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
Medicineauthors
Li SJ,Zhang YF,Ma SH,Yi Y,Yu HY,Pei L,Feng Ddoi
10.1097/MD.0000000000011861subject
Has Abstractpub_date
2018-08-01 00:00:00pages
e11861issue
33eissn
0025-7974issn
1536-5964pii
00005792-201808170-00031journal_volume
97pub_type
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