绞股蓝皂苷对光损伤小鼠皮肤中核因子κB、p38MAPK的影响  

Effects of gypenosides on nuclear factor KB and p38 mitogen activated protein kinase signaling pathways in photodamaged skin of mice

作　　者：邓丹琪[1] 李杨[1] 王医林[1] 袁李梅[1] 刘流[2] 

机构地区：[1]昆明医学院第二附属医院皮肤性病／风湿免疫科,650101 [2]昆明医学院第一附属医院头颈颌面外科

出　　处：《中华皮肤科杂志》2012年第3期195-198,共4页Chinese Journal of Dermatology

基　　金：云南省卫生厅科研基金（2009NS056）

摘　　要：目的观察绞股蓝皂苷（GP）对光损伤Balb／C小鼠皮肤中核转录因子kappa—B（NF—KB）、p38丝裂原活化蛋白激酶（p38MAPK）的影响，进一步探讨GP抗皮肤光损伤的可能机制。方法将80只雌性Balb／C小鼠随机分为8组，每组10只。①空白对照组：不做任何处理；@uvB模型组：UVB照射60S；③GP乳膏I组；@GP乳膏Ⅱ组；⑤维生素E乳膏I组；⑥维生素E乳膏Ⅱ组；⑦基质I组；⑧基质Ⅱ组。I组均先外涂相应的乳膏或基质，30min后照射UVB60s；1／组均先用UVB照射60S，30min后外涂相应的乳膏或基质。采用隔日UVB照射7次Balb／C小鼠建立皮肤光损伤动物模型，应用Western印迹法检测小鼠皮肤中NF—KB抑制蛋白（IKB蛋白）、KB抑制蛋白激酶（IKK蛋白）及p38MAPK、磷酸化p38MAPK（pp38）的表达。结果空白对照组小鼠表皮中IKB、IKK蛋白未见表达。UVB模型组小鼠表皮中IKB蛋白水平为0．40±0．07，IKK蛋白为2．01±1．75。GP乳膏I组与Ⅱ组IKB蛋白表达（分别为1．63±0．85和0．90±0．40）明显高于UVB模型组（P值均〈0．05），IKK蛋白表达（分别为0．23±0．12和0．45±0．29）明显低于UVB模型组（P值均〈0．05），与维生素E组小鼠皮肤中IKB蛋白、IKK蛋白的表达结果相似。各组p38MAPK表达量没有明显差异。GP乳膏I组与Ⅱ组磷酸化p38MAPK表达水平（分别为0．425±0．054和0．571±0．090）明显低于UVB模型组（0．835±0．049），与维生素E组相似。结论UVB照射能促使NF-KB活化，激活磷酸化p38MAPK；1．5％GP乳膏能抑制UVB诱导的NF—KB通路及p38MAPK的激活，可能是其抗炎、抗光损伤的作用机理之一。Objective To observe the effects of gypenosides （GP） on nuclear factor KB （NF-KB） 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 group I receiving topical GP treatment followed by UVB irradiation, GP group II receiving UVB irradiation followed by topical GP treatment, VitE group I receiving topical VitE treatment followed by UVB irradiation, VitE group II receiving UVB irradiation followed by topical VitE treatment, matrix group I receiving topical matrix treatment followed by UVB irradiation, matrix group II receiving 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-KB（IKB）, inhibitor of NF-KB kinase （IKK）, p38MAPK as well as phosphorylated p38MAPK （pp38） in skin tissue from the mice. Results No expressions of IKB or IKK were observed in the blank control group. The expression level of IgB 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 IKB or IKK proteins between the GP group I, II , VitE group I and II or in the expression of

关 键 词：绞股蓝皂甙 NF—KB I-KB激酶 P38丝裂原活化蛋白激酶类 辐射损伤 实验性 

分 类 号：R285.5[医药卫生—中药学]