Abstract Title:

Quercetin reduces neural tissue damage and promotes astrocyte activation after spinal cord injury in rats.

Abstract Source:

J Cell Biochem. 2017 Sep 2. Epub 2017 Sep 2. PMID: 28865131

Abstract Author(s):

Yeyang Wang, Wenjun Li, Mingsen Wang, Chuangxin Lin, Guitao Li, Xiaozhong Zhou, Junnan Luo, Dadi Jin

Article Affiliation:

Yeyang Wang


Spinal cord injury (SCI) is lead to locomotor impairment because of neurological damage after following trauma. Quercetin (Que) has been confirmed have a neuro-protective effect during nerve damage processes. The purpose of this study was to determine the roles of Que in functional recovery, cavity formation, astrocyte activation and nerve regeneration following SCI. Sprague-Dawley rats were randomly divided into 3 groups: Sham group, SCI group and Que + SCI group. A rat model of SCI was made at T10 using the modified Allen's method. In the Que + SCI group, animals underwent laminectomy and were then intraperitoneally injected with 20 mg/kg Que for 7 days. Locomotor function was determined with the Basso, Beattie, Bresnahan (BBB) scoresat 1, 3, 5 and 7 days post injury. At 7 days post injury, somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) were recorded. Hematoxylin-Eosin (HE) staining was used to investigate cavity formation. Astrocyte activation was assayed by immunohistochemistry staining with an antibody specific for glial fibrillary acidic protein (GFAP), as well as the expression of GFAP and S100β. Axons were stained using an antibody specific for neurofilament 200 (NF200) and 5-hydroxytryptamine (5-HT). In addition, the protein level of BDNF, p-JNK2 and p-STAT3 was detected using western blot. Que promoted locomotor function and electrophysiological recovery, reduced cavity formation, contributed to astrocyte activation and axonal regeneration after acute SCI. Moreover, Que up-regulated the expression of BDNF, but reduced p-JNK2 and p-STAT3 expression after acute SCI. Taken together,Que promoted locomotor and electrophysiological functional recovery, astrocyte activation and axonal regeneration after acute SCI, possibly through BDNF and JAK2/STAT3 signaling pathways. This article is protected by copyright. All rights reserved.

Study Type : Animal Study

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