紫外线致HeP-G2细胞调亡的分子机制初探

紫外线 (UV)是人类最常接触的具基因毒作用的因子。为探索紫外线辐射致细胞凋亡和组织损伤的分子机制 ,本研究采用免疫细胞化学技术与特异性抗体初步探索了经紫外线辐射处理的Hep G2细胞P5 3、Caspase3、bcl 2和P2 1等与细胞凋亡和生长抑制基因的表达情况。结果表明经紫外线辐射处理的Hep G2细胞的P5 3、Caspase3和bcl 2基因表达增加 ,而P2 1未见明显改变 ,提示P5 3、Caspase基因在紫外线辐射诱导的细胞凋亡中起重要作用 ,bcl 2增高可能有抑制细胞的过度凋亡 ,保持内在平衡的作用。P2 1保持不变或下降可能反映了细胞对DNA损伤应答的新途径。

Molecular events associated with cell apoptosis and tissue damage in ducedby ultraviolet radiation in Hep-G2

Ultraviolet radiation(UVR) is the genotoxie agents to induce DNA damage and cell apoptosis. In order to investigated the Molecular events associated with cell apoptosis and tissue damage induced by UVR, We used Immunocytochemistry technique and specific antibodies to measured the expression of p53, p21, bcl--2, and caspase3 in Hep--G2 after UV irradiation. The results indicated the expression of p53 ,caspase 3 and bcl--2 was increased at 4 and 48 h after irradiation, but P2t was kept to unchanged. Moreover, UVR caused an increase in the apoptotic activity. These results suggest Up--regulation of p53, bcl--2 and caspase 3 were involved in the altered balance between survival and apoptosis induced by UVR. It may be associated with novel insight into regulation of p21 protein and its role in the cellular response to DNA damage that p21 protein levels was kept to unchanged or degradation after UVR.