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栉孔扇贝多肽保护HaCaT细胞免受UVA加UVB诱导凋亡的分子机制

Molecular mechanisms of polypeptide from Chlamys farreri protecting HaCaT cells from apoptosis induced by UVA plus UVB.

作者信息

Gao Ming-qing, Guo Shen-bo, Chen Xue-hong, Du Wei, Wang Chun-bo

机构信息

Medical College, Qingdao University, Qingdao 266021, China.

出版信息

Acta Pharmacol Sin. 2007 Jul;28(7):1007-14. doi: 10.1111/j.1745-7254.2007.00594.x.

Abstract

AIM

To investigate the mechanism of polypeptide from Chlamys farreri (PCF) protecting HaCaT cells from apoptosis induced by UVA plus UVB in vitro.

METHODS

An apoptotic model of UV irradiation-induced HaCaT cells was established. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay, agarose gel electrophoresis, biochemical methods, and Western blotting were employed in the study.

RESULTS

PCF inhibited the UV irradiation-induced apoptosis of HaCaT cells. PCF strongly reduced the intracellular reactive oxygen species level, enhanced activities of superoxide dismutase and glutathione peroxidase and increased the total anti-oxidative capacity in HaCaT cells following UV irradiation. Furthermore, we found that PCF could inhibit the phosphorylation of c-Jun amino-terminal kinase and the activity of caspase-3 in a concentration-dependent manner.

CONCLUSION

PCF protected HaCaT cells from apoptosis induced by UVA plus UVB, mainly through decreasing the intracellular ROS level and increasing the activities of anti-oxidative enzymes to block the ROS-JNK-caspase-3-apoptosis signaling pathway.

摘要

目的

研究栉孔扇贝多肽(PCF)在体外保护HaCaT细胞免受UVA加UVB诱导凋亡的机制。

方法

建立紫外线照射诱导HaCaT细胞凋亡的模型。本研究采用3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2H-四氮唑溴盐法、琼脂糖凝胶电泳、生化方法和蛋白质免疫印迹法。

结果

PCF抑制紫外线照射诱导的HaCaT细胞凋亡。紫外线照射后,PCF可显著降低HaCaT细胞内活性氧水平,增强超氧化物歧化酶和谷胱甘肽过氧化物酶活性,并提高总抗氧化能力。此外,我们发现PCF能以浓度依赖的方式抑制c-Jun氨基末端激酶的磷酸化和半胱天冬酶-3的活性。

结论

PCF保护HaCaT细胞免受UVA加UVB诱导的凋亡,主要是通过降低细胞内活性氧水平和提高抗氧化酶活性来阻断活性氧-JNK-半胱天冬酶-3-凋亡信号通路。

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