摘要
Objective @#To investigate the mechanism by which Erastin affects ferroptosis in lung fibroblasts.@*Methods@#Mouse lung fibroblasts (C57/B6⁃L) were treated with varying concentrations of the iron death inducer Erastin, Cell viability was assessed using the cell counting Kit⁃8 (CCK⁃8) assay. Oxidative stress levels were visualize using a fluorescence microscope , and the expression of proteins related to the mitogen⁃activated protein kinase (MAPK) signaling pathway was analyzed using Western blot. Additionally , the p38 and extracellular regulated protein kinase (ERK) inhibitors SB203580 and U0126 were employed to further elucidate the mechanism by which Erastin induces iron death in lung fibroblasts. @*@#At a concentration of 100 μmol/L , Erastin effectively in⁃duced ferroptosis in lung fibroblasts , leading to an upregulation of oxidative stress. Furthermore , the phosphoryla⁃tion levels of p38 and ERK proteins in the MAPK pathway were elevated (P < 0. 05) . The addition of SB203580 and U0126 inhibitors resulted in a significant reduction in oxidative stress levels and a notable increased in cell actiivity in lung fibroblasts (P < 0. 05) . @*@#It can be concluded that Erastin induces ferroptosis in lung fibroblasts , potentially through the mediation of oxidative stress via the MAPK signaling pathway.
摘要
Objective:To evaluate the value of shear wave elastography (SWE) in skin assessment of Systemic sclerosis (SSc).Methods:A total of 58 SSc patients admitted to Peking University Third Hospital from May 2021 to October 2022 and 41 healthy volunteers were included in the study. Skin shear wave elastography (SWE) was performed at 17 sites defined in modified Rodnan skin score (mRSS) measurement, and shear wave velocity values were recorded to evaluate skin hardness. SPSS 22.0 software was used to analyze the skin hardness of SSc patients and healthy controls, and the correlation between skin hardness of SSc patients and clinical data was analyzed. A logistic regression model was constructed to evaluate the diagnostic efficacy of skin hardness at different sites of SSc patients, and to further select the most practical measurement site.Results:The SWE value of SSc patients was significantly higher than that of healthy control group ( P<0.05). There was a positive correlation between SWE and mRSS in the measurement of bilateral fingers, bilateral dorsal hands, bilateral forearms, fore-chest, abdomen, bilateral thighs, and bilateral dorsal feet. Skin stiffness measured by SWE was significantly correlated with SSc disease activity score (EScSG-DAI), ( r=0.71, P<0.001), disease injury score (SCTC-DI), (P=0.55, P=0.005) and functional score (HAQ-DI), ( r=0.46, P=0.003). Reducing the number of measurement sites to 12 (bilateral fingers, bilateral hands, bilateral forearms, bilateral upper arms, forehead, fore-chest, bilateral dorsum of feet) performs as well as all 17 measurement sites simultaneously in assessing disease activity. Conclusion:SWE is a good evaluation tool to reflect the skin lesions of SSc, which is of great value for the diagnosis and evaluation of the disease. We can further standardize the measurement sites and select the most appropriate evaluation strategy, so as to achieve better clinical application.