Wang Chun-Bo, Ding Bo-Xiao, Guo Shen-Bo, Wang Yu-Zhen, Han Yan-Tao, Wang Yue-Jun
Department of Pharmacology, Medical College, Qingdao University, Qingdao 266021, China.
Acta Pharmacol Sin. 2003 Jul;24(7):692-6.
To study the effect of polypeptide from Chlamys farreri (PCF) on mitochondria of human dermal fibroblasts irradiated by ultraviolet B (UVB) in vitro.
Malondialdehyde (MDA) and antioxidant enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were determined by biochemical methods. Mitochondrial transmembrane potential was measured by flow cytometry. Ultrastructure of fibroblasts was observed with transmission electron microscope.
UVB (1.176 x 10(-4) J/cm(2)) induced mitochondria damage in dermal fibroblast and PCF (0.25%-1%) reduced the damage in a concentration-dependent manner. Furthermore, PCF also concentration-dependently maintained the stability of mitochondrial transmembrane potential. PCF was able to reduce the MDA formation caused by UVB, meanwhile increased the activities of SOD and GSH-PX. The differences among the PCF groups and UVB model group were significant (P<0.05, P<0.01).
The UVB-induced mitochondria damage was alleviated by PCF in human dermal fibroblasts.
体外研究栉孔扇贝多肽(PCF)对紫外线B(UVB)照射后人皮肤成纤维细胞线粒体的影响。
采用生化方法测定丙二醛(MDA)以及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)等抗氧化酶。通过流式细胞术测量线粒体跨膜电位。用透射电子显微镜观察成纤维细胞的超微结构。
UVB(1.176×10⁻⁴ J/cm²)诱导皮肤成纤维细胞线粒体损伤,PCF(0.25% - 1%)以浓度依赖方式减轻损伤。此外,PCF还以浓度依赖方式维持线粒体跨膜电位的稳定性。PCF能够减少UVB引起的MDA形成,同时提高SOD和GSH-PX的活性。PCF组与UVB模型组之间的差异具有统计学意义(P<0.05,P<0.01)。
PCF减轻了UVB诱导的人皮肤成纤维细胞线粒体损伤。