The role of NLRP3 inflammasome in stroke and central poststroke pain.

Abstract:

BACKGROUND:NLRP3 inflammasome plays a prominent role in the pathogenesis and progression of many diseases, such as type 2 diabetes mellitus, obesity, atherosclerosis, and Alzheimer's disease. However, little knowledge is known about the role of NLRP3 inflammasome in central post-stroke pain (CPSP). METHODS:We selected relevant studies by searching PubMed, Embase, and Medline from inception through February, 2018. We systematically reviewed available publications according to the terms "NLRP3 inflammasome" and "stroke" or "central post-stroke pain" in the title/abstract field. RESULTS:We reviewed the articles and put forward two possible ways for NLRP3 inflammasome in CPSP. One way is that NLRP3 activation causes cerebral cortex injure, decreasing descending projection fiber to thalamus. Such condition may let GABAergic releases reduce, making the ventral basal (VB) neurons excitability increased. Finally, CPSP occur. Another way is that NLRP3 inflammasome leads to thalamic lesion and strengthens inflammatory response of microglia at the same time. Persistent inflammation causes GABAergic alteration in thalamus reticular neurons (TRN) to restrain VB interneurons functions, contributing to CPSP. CONCLUSIONS:These possible mechanisms will help become knowledgeable about the occurrence CPSP and provide potential therapy for CPSP.

journal_name

Medicine (Baltimore)

journal_title

Medicine

authors

Li SJ,Zhang YF,Ma SH,Yi Y,Yu HY,Pei L,Feng D

doi

10.1097/MD.0000000000011861

subject

Has Abstract

pub_date

2018-08-01 00:00:00

pages

e11861

issue

33

eissn

0025-7974

issn

1536-5964

pii

00005792-201808170-00031

journal_volume

97

pub_type

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