Objectives: This study aims to investigate the clinical effect of dexmedetomidine (DEX) combined with low concentrations of ropivacaine in ultrasound-guided continuous fem­oral nerve block for postoperative analgesia in elderly patients with total knee arthroplasty (TKA). Materials and Methods: Patients were divided into three groups: group C, group D1, and group D2. For postoperative analgesia, patients in group C were given 0.15% ropivacaine, patients in group D1 were given 0.15% ropivacaine + 0.02 μg × kg–1 × h–1 DEX, and patients in group D2 were given 0.15% ropivacaine + 0.05 μg × kg–1 × h–1 DEX. The visual analogue scores in the resting state, active state (AVAS), and passive functional exercise state (PVAS), degree of joint bending, and Ramsay scores were recorded. Results: The Ramsay scores were significantly higher, AVAS scores were significantly lower, PVAS scores were significantly decreased, the degree of joint bending was significantly higher, and the time to the first postoperative ambulation was shorter in groups D1 and D2 than group C. Furthermore, the time to the first postoperative ambulation was shorter in group D2 than in group D1, patients in groups D1 and D2 were more satisfied than patients in group C, and patients in group D2 were more satisfied than patients in group D1. Conclusion: The protocol of 0.05 μg × kg–1 × h–1 of DEX combined with 0.15% ro­pivacaine in ultrasound-guided continuous femoral nerve block for postoperative analgesia in elderly patients with TKA provides a better analgesic effect than without DEX performance.

Background Kidney ischemia–reperfusion injury is a common pathophysiological phenomenon in the clinic. A large number of studies have found that the tyrosine protein kinase/signal transducer and activator of transcription (JAK/STAT) pathway is involved in the development of a variety of kidney diseases and renal protection associated with multiple drugs. Edaravone (EDA) is an effective free radical scavenger that has been used clinically for the treatment of postischemic neuronal injury. This study aimed to identify whether EDA improved kidney function in rats with ischemia–reperfusion injury by regulating the JAK/STAT pathway and clarify the underlying mechanism. Methods Histomorphological analysis was used to assess pathological kidney injury, and mitochondrial damage was observed by transmission electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to detect tubular epithelial cell apoptosis. The expression of JAK2, P-JAK2, STAT3, P-STAT3, STAT1, P-STAT1, BAX and Bcl-2 was assessed by western blotting. Mitochondrial function in the kidney was assessed by mitochondrial membrane potential (ΔΨm) measurement. Results The results showed that EDA inhibited the expression of p-JAK2, p-STAT3 and p-STAT1, accompanied by downregulation of the expression of Bax and caspase-3, and significantly ameliorated kidney damage caused by ischemia–reperfusion injury (IRI). Furthermore, the JC-1 dye assay showed that edaravone attenuated ischemia–reperfusion-induced loss of kidney ΔΨm. Conclusion Our findings indicate that EDA protects against kidney damage caused by ischemia–reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.

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Our previous studies have shown that electroacupuncture (EA) enhances neurobehavioral functional recovery after ischemic stroke, however, the underlying regulatory mechanisms remain unclear. MicroRNAs (miRNAs) are abundant in the brain and are involved in post-transcriptional gene regulation. During cerebral ischemia reperfusion, miRNAs perform numerous biological functions in the central nervous system related to regeneration and repair of damaged nerves. Our previous studies also have shown that the expression of miRNA-132 (miR-132) is obviously down-regulated after stroke by middle cerebral artery occlusion (MCAO), which can be up-regulated by EA. This study aimed to identify whether up-regulation of miR-132 by EA improved the damaged nerves after stroke and to screen the potential target of miR-132. The results showed that EA up-regulated miR-132 thus suppressing SOX2 expression in vivo after MCAO, which obviously ameliorated neurobehavioral functional recovery. Moreover, our results also suggested that up-regulated miR-132 suppressed SOX2 in primary neurons after oxygen-glucose deprivation (OGD), which promoted neurite outgrowth. In conclusion, EA enhances neurobehavioral functional recovery against ischemic stroke through targeting of SOX2-mediated axonal regeneration by miR-132.