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姜黄素可预防中风并提高Notch细胞内结构域水平。

Curcumin protects against stroke and increases levels of Notch intracellular domain.

作者信息

Liu Shuang, Cao Yungang, Qu Man, Zhang Zheng, Feng Liang, Ye Zusen, Xiao Meijuan, Hou Sheng T, Zheng Rongyuan, Han Zhao

机构信息

a Department of Neurology , The Second Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.

b Department of Neurology , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.

出版信息

Neurol Res. 2016 Jun;38(6):553-9. doi: 10.1080/01616412.2016.1187804.

Abstract

OBJECTIVES

To investigate whether curcumin regulates Notch signaling to cause neuroprotection and neurogenesis after focal ischemia reperfusion injury.

METHOD

Focal ischemia reperfusion injury was modeled in rats by occluding the middle cerebral artery. These animals were given either curcumin (300 mg/kg) or corn oil (vehicle) by intraperitoneal injection starting 1 h after stroke and continuing for 7 d. In parallel, sham-operated control animals received vehicle. All animals were killed on day 12. The different treatment groups were compared in terms of neurobehavioral deficits, BrdU incorporation, and levels of doublecortin (DCX) and Notch intracellular domain (NICD) using immunohistochemistry, immunofluorescence and Western blotting.

RESULTS

Animals treated with curcumin showed significantly smaller neurobehavioral deficits than vehicle-treated animals after 3, 7, and 12 d of reperfusion (all p < 0.05). Tissue sections from curcumin-treated animals contained significantly greater numbers of BrdU-positive cells (p < 0.05) and BrdU/DCX-positive cells (p < 0.01), as well as significantly higher NICD levels (p < 0.01).

CONCLUSION

Curcumin may protect from focal cerebral ischemia reperfusion injury as well as stimulate neurogenesis by activating the Notch signaling pathway.

摘要

目的

研究姜黄素是否通过调节Notch信号通路来在局灶性缺血再灌注损伤后发挥神经保护和神经发生作用。

方法

通过阻断大脑中动脉在大鼠中建立局灶性缺血再灌注损伤模型。这些动物在中风后1小时开始腹腔注射姜黄素(300mg/kg)或玉米油(载体),并持续7天。同时,假手术对照动物接受载体。所有动物在第12天处死。使用免疫组织化学、免疫荧光和蛋白质印迹法比较不同治疗组在神经行为缺陷、BrdU掺入以及双皮质素(DCX)和Notch细胞内结构域(NICD)水平方面的差异。

结果

在再灌注3、7和12天后,接受姜黄素治疗的动物的神经行为缺陷明显小于接受载体治疗的动物(所有p<0.05)。姜黄素治疗动物的组织切片中BrdU阳性细胞(p<0.05)和BrdU/DCX阳性细胞数量明显更多(p<0.01),NICD水平也明显更高(p<0.01)。

结论

姜黄素可能通过激活Notch信号通路对局灶性脑缺血再灌注损伤起到保护作用,并刺激神经发生。

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