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

• Published in: Journal of cellular biochemistry Vol. 119; no. 2; pp. 2298 - 2306
• Main Authors: Wang, Yeyang, Li, Wenjun, Wang, Mingsen, Lin, Chuangxin, Li, Guitao, Zhou, Xiaozhong, Luo, Junnan, Jin, Dadi
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.02.2018
• Subjects: Activation; Animals; astrocyte activation; Astrocytes - drug effects; axonal regeneration; Axons; Brain-derived neurotrophic factor; Damage; Disease Models, Animal; Evoked potentials; Glial fibrillary acidic protein; Glial Fibrillary Acidic Protein - metabolism; Immunohistochemistry; Injections, Intraperitoneal; Injuries; JAK2/STAT3 signaling pathway; Janus kinase 2; JNK protein; Locomotion - drug effects; locomotor functional recovery; Motor Activity - drug effects; Motor evoked potentials; Neurological complications; Quercetin; quercetin (Que); Quercetin - administration & dosage; Quercetin - pharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Recovery; Recovery of Function; Regeneration; Rodents; S100 Calcium Binding Protein beta Subunit - metabolism; Signal Transduction - drug effects; Signaling; Somatosensory evoked potentials; Spinal cord injuries; Spinal Cord Injuries - drug therapy; Spinal Cord Injuries - metabolism; Spinal Cord Injuries - physiopathology; spinal cord injury (SCI); Staining; Stat3 protein; Trauma; quercetin (Que); axonal regeneration; locomotor functional recovery; spinal cord injury (SCI); JAK2/STAT3 signaling pathway; astrocyte activation
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.26392

Spinal cord injury (SCI) is lead to locomotor impairment because of neurological damage after following trauma. Quercetin (Que) has been confirmed to 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 three 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) scores at 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. Taken together, Que promoted locomotor functional recovery and astrocyte activation and axonal regeneration after acute SCI, possibly through the BDNF and JAK2/STAT3 signaling pathways.