Introduction Ketamine, which is widely used in anesthesia, can induce cortical neurotoxicity in patients. This study aims to investigate the effects of long non-coding RNA LINC00641 on the ketamine-induced neural injury. Materials and Methods In this study, rat pheochromocytoma cells (PC12 cells) were used as a cell model and Sprague–Dawley postnatal day 7 rats were used for experiments in vivo . Ketamine-induced aberrant expression levels of LINC00641, miR-497-5p and brain-derived neurotrophic factor (BDNF) were examined by qRT-PCR. The effects of LINC00641 and miR-497-5p on ketamine-induced neural injury were then examined by MTT assays and TUNEL analysis. In addition, the activity of ROS and caspase-3 was measured. The regulatory relationships between LINC00641 and miR-497-5p, miR-497-5p and BDNF were detected by dual-luciferase reporter assay, respectively. Results Ketamine induced the apoptosis of PC12 cells, accompanied by down-regulation of LINC00641 and BDNF, and up-regulation of miR-497-5p. LINC00641 overexpression enhanced the resistance to the apoptosis of PC12 cells, while transfection of miR-497-5p had opposite effects. Furthermore, LINC00641 could bind to miR-497-5p and reduce its expression, but indirectly increase the BDNF expression, which was considered as a protective factor in neural injury and activated TrkB/PI3K/Akt pathway. Conclusion Collectively, LINC00641/miR-497-5p/BDNF axis was validated to be an important signaling pathway in modulating ketamine-induced neural injury.

Bone pain associated with advanced tumor metastasis is the most severe threat to life quality of patients. Highly efficient and low-toxic therapeutics is of urgent need for this complication. Bone tumor metastasis was established by direct bone inoculation of Walker 256 mammary gland carcinoma cells. Bone nociception was measured by mechanical allodynia, thermal hyperalgesia and spontaneous flinches. P2X7R level was determined by immunoblotting. The inward current was recorded by a patch clamp. The related cytokines were determined by ELISA. Our results showed that teniposide (TN) treatment significantly ameliorated bone nociception associated with tumor inoculation to a comparable extent with P2X7-specific inhibitor, BBG, in rat model. The efficient blockade of inward current generation and pro-inflammatory cytokines secretion were observed upon administration with TN. Our data highlighted the therapeutic potency of TN in this complication associated with tumor metastasis and warrants further clinical investigations.