Abstract: Aim to explore the schisandrin B (SchB) on the long wave ultraviolet (UVA) induced permanent resident human keratinocytes (HaCat) injury and its possi-ble mechanism. Irradiated with UVA HaCat 5Jcm2, treated with different concentrations of SchB (0.0001umol/L 0.001 umol/L 0.01 umol/L 0.1 umol/L) treatment after UVA damage of HaCat cells, the detection cell superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, lactate dehydrogenase (LDH) and nitric oxide (ON) content. After HaCat cell was irradiated by UVA, the result of which reduced the SOD, GSH-Px activity, increased LDH and ON content, treated with different concentrations of SchB , which could increase significantly the SOD, GSH-Px activity, decrease LDH , to improve the survival rate HaCat cells, especially with the protection of the 0.001 umol/L SchB do with strongest （UVA+0.001umol/L SchB to UVA UVA model group：the cell survival rate:98.39%±3.23% to 77.110%±3.33%. GSH:8.34μmol/L±0.33μmol/L to 2.54μmol/L±0.34μmol/L, SOD:7.79 U/mL±1.22 U/mL to 3.22U/mL±0.15U/mL, LDH: 4.00 U/mL±0.98 U/mL to 7.8U/mL±1.06U/mL, NO: 0.19υmol／L±0.02υmol／L to 0.38υmol±0.03υmol , the above compared between groups p＜0.05） The conclusion is that SchB can be a cert ain extent and reduce the UVA damage of HaCat cells. As the concentration decreased, its protective effect gradually increase, when it is reaching the optimum concentration (0.001 umol/L), the protective effect of reducing mechanism, oxidative damage and inhibition of SchB cells enhance the ability of anti.

Key words: schisandrin B, Ultraviolet, long wave ultraviolet, human keratinocytes