Expression of the NLRP3 Inflammasome in Cerebral Cortex After Traumatic Brain Injury in a Rat Model

Inflammatory response plays an important role in the pathogenesis of secondary damage after traumatic brain injury (TBI). The inflammasome is a multiprotein complex involved in innate immunity and a number of studies have suggested that the inflammasome plays a critical role in a host inflammatory s...

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Bibliographic Details
Published in:Neurochemical research 2013-10, Vol.38 (10), p.2072-2083
Main Authors: Liu, Huan-Dong, Li, Wei, Chen, Zhen-Rui, Hu, Yang-Chun, Zhang, Ding-Ding, Shen, Wei, Zhou, Meng-Liang, Zhu, Lin, Hang, Chun-Hua
Format: Article
Language:English
Subjects:
Animals
Apoptosis Regulatory Proteins
Biochemistry
Biomedical and Life Sciences
Biomedicine
Brain Injuries - immunology
Brain Injuries - metabolism
CARD Signaling Adaptor Proteins
Carrier Proteins
Caspase 1 - metabolism
Cell Biology
Cerebral Cortex - metabolism
Cytoskeletal Proteins - biosynthesis
Immunity, Innate
Inflammasomes - biosynthesis
Inflammation - immunology
Inflammation - metabolism
Interleukin-18 - physiology
Interleukin-1beta - physiology
Neurochemistry
Neurology
Neurosciences
NLR Family, Pyrin Domain-Containing 3 Protein
Original Paper
Rats
Rats, Sprague-Dawley
Receptors, Cytoplasmic and Nuclear - biosynthesis
Receptors, Cytoplasmic and Nuclear - physiology
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Summary:Inflammatory response plays an important role in the pathogenesis of secondary damage after traumatic brain injury (TBI). The inflammasome is a multiprotein complex involved in innate immunity and a number of studies have suggested that the inflammasome plays a critical role in a host inflammatory signaling. Nucleotide-binding domain, leucine-rich repeat, pyrin domain containing 3 (NLRP3) is a key component of the NLRP3-inflammasome, which also includes apoptotic speck-containing protein (ASC) with a cysteine protease (caspase) -activating recruitment domain and pro-caspase1. Activation of the NLRP3-inflammasome causes the processing and release of the interleukin 1 beta (IL-1β) and interleukin 18 (IL-18). Based on this, we hypothesized that the NLRP3-inflammasome could participate in the inflammatory response following TBI. However, the expression of NLRP3-inflammasome in cerebral cortex after TBI is not well known. Rats were randomly divided into control, sham and TBI groups (including 6 h, 1 day, 3 day and 7 day sub-group). TBI model was induced, and animals were sacrificed at each time point respectively. The expression of NLRP3-inflammasome was measured by quantitative real-time polymerase chain reaction, western blot and immunohistochemistry respectively. Immunofluorescent double labeling was performed to identify the cell types of NLRP3-inflammasome’s expression. Moreover, enzyme linked immunosorbent assay was used to detect the alterations of IL-1β and IL-18 at each time point post-injury. The results showed that, TBI could induce assembly of NLRP3-inflammasome complex, increased expression of ASC, activation of caspase1, and processing of IL-1β and IL-18. These results suggested that NLRP3-inflammasome might play an important role in the inflammation induced by TBI and could be a target for TBI therapy.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-013-1115-z