4-hydroxybenzyl aldehyde can prevent the acute cerebral ischemic injury in rats
10.3969/j.issn.1001-1528.2017.08.005
- VernacularTitle:对羟基苯甲醛可预防大鼠急性脑缺血后神经炎症
- Author:
Bin XIANG
;
Chun XIAO
;
Ting SHEN
;
Shi JIANG
;
Qing LIN
;
Xiufang LI
- Keywords:
Gastrodia elata Blume;
4-hydroxybenzyl aldehyde (4-HBAL);
acute cerebral ischemic injury;
neuro-inflammation
- From:
Chinese Traditional Patent Medicine
2017;39(8):1572-1576
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate the anti-neuroinflammation effects of 4-hydroxybenzyl aldehyde (4-HBAL) from Gastrodia elata Blume on acute cerebral ischemic injury in rats and its nechanism of action.METHODS The rat model of acute cerebral ischemic injury was induced by injecting arachidonic acid via intracarotid artery.Brain tissue samples were taken from the animals 3 h after the model of acute cerebral ischemic injury.Tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) were detected in brain tissue to evaluate the effects of 4-HBAL in vivo.Lipopolysaccharid (LPS)-induced activation of BV-2 microglia cells model was used to explore the anti-neuroinflammation mechanism of 4-HBAL.RESULTS The experimental results showed that 4-HBAL had a significant protective effect on acute cerebral ischemic injury.It could significandy decrease the contents of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β),and obviously inhibit the production of nitric oxide (NO),prostaglandin E2 (PGE2) and TNF-α in LPS-stimulated BV-2 cell,and increase the production of interleukin-10 (IL-10) and transforming growth factors-β (TGF-β) in BV-2 cell.CONCLUSION The mechanism of 4-HBAL may be related to the suppression of the excessive activation of microglia after cerebral ischemia and the promotion of the transformation of microglia into anti-inflammatory phenotype.
