AIM:To investigate how the stearoyl-CoA desaturase-1(SCD1)inhibitor CAY-10566 induc-es ferroptosis in oral squamous cell carcinoma(OS-CC)cells and enhances their sensitivity to cisplatin,with preliminary exploration of the underlying mo-lecular mechanisms.METHODS:Bioinformatics analysis and clinical specimens were used to evalu-ate SCD1 expression in OSCC tissues.OSCC cell lines(Cal27 and HSC3)were treated with CAY-10566,cis-platin,the ferroptosis inhibitor Ferrostatin-1(Fer-1),or their combinations.Cell viability was assessed using the CCK-8 assay,while reactive oxygen spe-cies(ROS)and lipid ROS levels were measured by flow cytometry.Malondialdehyde(MDA)and re-duced glutathione(GSH)levels were quantified us-ing commercial assay kits.Western blotting was performed to analyze the protein expression of glu-tathione peroxidase 4(GPX4),mechanistic target of rapamycin(mTOR),mature sterol regulatory ele-ment-binding protein 1(m-SREBP1),SCD1,and heme oxygenase 1(HMOX1).RESULTS:SCD1 was significantly overexpressed in OSCC tissues(P＜0.01).Combined treatment with CAY-10566 and cis-platin markedly reduced OSCC cell viability(P＜0.01)and increased lipid peroxidation(P＜0.001),while suppressing GPX4 expression-effects that were re-versed by Fer-1(P＜0.001).CAY-10566 upregulated HMOX1 expression and inhibited mTOR,m-SREBP1,and SCD1 protein levels(P＜0.001).CONCLUSION:CAY-10566 promotes ferroptosis and cisplatin sensi-tivity in OSCC cells,potentially through HMOX1 up-regulation and suppression of the mTOR/SREBP1/SCD1 axis.

AIM:To investigate how the stearoyl-CoA desaturase-1(SCD1)inhibitor CAY-10566 induc-es ferroptosis in oral squamous cell carcinoma(OS-CC)cells and enhances their sensitivity to cisplatin,with preliminary exploration of the underlying mo-lecular mechanisms.METHODS:Bioinformatics analysis and clinical specimens were used to evalu-ate SCD1 expression in OSCC tissues.OSCC cell lines(Cal27 and HSC3)were treated with CAY-10566,cis-platin,the ferroptosis inhibitor Ferrostatin-1(Fer-1),or their combinations.Cell viability was assessed using the CCK-8 assay,while reactive oxygen spe-cies(ROS)and lipid ROS levels were measured by flow cytometry.Malondialdehyde(MDA)and re-duced glutathione(GSH)levels were quantified us-ing commercial assay kits.Western blotting was performed to analyze the protein expression of glu-tathione peroxidase 4(GPX4),mechanistic target of rapamycin(mTOR),mature sterol regulatory ele-ment-binding protein 1(m-SREBP1),SCD1,and heme oxygenase 1(HMOX1).RESULTS:SCD1 was significantly overexpressed in OSCC tissues(P＜0.01).Combined treatment with CAY-10566 and cis-platin markedly reduced OSCC cell viability(P＜0.01)and increased lipid peroxidation(P＜0.001),while suppressing GPX4 expression-effects that were re-versed by Fer-1(P＜0.001).CAY-10566 upregulated HMOX1 expression and inhibited mTOR,m-SREBP1,and SCD1 protein levels(P＜0.001).CONCLUSION:CAY-10566 promotes ferroptosis and cisplatin sensi-tivity in OSCC cells,potentially through HMOX1 up-regulation and suppression of the mTOR/SREBP1/SCD1 axis.

Objective:To investigate the inflammatory state and immune function of patients experiencing acute exacerbation of chronic obstructive pulmonary disease complicated by hypercapnia before and after noninvasive mechanical ventilation.Methods:The clinical data of 120 patients experiencing acute exacerbation of chronic obstructive pulmonary disease complicated by hypercapnia who received treatment in Taizhou Central Hospital from August 2018 to August 2019 were retrospectively analyzed. According to different treatment methods, they were divided into a noninvasive ventilation group ( n = 57) and a conventional treatment group ( n = 63). The therapeutic effect was observed in each group. Before and after treatment, serum levels of inflammatory factors (tumor necrosis factor-α, interleukin-6, C-reactive protein), immune indexes (CD 4+, CD 8+, CD 4+/CD 8+), blood gas analysis indexes (PaCO 2, PaO 2, pH) and pulmonary function indexes (forced expiratory volume in 1 second, forced vital capacity, peak expiratory flow) were measured in each group. Adverse reactions such as sputum obstruction and gastric distension during treatment were statistically analyzed. Results:Total effective rate in the noninvasive ventilation group was significantly higher than that in the conventional treatment group ( P < 0.05). After treatment, serum levels of tumor necrosis factor-α, interleukin-6, C-reactive protein were (61.98 ± 5.16) ng/L, (19.77 ± 3.41) ng/L, (15.39 ± 3.22) mg/L respectively in the noninvasive ventilation group, which were significantly lower than those in the conventional treatment group [(68.24 ± 5.12) ng/L, (21.04 ± 3.52) ng/L, (19.28 ± 3.50) mg/L, t = 6.664, 2.003, 6.314, all P < 0.05]. After treatment, CD 4+ and CD 4+/CD 8+ were (29.28 ± 2.81) and (1.18 ± 0.17) respectively in the non-invasive ventilation group, which were significantly higher than (27.34 ± 2.96) and (1.09 ± 0.15) in the conventional treatment group ( t = 3.672, 3.081, both P < 0.05). After treatment, PaCO 2 [(48.34 ± 6.92) mmHg] in the noninvasive ventilation group was lower than that in the conventional treatment group [(53.09 ± 7.07) mmHg, t = 3.712, P < 0.05]. PaO 2, pH, forced expiratory volume in 1 second, forced vital capacity and peak expiratory flow were (70.61 ± 9.82) mmHg, (7.35 ± 0.15), (2.39 ± 0.48) L, (2.50 ± 0.46) L, (4.65 ± 0.75) L/s, respectively in the non-invasive ventilation group, which were significantly higher than those in the conventional treatment group [(65.19 ± 8.23) mmHg, (7.29 ± 0.14), (2.16 ± 0.47) L, (2.21 ± 0.45) L, (4.06 ± 0.69) L/s, t = 3.287, 2.266, 2.650, 3.488, 4.488, all P < 0.05]. There was no significant difference in the incidence of adverse reactions between the two groups ( P > 0.05). Conclusion:Noninvasive mechanical ventilation for patients experiencing acute exacerbation of chronic obstructive pulmonary disease complicated by hypercapnia can improve the inflammatory state and immune function, enhance lung function and reduce the degree of hypoxia.