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Updated: Mar 26, 2026
Partial Sciatic Nerve Ligation: A Mouse Model of Chronic Neuropathic Pain to Study the Antinociceptive Effect of Novel Therapies
Published on: October 6, 2022
MiR-155 modulates the progression of neuropathic pain through targeting SGK3
Shaoxing Liu1, Bo Zhu1, Yan Sun1
1Department of Anesthesiology, Chengdu Hospital Affiliated to Zunyi Medical College and Chengdu Second People's Hospital Chengdu 610017, China.
Abstract:
This study aimed to illustrate the potential effects of miR-155 in neuropathic pain and its potential mechanism. Spragure-Dawley (SD) rats were used for neuropathic pain model of bilateral chronic constriction injury (bCCI) construction. Effects of miR-155 expression on pain threshold of mechanical stimuli (MWT), paw withdrawal threshold latency (PMTL) and cold threshold were analyzed. Target for miR-155 was analyzed using bioinformatics methods. Moreover, effects of miR-155 target gene expression on pain thresholds were also assessed. Compared with the controls and sham group, miR-155 was overexpressed in neuropathic pain rats (P<0.05), but miR-155 slicing could significantly decreased the pain thresholds (P<0.05). Serum and glucocorticoid regulated protein kinase 3 (SGK3) was predicted as the target gene for miR-155, and miR-155 expression was negatively correlated to SGK3 expression. Furthermore, SGK3 overexpression could significantly decreased the pain thresholds which was the same as miR-155 (P<0.05). Moreover, miR-155 slicing and SGK3 overexpression could significantly decrease the painthreshold. The data presented in this study suggested that miR-155 slicing could excellently alleviate neuropathic pain in rats through targeting SGK3 expression. miR-155 may be a potential therapeutic target for neuropathic pain treatment.
Insights
MicroRNA-155 (miR-155) slicing alleviates neuropathic pain in rats by targeting SGK3. This suggests miR-155 may be a novel therapeutic target for treating neuropathic pain.
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Neuropathic pain is a debilitating condition with limited treatment options.
- MicroRNAs (miRNAs) play crucial roles in regulating gene expression and are implicated in pain pathways.
- miR-155 has emerged as a potential regulator in various biological processes, including inflammation and cell signaling.
Purpose of the Study:
- To investigate the role of miR-155 in the development and progression of neuropathic pain.
- To elucidate the underlying molecular mechanism of miR-155 in neuropathic pain.
- To evaluate miR-155 as a potential therapeutic target for neuropathic pain.
Main Methods:
- A rat model of neuropathic pain was established using bilateral chronic constriction injury (bCCI).
- miR-155 expression levels were quantified in pain model rats.
- Bioinformatics analysis was employed to predict miR-155 targets.
- The effects of miR-155 and its target gene on pain thresholds were assessed.
Main Results:
- miR-155 was significantly overexpressed in rats with neuropathic pain.
- miR-155 inhibition (slicing) markedly reduced pain thresholds.
- Serum and glucocorticoid regulated protein kinase 3 (SGK3) was identified as a direct target of miR-155.
- SGK3 overexpression mimicked the analgesic effect of miR-155 inhibition, reducing pain thresholds.
Conclusions:
- miR-155 plays a critical role in the pathogenesis of neuropathic pain.
- miR-155 alleviates neuropathic pain by downregulating SGK3 expression.
- Targeting miR-155 presents a promising therapeutic strategy for neuropathic pain management.
