Literature DB >> 31267316

Effects of NLRP6 in Cerebral Ischemia/Reperfusion (I/R) Injury in Rats.

Changchang Meng1, Jinyan Zhang2, Luyu Zhang3, Yueting Wang1, Zhenyu Li2, Jing Zhao4.   

Abstract

The NOD-like receptor protein 6 (NLRP6), an intracytoplasmic pattern recognition receptor in the nucleotide-binding domain, leucine-rich repeat-containing (NLR) innate immune receptor family, influences the inflammation reaction. The role of NLRP6 in cerebral ischemia-reperfusion (I/R) injury in rats is unclear. We explore the function of NLRP6 in cerebral I/R injury. The investigators used a middle cerebral artery occlusion/reperfusion model (MCAO) to imitate ischemic injury. We found the peak expression of NLRP6 is in 48-h post-cerebral I/R injury. The expression of NLRP6 siRNA, as well as the expression of protein and mRNA, was detected by Western blot and qRT-PCR. The degree of IL-1β and IL-18 was assessed by ELISA. After downregulating NLRP6, the expression of IL-1β, IL-18, cleaved Caspase-1, and myeloperoxidase (MPO) were reduced. In HE and Nissl staining, pathological injury of brain tissue after downregulating NLRP6 was improved. NLRP6 siRNA decreased the NLRP6-ASC binding states by CO-IP. NRP6 has a pro-inflammatory effect in cerebral I/R injury, which may provide a new target for the treatment of cerebral I/R injury.

Entities:  

Keywords:  Cerebral ischemia/reperfusion injury; IL (interleukin)-18; IL (interleukin)-1β; Inflammation; NLRP6

Mesh:

Substances:

Year:  2019        PMID: 31267316     DOI: 10.1007/s12031-019-01370-4

Source DB:  PubMed          Journal:  J Mol Neurosci        ISSN: 0895-8696            Impact factor:   3.444


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9.  Tetrandrine alleviates cerebral ischemia/reperfusion injury by suppressing NLRP3 inflammasome activation via Sirt-1.

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10.  Role of promoting inflammation of Krüppel-like factor 6 in acute kidney injury.

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