RESUMEN
Objective:To investigate the clinical efficacy of wrist-ankle acupuncture combined with rehabilitation for dysphagia caused by achalasia of the cricopharyngeal muscle after stroke.Methods:Sixty patients with dysphagia caused by achalasia of the cricopharyngeal muscle after stroke who received treatment in Wenzhou Hospital of Traditional Chinese Medicine from June 2019 to March 2020 were included in this study. They were randomly divided into a treatment group and a control group ( n = 30). All patients received routine drug treatment and swallowing rehabilitation training. The control group underwent routine acupuncture treatment. The treatment group received wrist-ankle acupuncture based on routine acupuncture treatment. Both groups were treated for 4 consecutive weeks. The clinical efficacy in the two groups was evaluated using the Video Fluoroscopic Swallowing Study (VFSS), Standardized Swallowing Assessment (SSA), and Swallow Quality-of-Life Questionnaire (SWAL-QOL). Results:Before treatment, there were no significant differences in VFSS, SSA, and SWAL-QOL scores between the two groups. After treatment, VFSS, SSA, and SWAL-QOL scores in the treatment group were (8.21 ± 0.77) points, (21.19 ± 1.42) points, (200.24 ± 11.12) points, and they were (6.01 ± 0.36) points, (23.31 ± 1.45) points, and (182.37 ± 12.06) points in the control group ( t = 3.26, 5.50, 6.31, all P < 0.05). Conclusion:Wrist-ankle acupuncture combined with rehabilitation is an effective treatment method for dysphagia caused by achalasia of the cricopharyngeal muscle after stroke. It can alleviate dysphagia and improve quality of life.
RESUMEN
Objective:To investigate whether the necroptosis pathway receptor interacting protein 1-receptor interacting protein 3-mixed lineage kinase domain-like protein (RIP1-RIP3-MLKL) is involved in fluoride-induced osteoblastic death.Methods:Human osteosarcoma cell line (Saos-2 cells) were cultured in vitro and divided into NC group, sodium fluoride (NaF) groups (5.0, 10.0, 20.0 and 40.0 mg/L NaF), necroptosis inhibitor Necrostatin-1 (Nec-1) group (50.0 μmol/L Nec-1) and NaF + Nec-1 groups (5.0, 10.0, 20.0 and 40.0 mg/L NaF + 50.0 μmol/L Nec-1). After cultured for 24 and 48 h, respectively, cell proliferation was determined via the CCK-8 method, and the activity of lactate dehydrogenase (LDH) was determined by chemical colorimetry. To further analyze the influence of NaF on RIP1-RIP3-MLKL pathway, Saos-2 cells were divided into NCⅡgroup and NaFⅡgroups (2.5, 5.0, 10.0, 20.0 and 40.0 mg/L NaF). After cultured for 24 and 48 h, respectively, the protein expression levels of RIP1, RIP3 and MLKL were determined by Western blotting. Results:The cell proliferation rates (%: 100.00 ± 0.59, 104.90 ± 0.44, 104.16 ± 0.41, 82.45 ± 1.91, 64.59 ± 1.83, 103.56 ± 0.41, 107.18 ± 0.87, 105.35 ± 1.28, 89.63 ± 1.20, 77.51 ± 1.30; 100.00 ± 0.33, 107.92 ± 0.44, 101.78 ± 1.06, 75.45 ± 0.39, 57.94 ± 1.17, 106.74 ± 0.21, 111.85 ± 0.21, 107.82 ± 0.68, 82.34 ± 0.56, 70.19 ± 0.99) among all groups were significantly different at both 24 and 48 h ( F = 77.13, 2 313.43, P < 0.05). Except the cell proliferation rate of the 10.0 mg/L NaF + Nec-1 group that was not significantly different with that of the 10.0 mg/L NaF group at 24 h ( P > 0.05), the cell proliferation rates of other NaF + Nec-1 groups were significantly higher than those of corresponding NaF groups at both 24 and 48 h ( P < 0.05). The proliferation rate was negatively correlated with fluoride concentration ( r24 h = - 0.976, r48 h = - 0.969, P < 0.001). The LDH activity in all concentrations of NaF groups was significantly higher than that in NC group and corresponding NaF + Nec-1 groups at both 24 and 48 h ( P < 0.05). The LDH activity was positively correlated with fluoride concentration ( r24 h = 0.985, r48 h = 0.988, P < 0.001). The protein expression levels of RIP1, RIP3 and MLKL of 5.0 mg/L NaFⅡ group at 24 h, RIP3 of 5.0 mg/L NaFⅡ group at 48 h, and RIP1, RIP3 and MLKL of 10.0, 20.0 and 40.0 mg/L NaFⅡ groups at both 24 and 48 h were higher than that in NCⅡ group ( P < 0.05). The protein expression levels of RIP1, RIP3 and MLKL were positively correlated with fluoride concentration ( r24 h-RIP1 = 0.881, r48 h-RIP1 = 0.952, r24 h-RIP3 = 0.867, r48 h-RIP3 = 0.938, r24 h-MLKL = 0.758, r48 h-MLKL = 0.907, P < 0.001). Conclusion:Fluoride can directly cause necroptosis of osteoblasts through the RIP1-RIP3-MLKL pathway, and the severity of cell damage is closely related to fluoride concentration, Nec-1 has partially reversed the effects of fluoride.