The UVC was sent via an isopore plastic filter to generate local DNA injury areas and the CPD were found with microscopy and immunofluorescent staining. the mechanisms whereby NG displays its antiapoptotic result independent of p53. The protective effect of several naturally occurring botanicals, including flavonoids, against various apoptotic inducers and UV induced damage has previously been demonstrated. Lee et Dasatinib structure al. has reported that 3,4 dihydroxy flavone protects HaCaT cells from etoposide induced apoptosis through different mechanisms, including caspase pathway. Recently, the flavonoid eriodictyol was shown to apply antiapoptotic effect in HaCaT cell line and normal human keratinocyte exposed to UV light and the effect was proposed to arise through modulation of caspase route and attenuation of ROS generation. Maalouf et al. has reported the protective effect of vitamin E against UVB induced injury in keratinocytes. Now, delphinidin, an important anthocyanidin contained in many pigmented fruits and vegetables, is reported to protect HaCaT cells and mouse skin against UVB caused damage and apoptosis. The view that UVB induced apoptosis occurs through the intrinsic pathway is suggested to be due Mitochondrion to the ability of Bcl2 household proteins to inhibit the apoptosis following UV irradiation. Improved Bax/Bcl2 Icotinib ratio contributes to the release of cytochrome c from mitochondria, and therefore the initiation of caspase activation. In our study, we noticed that UVB induced alteration in Bax/Bcl2 percentage was modulated upon NG therapy. The UVBirradiated cells treated with NG kept the normal level of Bcl2 expression and displayed a gradual decline in the level of proapoptotic protein Bax. This modulation is relative to the inhibitory effect of NG on caspase activation. Besides apoptotic process, normal cell cycle can be damaged upon experience of DNA damaging agents. Arrest at these phases allows time for DNA repair or initiation of cell death. 6, the lower dose of UVB irradiation caused a G/ M charge using a slight change in S phase populace in HaCaT cells. The absence of S phase arrest is possibly caused by the mutation of p53 in HaCaT cells.