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Pioglitazone ameliorates neuronal damage after traumatic brain injury via the PPARγ/NF-κB/IL-6 signaling pathway by Yongbing Deng; Xue Jiang; Xiaoyan Deng; Hong Chen; Jie Xu; Zhaosi Zhang; Geli Liu; Zhu Yong; Chengfu Yuan; Xiaochuan Sun; Changdong Wang is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Traumatic brain injury (TBI) is the major cause of high mortality and disability rates worldwide. Pioglitazone is an activator of peroxisome proliferator-activated receptor-gamma (PPARγ) that can reduce inflammation following TBI. Clinically, neuroinflammation after TBI lacks effective treatment. Although there are many studies on PPARγ in TBI animals, only few could be converted into clinical, since TBI mechanisms in humans and animals are not completely consistent. The present study, provided a potential theoretical basis and therapeutic target for neuroinflammation treatment after TBI. First, we detected interleukin-6 (IL-6), nitric oxide (NO) and Caspase-3 in TBI clinical specimens, confirming a presence of a high expression of inflammatory factors. Western blot (WB), quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) were used to detect PPARγ, IL-6, and p-NF-κB to identify the mechanisms of neuroinflammation. Then, in the rat TBI model, neurobehavioral and cerebral edema levels were investigated after intervention with pioglitazone (PPARγ activator) or T0070907 (PPARγ inhibitor), and PPARγ, IL-6 and p-NF-κB were detected again by qRT-PCR, WB and immunofluoresc

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Author

Yongbing Deng; Xue Jiang; Xiaoyan Deng; Hong Chen; Jie Xu; Zhaosi Zhang; Geli Liu; Zhu Yong; Chengfu Yuan; Xiaochuan Sun; Changdong Wang

Publisher

Elsevier BV

Published

2019

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)