Abstract
The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is the most frequently studied in the central nervous system and has been linked to neuropathic pain. In this study, a post-translational mechanism of microRNA (miR)-186 via regulating the expression of NLRP3 in the complete Freund's adjuvant (CFA)-treated mice was investigated. The injection of CFA was used to induce trigeminal neuropathic pain in mice. miRs microarray chip assay was performed in trigeminal ganglions (TGs). CFA treatment significantly increased the mRNA expression of NLRP3, interleukin (IL)-1β, and IL-18 in TGs compared to the control group. Moreover, 26 miRs were differentially expressed in TGs from trigeminal neuropathic pain mice, and the expression of miR-186 showed the lowest level of all the miRs. Further examination revealed that NLRP3 was a candidate target gene of miR-186. We delivered miR-186 mimics to CFA-treated mice. The head withdrawal thresholds of the CFA-treated mice were significantly increased by miR-186 mimics injection compared with CFA single treatment. The mRNA and protein expression of NLRP3, IL-1β, and IL-18 in TGs from trigeminal neuropathic pain mice were significantly inhibited by miR-186 mimics treatment compared to the CFA group. miR-186 was able to suppress the neuropathic pain via regulating the NLRP3 inflammasome signaling.
Highlights
Neuropathic pain is one of the most intractable nervous system diseases and is characterized by spontaneous pain, allodynia, and hyperalgesia [1,2]
The differentially expressed miRs were further validated by qRT-PCR, and the results indicated that miR-186 and miR-223 were significantly inhibited from 1 h to day 6 in complete Freund’s adjuvant (CFA) injection mice compared to the control group
Our study demonstrated that miR-186 was involved in the regulation of trigeminal neuropathic pain and neuroinflammation in a CFA-induced mice model
Summary
Neuropathic pain is one of the most intractable nervous system diseases and is characterized by spontaneous pain, allodynia, and hyperalgesia [1,2]. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome complex (including NOD-like receptor NLRP3, the adaptor molecule apoptosis-associated speck-like protein containing a caspase-recruitment domain, and the effector molecule procaspase-1) play a critical role in the pathogenesis of neuropathic pain [2,5]. The NLRP3 inflammasome is the most frequently studied in the central nervous system and has been linked to Parkinson’s and Alzheimer’s diseases [6,7]. In the mice spared nerve injury model, the expression of NLRP3 is increased and has a role in acute and chronic pain following peripheral nerve injury [2]
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