Surgery-induced acute postoperative pain and stress response can lead to prolonged convalescence. The present study was designed to investigate the effects of intraoperative dexmedetomidine on postoperative analgesia and recovery following abdominal hysterectomy surgeries. Sixty-four patients scheduled for abdominal hysterectomy under general anesthesia were divided into two groups that were maintained using propofol/remifentanil/dexmedetomidine (PRD) or propofol/remifentanil/saline (PRS). During surgery, patients in the PRD group had a lower bispectral index (BIS) value, which indicated a deeper anesthetic state, and a higher sedation score immediately after extubation than patients in the PRS group. During the first 24 hours post-surgery, PRD patients consumed less morphine with patient-controlled analgesia (PCA) and had lower scores on a visual analogue scale (VAS) than their controls from the PRS group. The global 40-item quality of recovery questionnaire and 9-question fatigue severity score both showed higher recovery scores from day 3 after surgery in the PRD group. with the data are considered together, intraoperative administration of dexmedetomidine appeared to promote the analgesic properties of morphine-based PCA and to expedite recovery following surgery in patients undergoing abdominal hysterectomy.

Surgery-induced acute postoperative pain and stress response may lead to prolonged convalescence. The present study was designed to investigate the effects of intraoperative dexmedetomidine on postoperative analgesia and recovery after abdominal colectomy surgeries.Sixty-seven patients scheduled for abdominal colectomy under general anesthesia were divided into two groups, which were maintained using propofol/remifentanil/dexmedetomidine (PRD) or propofol/remifentanil/saline (PRS).During surgery, patients in the PRD group had a lower bispectral index value, which indicated a deeper anesthetic state and a higher sedation score right after extubation, than patients in the PRS group. During the first 24 hours after surgery, PRD patients consumed less morphine in patient-controlled analgesia, and had a lower score in visual analog scale, than their controls from the PRS group. The global 40-item quality of recovery questionnaire and 9-question fatigue severity score both showed a higher recovery score from day 3 after surgery in the PRD group.Intraoperative administration of dexmedetomidine seems to promote the analgesic property of morphine-based patient-controlled analgesia, and speed recovery from surgery in patients after abdominal colectomy.

Emerging evidence has suggested that microRNAs play a critical role in neuropathic pain development. However, the biological role of miRNAs in regulating neuropathic pain remains barely known. In our present study, we found that miR‐124‐3p was significantly downregulated in rats after chronic sciatic nerve injury (CCI). In addition, it was showed that overexpression of miR‐124‐3p obviously repressed mechanical allodynia and heat hyperalgesia. Meanwhile, it has been reported that neuroinflammation can contribute a lot to neuropathic pain progression. Here, we found that inflammatory cytokine (IL‐6, IL‐1β, and TNF‐⍺) protein expression in rats after CCI greatly increased and miR‐124‐3p mimics depressed inflammation cytokine levels. Consistently, miR‐124‐3p alleviated inflammation production in lipopolysaccharide‐incubated spinal microglial cells. Bioinformatics analysis revealed that EZH2 acted as a direct target of miR‐124‐3p, which participated in the miR‐124‐3p‐modulated effects on neuropathic pain development and neuroinflammation. We observed that miR‐124‐3p was able to promote neuroinflammation and neuropathic pain through targeting EZH2. The direct correlation between them was validated in our current study using dual‐luciferase reporter assays. Subsequently, it was manifested that EZH2 abrogated the inhibitory role of miR‐124‐3p on neuropathic pain progression in CCI rats. Taken these together, our findings highlighted a novel contribution of miR‐124‐3p to neuropathic pain and indicated the possibilities for developing novel therapeutic options for neuropathic pain.

No abstract

Surgery-induced acute postoperative pain may lead to prolonged convalescence. The present study was designed to investigate the effects of intraoperative dexmedetomidine on postoperative analgesia following abdominal colectomy surgeries. Eighty patients scheduled for abdominal colectomy surgery under general anesthesia were divided into 2 groups, which were maintained using propofol/remifentanil/dexmedetomidine (PRD) or propofol/remifentanil/saline (PRS). During surgery, patients in the PRD group had a lower bispectral index (BIS) value, which indicated a deeper anesthetic state, and a higher sedation score right after extubation than patients in the PRS group. During the first 24 hours post surgery, PRD patients consumed less morphine in patient-controlled analgesia (PCA) and had a lower score in the visual analog scale (VAS) testing than their controls from the PRS group. Intraoperative administration of dexmedetomidine appears to promote the analgesic property of morphine-based PCA in patients after abdominal colectomy.

Supplemental Digital Content is available in the text

BackgroundThe aim of this study was to investigate the protective effect of β-casomorphin-7 (β-CM-7) and its possible mechanisms on acute kidney injury (AKI).Material/MethodsRats were randomly divided into a sham group, a cecal ligation and puncture (CLP) group, and a CLP+β-CM-7 group. Kidney index, kidney function, and histopathology changes were assessed. The expression of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (Kim-1), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα), and p-IκBα in kidney tissues were detected by Western blotting. Inflammatory and oxidative stress factors were detected by ELISA kits.ResultsThe results showed that treatment with β-CM-7 reduced the levels of creatinine (Cre), blood urea nitrogen (BUN), NGAL, and Kim-1 induced by CLP, weakening the pathological damage. In the CLP + β-CM-7 group, the tumor necrosis factor-α (TNF-α) level and the DNA-binding activity of NF-κB p65 were significantly reduced and the interleukin-10 (IL-10) level was significantly increased compared with the CLP group. b-CM-7 decreased the expression of p-IκBα/IκBα. In addition, β-CM-7 increased the activity of superoxide dismutase (SOD) and decreased the level of malondialdehyde (MDA) in kidney tissue.Conclusionsβ-CM-7 attenuated sepsis-induced AKI through reducing inflammation and oxidative stress and by inhibition of nuclear factor (NF)-κB activities. This study provides a new therapeutic agent for attenuating sepsis-induced kidney injury.

Neuropathic pain, resulting from somatosensory nervous system dysfunction, remains a serious public health problem worldwide. microRNAs are involved in the physiological processes of neuropathic pain. However, the biological roles of miR-98 in neuropathic pain development have not been investigated. Therefore, in our current study, we focused on the effects of miR-98 in neuropathic pain. It was shown that miR-98 was significantly downregulated in chronic sciatic nerve injury (CCI) rat models. In addition, high mobility group A2 (HMGA2) was obviously upregulated in CCI rats. Overexpression of miR-98 inhibited neuropathic pain progression, including mechanical and thermal hyperalgesia. By a bioinformatics analysis, HMGA2 was predicted as a direct target of miR-98. The negative correlation between miR-98 and HMGA2 was validated in our present study. Furthermore, overexpression of miR-98 dramatically repressed HMGA2 protein and messenger RNA (mRNA) expression. Neuroinflammation participates in neural-immune interactions, which can contribute to the neuropathic pain development. Meanwhile, we found that inflammatory cytokine (interleukin [IL]-6, IL-1β, and COX-2) protein expression in rats infected with LV-miR-98 was greatly suppressed. Taking these results together, we concluded that miR-98 might depress neuropathic pain development through modulating HMGA2. K E Y W O R D S high mobility group A2 (HMGA2), miR-98, neuropathic pain Zhang and Su have contributed equally to this work. How to cite this article: Zhang Y, Su Z, An L-J, et al. miR-98 acts as an inhibitor in chronic constriction injury-induced neuropathic pain via downregulation of high-mobility group AT-hook 2.