Objective: This study was designed to investigate preoperative anxiety situations and postoperative pain degree in Chinese patients undergoing laparoscopic hysterectomy and to analyze the related factors of preoperative anxiety and the correlation between preoperative anxiety and postoperative pain to provide a reference for effective postoperative analgesia management.Methods: A total of 100 female patients undergoing laparoscopic hysterectomy were enrolled in this study and randomly divided into two groups (n = 50, each). In group A, the patients were treated with dexmedetomidine and sufentanil for postoperative analgesia. In group B, the patients were treated with sufentanil alone for postoperative analgesia. All patients were evaluated with a self-rating anxiety scale (SAS) 1 day before the operation. The patients’ pain was evaluated using the numerical rating scale (NRS) 1 day after the operation, and data were recorded.Results: In these 100 patients, the highest preoperative SAS score was 48, and the average score was 40.99 ± 4.55 points, which is higher than the norm in China. There were significant differences in preoperative SAS scores among patients with different occupations and previous surgical experience (P < 0.05). There was no significant difference in SAS scores among patients with different education levels (P > 0.05). The postoperative NRS score of group A was significantly higher than that of group B, and the difference was statistically significant (P < 0.05). The correlation coefficients between SAS scores and NRS scores in groups A and B were 0.836 and 0.870, respectively, presenting with a significantly positive correlation.Conclusion: Preoperative anxiety is an important predictor of postoperative pain. Patients undergoing laparoscopic hysterectomy have preoperative anxiety. The degree of anxiety is influenced by the occupation and previous operation experience of the patients, and patients with higher preoperative anxiety have greater postoperative pain. In addition, we should not neglect the management of postoperative pain because of the small trauma of laparoscopic surgery, and dexmedetomidine combined with sufentanil can improve the postoperative analgesic effect.

The aim of the present study was to determine the roles of the chemotactic factor, chemokine ligand 2 (CCL2), and its receptor, chemokine receptor type 2 (CCR2), in the hippocampus of rats with cerebral ischemia/reperfusion injury. In total, 24 Sprague-Dawley rats, weighting 250–300 g, were randomly divided into three groups (n=8): Sham-operated (C group), cerebral ischemia/reperfusion injury (I/R group) and propofol-intervention (P group) groups. The rats were sacrificed at 6 h after the ischemia/reperfusion surgery, and the brains were obtained to isolate the hippocampus. The mRNA expression levels of CCL2 and CCR2 in the hippocampus were analyzed by quantitative polymerase chain reaction, while the protein expression levels of CCL2 and CCR2 were determined by western blot analysis. The expression levels of CCL2 and CCR2 in the procerebrum were markedly elevated in the I/R and P groups at 6 h after the ischemia/reperfusion surgery when compared with the C group (P<0.05). In addition, the mRNA expression levels of CCL2 and CCR2 decreased significantly in the P group as compared with that in the I/R group (P<0.05). Therefore, CCL2 and CCR2 may be involved in the mechanisms underlying cerebral ischemia/reperfusion injury, and propofol may protect the brain through regulating the expression of CCL2 and CCR2.

Diabetic neuropathy (DNP) is the most common complication of diabetes mellitus affecting approximately 50% of diabetes patients. Studying the effect of potential drugs with antioxidant properties and minimal toxicities on neural cells may lead to the development of new and safe pharmacotherapy. Dexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, is a clinically used sedative also known to have neural protection effect. In the present study, we aimed to investigate the protective role of DEX in high glucose (HG)-induced neural injury and its potential miRNA-related mechanisms. Our results showed that DEX exerted neuroprotective effects during high glucose-induced damage to PC12 cells in a dose-dependent manner. DEX restored cell viability and repressed LDH, Caspase-3 activity, ROS production, and cell apoptosis in HG-treated PC12 cells. MiR-125b-5p was significantly up-regulated in PC12 cells upon HG treatment and it was demonstrated as an target for DEX. The neuroprotective effects of DEX on HG-induced cellular injury were reversed through miR-125b-5p overexpression, and vitamin D receptor (VDR) is a direct targeted of the miR-125b-5p. Together, our results indicate that DEX displays neuroprotective effects on PC-12 cells under high glucose through regulating miR-125b-5p/VDR axis. Our findings might raise the possibility of potential therapeutic application of DEX for managing diabetic neuropathy neural injuries.

No abstract