decreased level of phosphorylation of PI3K, Akt, mTOR, whereas this effect was blocked in the LY294002 (PI3K inhibitor) treatment group. Conclusions: AET improved the survival of OGD/R-injured HT-22 cells by activating the PI3K/Akt/mTOR pathway. Based on the results above, aqueous extract of turnip has a protective effect on focal cerebral ischemic injury.

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