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Background: To observe the effects of triptolide (TP) on the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of glioma cells, and to explore the possible mechanisms of phenotypic changes in EMT.Methods: The U87 and U251 glioma cell lines were treated TP. The Cell Counting Kit-8 (CCK-8) method was used to detect the half-maximal inhibitory concentration (IC 50 ) of TP in these two cell lines and the inhibition of cell proliferation at the IC 50 concentration. The wound-healing experiment and Transwell invasion assay were used to detect the cells' migration and invasion abilities, respectively. Using western blot protocol, the expression levels of the EMT markers were analyzed, and the levels of the autophagy markers were also detected. The pEGFP-C2-LC3B plasmid was transfected into glioma cells, and the effect of TP on autophagy was detected by immunofluorescence. A subcutaneous tumor model in nude mice was established to observe the effect of TP on cell proliferation in vivo, and immunohistochemistry (IHC) was used to detect the expression levels of EMT markers in mouse tumor tissues.Results: TP significantly inhibited the proliferation of U87 and U251 cells in a dose-and time-dependent manner. TP had a significant inhibitory effect on the migration and invasion of U87 and U251 cells. Western blot showed that TP reversed the process of EMT in glioma cells, which was evidenced by the upregulated expression of the epithelial marker E-cadherin, and the downregulated expression of the mesenchymal markers N-cadherin, Vimentin, ZEB1, Snail, and Slug. TP increased autophagy in glioma cells, increased the LC3B II/I ratio, and upregulated Beclin-1 and Atg-7 expression. Immunofluorescence showed that the number of autophagosomes increased significantly after TP was applied to cells. In the nude mouse subcutaneous tumor model, experiments revealed an inhibitory effect of TP on glioma cell proliferation in vivo. IHC confirmed that the expression of E-cadherin was upregulated in mouse tumor tissues, while the expression levels of N-Cadherin and Vimentin were downregulated.Conclusions: TP can inhibit glioma cell proliferation, migration, and invasion, and reverse EMT progression. The possible mechanism of EMT reversal in glioma cells is that TP induces autophagy.

Objective The treatment experience and the technical skill with percutaneous balloon compression (PBC) for treatment of primary trigeminal neuralgia (TN) were summarised in a single institution. Methods This is a retrospective review including consecutive patients with typical symptoms of uni-lateral primary TN who underwent PBC from June 2020 to September 2021 in our institution. We excluded secondary aetiologies of TN. Patient demographics, surgical techniques and outcomes were reviewed. All included patients were initially managed with carbamazepine before PBC. Results A total of 70 patients were included. The mean length of follow-up was 10.6 months. Sixty-nine (98.6%) were successfully treated, and only one patient failed due to particularly narrow foramen ovale. Amongst successfully treated patients, 68 (97.1%) had immediate pain relief, with one having delayed relief. Sixty-eight patients (97.1%) had immediate facial numbness post-operatively and one (1.4%) presented delayed numbness 7 days after surgery. In the last follow-up, regarding facial numbness, 22 (31.9%) patients had complete resolution, whilst 46 (67.6%) had different degrees of benefit. Forty-nine (71.0%) patients developed masseter muscle weakness with recovery at 3-month follow-up. No anaesthesia dolorosa, keratitis, intracranial infection or death occurred in this study. Conclusion PBC for treatment of TN has quick and effective result, and could be safely performed under general anaesthesia without discomfort to the patient. The common postoperative complications are facial numbness and masseter muscle weakness, with most being improved or recovered at follow-up.