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Gynura procumbens Root Extract Ameliorates Ischemia-Induced Neuronal Damage in the Hippocampal CA1 Region by Reducing Neuroinflammationopen access

Authors
Kim, WoosukJung, Hyo YoungYoo, Dae YoungKwon, Hyun JungHahn, Kyu RiKim, Dae WonYoon, Yeo SungChoi, Soo YoungHwang, In Koo
Issue Date
Jan-2021
Publisher
Multidisciplinary Digital Publishing Institute (MDPI)
Keywords
Gynura procumbens root extract; neuroprotection; pro-inflammatory cytokines; microglia; ischemia
Citation
Nutrients, v.13, no.1
Journal Title
Nutrients
Volume
13
Number
1
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/2112
DOI
10.3390/nu13010181
ISSN
2072-6643
Abstract
Gynura procumbens has been used in Southeast Asia for the treatment of hypertension, hyperglycemia, and skin problems induced by ultraviolet irradiation. Although considerable studies have reported the biological properties of Gynura procumbens root extract (GPE-R), there are no studies on the effects of GPE-R in brain damages, for example following brain ischemia. In the present study, we screened the neuroprotective effects of GPE-R against ischemic damage and neuroinflammation in the hippocampus based on behavioral, morphological, and biological approaches. Gerbils received oral administration of GPE-R (30 and 300 mg/kg) every day for three weeks and 2 h after the last administration, ischemic surgery was done by occlusion of both common carotid arteries for 5 min. Administration of 300 mg/kg GPE-R significantly reduced ischemia-induced locomotor hyperactivity 1 day after ischemia. Significantly more NeuN-positive neurons were observed in the hippocampal CA1 regions of 300 mg/kg GPE-R-treated animals compared to those in the vehicle-treated group 4 days after ischemia. Administration of GPE-R significantly reduced levels of pro-inflammatory cytokines such as interleukin-1 beta, -6, and tumor necrosis factor-alpha 6 h after ischemia/reperfusion. In addition, activated microglia were significantly decreased in the 300 mg/kg GPE-R-treated group four days after ischemia/reperfusion compared to the vehicle-treated group. These results suggest that GPE-R may be one of the possible agents to protect neurons from ischemic damage by reducing inflammatory responses.
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