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小白菊内酯可抑制过氧化氢诱导的人晶状体上皮细胞凋亡。

Hydrogen peroxide-induced apoptosis of human lens epithelial cells is inhibited by parthenolide.

作者信息

Shentu Xing-Chao, Ping Xi-Yuan, Cheng Ya-Lan, Zhang Xin, Tang Ye-Lei, Tang Xia-Jing

机构信息

Eye Center, the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, Zhejiang Province, China.

The Second Affiliated Hospital of Zhejiang University the School of Medicine, Hangzhou 310000, Zhejiang Province, China.

出版信息

Int J Ophthalmol. 2018 Jan 18;11(1):12-17. doi: 10.18240/ijo.2018.01.03. eCollection 2018.

Abstract

AIM

To explore the effect of parthenolide on hydrogen peroxide (HO)-induced apoptosis in human lens epithelial (HLE) cells.

METHODS

The morphology and number of apoptotic HLE cells were assessed using light microscopy and flow cytometry. Cell viability was tested by MTS assay. In addition, the expression of related proteins was measured by Western blot assay.

RESULTS

Apoptosis of HLE cells was induced by 200 µmol/L HO, and the viability of these cells was similar to the half maximal inhibitory concentration (IC50), as examined by MTS assay. In addition, cells were treated with either different concentrations (6.25, 12.5, 25 and 50 µmol/L) of parthenolide along with 200 µmol/L HO or only 50 µmol/L parthenolide or 200 µmol/L HO for 24h. Following treatment with higher concentrations of parthenolide (50 µmol/L), fewer HLE cells underwent HO-induced apoptosis, and cell viability was increased. Further, Western blot assay showed that the parthenolide treatment reduced the expression of caspase-3 and caspase-9, which are considered core apoptotic proteins, and decreased the levels of phosphorylated nuclear factor-κB (NF-κB), ERK1/2 [a member of the mitogen-activated protein kinase (MAPK) family], and Akt proteins in HLE cells.

CONCLUSION

Parthenolide may suppress HO-induced apoptosis in HLE cells by interfering with NF-κB, MAPKs, and Akt signaling.

摘要

目的

探讨小白菊内酯对过氧化氢(H₂O₂)诱导的人晶状体上皮(HLE)细胞凋亡的影响。

方法

采用光学显微镜和流式细胞术评估凋亡HLE细胞的形态和数量。通过MTS法检测细胞活力。此外,采用蛋白质免疫印迹法检测相关蛋白的表达。

结果

200μmol/L H₂O₂可诱导HLE细胞凋亡,MTS法检测显示这些细胞的活力与半数最大抑制浓度(IC50)相似。此外,将细胞分别用不同浓度(6.25、12.5、25和50μmol/L)的小白菊内酯与200μmol/L H₂O₂共同处理,或仅用50μmol/L小白菊内酯或200μmol/L H₂O₂处理24小时。用较高浓度(50μmol/L)的小白菊内酯处理后,发生H₂O₂诱导凋亡的HLE细胞较少,且细胞活力增加。此外,蛋白质免疫印迹法显示,小白菊内酯处理降低了被认为是核心凋亡蛋白的半胱天冬酶-3和半胱天冬酶-9的表达,并降低了HLE细胞中磷酸化核因子-κB(NF-κB)、细胞外调节蛋白激酶1/2[丝裂原活化蛋白激酶(MAPK)家族成员]和Akt蛋白的水平。

结论

小白菊内酯可能通过干扰NF-κB、MAPK和Akt信号传导来抑制H₂O₂诱导的HLE细胞凋亡。

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