Objective:To observe the effect of sorafenib on ferroptosis in thyroid cancer TPC-1 cells, and to provide a new strategy for the treatment of thyroid cancer.Methods:Thyroid cancer TPC-1 cells were cultured in vitro, treated and divided into sorafenib group and negative control group, and cell counting kit-8 (CCK-8) assay was used to detect cell viability; Dichlorofluorescein (DCFH-DA) probe was used to detect reactive oxygen species (ROS) production; Western blotting experiment was used to detect the protein expression levels of ACSL4, SLC7A11 and GPX4; Malondialdehyde (MDA) kit was used to detect the content of MDA in thyroid cancer cells. Analysis of variance was used for the mean comparison between multiple groups, and t-test was used for the comparison between the two groups. Results:The cell absorbance value of sorafenib intervention group (1.29±0.17) was significantly lower than that of control group (1.86±0.23, t=2.695, P<0.05); The fluorescence intensity of ROS in TPC-1 cells treated with sorafenib (1.833±0.293) was significantly higher than that in the control group (0.825±0.186, t=2.801, P<0.05); Western blotting experiments showed that the expression level of ACSl4 protein (0.954±0.091) after sorafenib intervention was higher than that in the control group (0.442±0.132, t=5.314, P<0.05), and the protein expression level of SLC7A11 (0.293±0.087) was significantly lower than that in the control group (0.897±0.098, t=7.916, P<0.05), the protein expression level of GPx4 (0.325±0.051) was also lower than that of control cells (0.893±0.069, t=9.325, P<0.05). The results of MDA detection showed that the expression level of MDA in sorafenib intervention group (30.661±3.192) was significantly higher than that in control group (19.285±1.406, t=5.901, P<0.05). Conclusion:Sorafenib can promote the ferroptosis process of thyroid cancer cells and accelerate the death of thyroid cancer cells.

目的：探讨氨基胍在骨骼肌缺血再灌注肺损伤中的作用机制。方法将24只雄性Wister大鼠随机分为4组（n＝6），Ⅰ组为对照组，Ⅱ组为缺血组，Ⅲ组为缺血再灌注组，Ⅳ组为缺血再灌注＋氨基胍治疗组，检测各组血清中乳酸脱氢酶、NO含量、肺组织中髄过氧化物酶含量及细胞间黏附分子1（ICAM-1）在肺组织中的表达情况。结果ICAM-1表达Ⅰ组不明显，在Ⅱ、Ⅲ组呈上升趋势，Ⅳ组表达下调，其余3组与Ⅰ组比较，差异有统计学意义（P均＜0．05）；Ⅳ组与Ⅲ组比较，差异有统计学意义（ P＜0．05）。与Ⅰ组比较，血清乳酸脱氢酶、NO及肺组织髄过氧化物酶含量Ⅱ、Ⅲ组明显升高（P均＜0．05）；Ⅳ组相应下降，与Ⅲ组比较，差异有统计学意义（P均＜0．05）。结论氨基胍可明显抑制ICAM-1表达上调，降低血清乳酸脱氢酶、NO及肺组织髄过氧化物酶含量，减少肺组织损伤。