Fig. 2. GA prevents HDFs from UV-B induced Oxidative stress (ROS) mediated ER stress response. UV-B -irradiation to HDFs induces immediate as well as secondary ROS in 3, 6, & 24 h post UV-B -irradiation, which is significantly quenched by GA pre-treatment to HDFs in an intensity dependent manner,(Fig. 2A & 2B), (*#p<0.001 as compared to UV-B treated), depicting its role as strong antioxidant. UV-B -irradiation up-regulates the anti-oxidant defence protein SOD1 and down-regulates the Catalase post-UV-B -irradiation whereas GA maintains the anti-oxidant balance in HDFs in both 6 & 24 Hr post UV-B -irradiation (Fig. 2C & 2D). UV-B -irradiation to HDFs induces ER stress response in 6 & 24 h post UV-B -irradiation whereas GA pre-treatment significantly relieves HDFs from oxidative stress-mediated manifestation of ER stress, (Fig. 2C, 2D & 2E), (*^#p<0.001, **p<0.01 as compared to UV-B treated alone). Thapsigargin (1µg/ml) was used as a positive control for comparative analysis of intracellular Calcium changes.