Abstract:

Objective To observe the effects of gypenosides （GP） on nuclear factorκB （NF-κB） and p38 mitogen activated protein kinase （p38MAPK） signaling pathways in photodamaged skin of mice, and to explore the mechanisms underlying the protective effects of GP against photodamage. Methods Eighty Balb/C female mice were randomly divided into 8 groups: blank control group receiving no treatment, ultraviolet B （UVB） model group receiving UVB irradiation for 60 seconds, GP groupⅠreceiving topical GP treatment followed by UVB irradiation, GP group Ⅱreceiving UVB irradiation followed by topical GP treatment, VitE groupⅠreceiving topical VitE treatment followed by UVB irradiation, VitE groupⅡreceiving UVB irradiation followed by topical VitE treatment, matrix groupⅠreceiving topical matrix treatment followed by UVB irradiation, matrix groupⅡreceiving UVB irradiation followed by topical matrix treatment. UVB irradiation lasted 60 seconds at one time, and was given once every other day for 7 times to establish a skin model of photodamage. The interval between irradiation and topical treatment was 30 minutes in all the groups except the control group and UVB model group. After the last treatment, mice were sacrificed. Western blot was performed to measure the protein expressions of inhibitor of NF-κB（I-κB）, inhibitor of NF-κB kinase （IKK）, p38MAPK as well as phosphorylated p38MAPK （pp38） in skin tissue from the mice. Results No expressions of I-κB or IKK were observed in the blank control group. The expression level of I-κB was 0.40 ± 0.07 in UVB model group, significantly lower than that in GP group I （1.63 ± 0.85, P < 0.05） and GP group II （0.90 ± 0.40, P < 0.05）, whereas the level of IKK protein was higher in UVB model group than in the GP group I and II （2.01 ± 1.75 vs. 0.23 ± 0.12 and 0.45 ± 0.29, both P < 0.05）. No significant difference was observed in the expression of I-κB or IKK proteins between the GP group I, II , VitE group I and II or in the expression of p38MAPK between the 8 groups. The phosphorylated p38MAPK expression in UVB model group was significantly higher than that in GP group I and II （0.835 ± 0.049 vs. 0.425 ± 0.054 and 0.571 ± 0.090, both P < 0.05）, but similar to that in VitE groups. Conclusions UVB can activate NF-κB and phosphorylated p38MAPK signaling pathways; GP 1.5% cream can inhibit UVB-induced activation of NF-?Objective To observe the effects of gypenosides （GP） on nuclear factorκB （NF-κB） and p38 mitogen activated protein kinase （p38MAPK） signaling pathways in photodamaged skin of mice, and to explore the mechanisms underlying the protective effects of GP against photodamage. Methods Eighty Balb/C female mice were randomly divided into 8 groups: blank control group receiving no treatment, ultraviolet B （UVB） model group receiving UVB irradiation for 60 seconds, GP groupⅠreceiving topical GP treatment followed by UVB irradiation, GP group Ⅱreceiving UVB irradiation followed by topical GP treatment, VitE groupⅠreceiving topical VitE treatment followed by UVB irradiation, VitE groupⅡreceiving UVB irradiation followed by topical VitE treatment, matrix groupⅠreceiving topical matrix treatment followed by UVB irradiation, matrix groupⅡreceiving UVB irradiation followed by topical matrix treatment. UVB irradiation lasted 60 seconds at one time, and was given once every other day for 7 times to establish a skin model of photodamage. The interval between irradiation and topical treatment was 30 minutes in all the groups except the control group and UVB model group. After the last treatment, mice were sacrificed. Western blot was performed to measure the protein expressions of inhibitor of NF-κB（I-κB）, inhibitor of NF-κB kinase （IKK）, p38MAPK as well as phosphorylated p38MAPK （pp38） in skin tissue from the mice. Results No expressions of I-κB or IKK were observed in the blank control group. The expression level of I-κB was 0.40 ± 0.07 in UVB model group, significantly lower than that in GP group I （1.63 ± 0.85, P < 0.05） and GP group II （0.90 ± 0.40, P < 0.05）, whereas the level of IKK protein was higher in UVB model group than in the GP group I and II （2.01 ± 1.75 vs. 0.23 ± 0.12 and 0.45 ± 0.29, both P < 0.05）. No significant difference was observed in the expression of I-κB or IKK proteins between the GP group I, II , VitE group I and II or in the expression of p38MAPK between the 8 groups. The phosphorylated p38MAPK expression in UVB model group was significantly higher than that in GP group I and II （0.835 ± 0.049 vs. 0.425 ± 0.054 and 0.571 ± 0.090, both P < 0.05）, but similar to that in VitE groups. Conclusions UVB can activate NF-κB and phosphorylated p38MAPK signaling pathways; GP 1.5% cream can inhibit UVB-induced activation of NF-κB and p38MAPK pathways, which may be one of the mechanisms underlying its protective effects against inflammation and photodamage

Key words: p38 mitogen activated protein kinases