Neuropathic pain has been reported as a type of chronic pain due to the primary dysfunction of the somatosensory nervous system. It is the most serious types of chronic pain, which can lead to a significant public health burden. But, the understanding of the cellular and molecular pathogenesis of neuropathic pain is barely complete. Long noncoding RNAs (lncRNAs) have recently been regarded as modulators of neuronal functions. Growing studies have indicated lncRNAs can exert crucial roles in the development of neuropathic pain. Therefore, our present study focused on the potential role of the lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) in neuropathic pain progression. Firstly, a chronic constrictive injury (CCI) rat model was built. CRNDE was obviously increased in CCI rats. Interestingly, overexpression of CRNDE enhanced neuropathic pain behaviors. Neuroinflammation was induced by CRNDE and as demonstrated, interleukin-10 (IL-10), IL-1, IL-6, and tumor necrosis factor-α (TNF-α) protein levels in CCI rats were activated by LV-CRNDE. For another, miR-136 was obviously reduced in CCI rats. Previously, it is indicated that miR-136 participates in the spinal cord injury via an inflammation in a rat model. Here, firstly, we verified miR-136 could serve as CRNDE target. Loss of miR-136 triggered neuropathic pain remarkably via the neuroinflammation activation. Additionally, IL6R was indicated as a target of miR-136 and miR-136 regulated its expression. Subsequently, we confirmed that CRNDE could induce interleukin 6 receptor (IL6R) expression positively.Overall, it was implied that CRNDE promoted neuropathic pain progression via modulating miR-136/IL6R axis in CCI rat models.

MicroRNA (miRNA) are emerging as critical regulators of neuropathic pain development. Neuroinflammation contributes to the development of neuropathic pain. miR‑142‑3p has been characterized as an inflammation‑related miRNA in various pathological processes. However, little is known about the role of miR‑142‑3p in neuroinflammation and neuropathic pain. The present study aimed to investigate the function of miR‑142‑3p in neuropathic pain by creating a murine model using spinal nerve ligation (SNL). A significant reduction in miR‑142‑3p expression was observed in the dorsal root ganglion of mice with SNL (P<0.05) compared with control mice. Overexpression of miR‑142‑3p significantly inhibited neuropathic pain and neuroinflammation in mice with SNL (P<0.05). High mobility group box 1 (HMGB1) was identified as a direct target gene of miR‑142‑3p by bioinformatic analysis and dual‑luciferase reporter assays. Overexpression of miR‑142‑3p significantly reduced the mRNA and protein expression levels of HMGB1 in vitro and in vivo (P<0.05). In addition, HMGB1 mRNA expression and miR‑142‑3p expression were inversely correlated in mice with SNL. Furthermore, overexpression of HMGB1 significantly reversed the inhibitory effect of miR‑142‑3p on neuroinflammation and neuropathic pain development (P<0.05). Overall, these results suggest that miR‑142‑3p functions as a negative regulator of neuropathic pain development through the downregulation of HMGB1, indicating that miR‑142‑3p may serve as a potential therapeutic target for neuropathic pain.

Background: Remimazolam tosilate is an ultra-short-acting sedative drug with the advantages of rapid onset, rapid recovery, and mild respiratory and circulatory inhibition. We aim to compare the incidence of hypotension of remimazolam with propofol in patients undergoing painless colonoscopy and explore the stability of remimazolam in circulation. Methods: This is a randomized, double-blind trial. 116 patients with outpatient appointment for painless colonoscopy in our hospital from December 2020 to March 2021 were randomly divided into the remimazolam group and the propofol group. The modified observer’s assessment of alert/sedative (MOAA/S) was used to evaluate the depth of the patient's sedation. The Narcotrend score was monitored throughout the whole process. Taking the incidence of hypotension as the primary outcome indicators, records the incidence of respiratory depression, nausea, vomiting and other adverse events during sedation in the two groups of patients, and record the effective time of anesthesia, awakening time, sedative success rate, etc. to evaluate the effect of remimazolam on circulation. Results：The incidence of hypotension during sedation (13.8%) in the remimazolam group was significantly lower than that in propofol (37.9%), and the success rate of remimazolam (98.3%) was slightly lower than propofol (100.0%), but the awakening time was significantly shorter (P<0.001); The incidence of respiratory inhibition, nausea, vomiting and other adverse events during colonoscopy, remimazolam was significantly lower than that of propofol (P<0.05). Conclusion：Remimazolam tosilate has higher circulatory stability in patients undergoing painless colonoscopy. Trial registration: The trial was registered at the Chinese Clinical Trial Registry (ChiCTR2000040398), data of registration: 28/11/2020.