Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury

The peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone inhibits NF-κB expression and endogenous neural stem cell differentiation into neurons and reduces the inflammatory cascade after spinal cord injury (SCI). The aim of this study was to explore the mechanisms underlyi...

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Main Authors: Qing-qi Meng, Wei Lei, Hao Chen, Zhen-cheng Feng, Li-qiong Hu, Xing-liang Zhang, Siming Li
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2018/3897478
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author Qing-qi Meng
Wei Lei
Hao Chen
Zhen-cheng Feng
Li-qiong Hu
Xing-liang Zhang
Siming Li
author_facet Qing-qi Meng
Wei Lei
Hao Chen
Zhen-cheng Feng
Li-qiong Hu
Xing-liang Zhang
Siming Li
author_sort Qing-qi Meng
collection DOAJ
description The peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone inhibits NF-κB expression and endogenous neural stem cell differentiation into neurons and reduces the inflammatory cascade after spinal cord injury (SCI). The aim of this study was to explore the mechanisms underlying rosiglitazone-mediated neuroprotective effects and regulation of the balance between the inflammatory cascade and generation of endogenous spinal cord neurons by using a spinal cord-derived neural stem cell culture system as well as SD rat SCI model. Activation of PPAR-γ could promote neural stem cell proliferation and inhibit PKA expression and neuronal formation in vitro. In the SD rat SCI model, the rosiglitazone + forskolin group showed better locomotor recovery compared to the rosiglitazone and forskolin groups. MAP2 expression was higher in the rosiglitazone + forskolin group than in the rosiglitazone group, NF-κB expression was lower in the rosiglitazone + forskolin group than in the forskolin group, and NeuN expression was higher in the rosiglitazone + forskolin group than in the forskolin group. PPAR-γ activation likely inhibits NF-κB, thereby reducing the inflammatory cascade, and PKA activation likely promotes neuronal cell regeneration.
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institution Kabale University
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language English
publishDate 2018-01-01
publisher Wiley
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series PPAR Research
spelling doaj-art-9689a1cba8734170827b684debeb77682025-02-03T05:51:56ZengWileyPPAR Research1687-47571687-47652018-01-01201810.1155/2018/38974783897478Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord InjuryQing-qi Meng0Wei Lei1Hao Chen2Zhen-cheng Feng3Li-qiong Hu4Xing-liang Zhang5Siming Li6Department of Orthopedics, Guangzhou Red Cross Hospital, Jinan University, 396 Tongfu Road, Guangzhou 510120, ChinaLaboratory Research Center, Guangdong Medical University, Zhanjiang 524001, ChinaDepartment of Gastroenterology, Guangdong General Hospital and Guangdong Academy of Medical Sciences, Guangzhou 51000, ChinaDepartment of Orthopedics, Guangzhou Red Cross Hospital, Jinan University, 396 Tongfu Road, Guangzhou 510120, ChinaDepartment of Orthopedics, Guangzhou Red Cross Hospital, Jinan University, 396 Tongfu Road, Guangzhou 510120, ChinaLaboratory Research Center, Guangdong Medical University, Zhanjiang 524001, ChinaDepartment of Orthopedics, Guangzhou Red Cross Hospital, Jinan University, 396 Tongfu Road, Guangzhou 510120, ChinaThe peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist rosiglitazone inhibits NF-κB expression and endogenous neural stem cell differentiation into neurons and reduces the inflammatory cascade after spinal cord injury (SCI). The aim of this study was to explore the mechanisms underlying rosiglitazone-mediated neuroprotective effects and regulation of the balance between the inflammatory cascade and generation of endogenous spinal cord neurons by using a spinal cord-derived neural stem cell culture system as well as SD rat SCI model. Activation of PPAR-γ could promote neural stem cell proliferation and inhibit PKA expression and neuronal formation in vitro. In the SD rat SCI model, the rosiglitazone + forskolin group showed better locomotor recovery compared to the rosiglitazone and forskolin groups. MAP2 expression was higher in the rosiglitazone + forskolin group than in the rosiglitazone group, NF-κB expression was lower in the rosiglitazone + forskolin group than in the forskolin group, and NeuN expression was higher in the rosiglitazone + forskolin group than in the forskolin group. PPAR-γ activation likely inhibits NF-κB, thereby reducing the inflammatory cascade, and PKA activation likely promotes neuronal cell regeneration.http://dx.doi.org/10.1155/2018/3897478
spellingShingle Qing-qi Meng
Wei Lei
Hao Chen
Zhen-cheng Feng
Li-qiong Hu
Xing-liang Zhang
Siming Li
Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
PPAR Research
title Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
title_full Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
title_fullStr Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
title_full_unstemmed Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
title_short Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury
title_sort combined rosiglitazone and forskolin have neuroprotective effects in sd rats after spinal cord injury
url http://dx.doi.org/10.1155/2018/3897478
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