摘要
目的研究绞股蓝皂甙(GP)抗小鼠皮肤光损伤作用,探讨其抗损伤作用的可能机制.方法采用7次隔日UVB照射Balb/C小鼠建立皮肤光损伤的动物模型,应用Brad-Ford进行蛋白浓度的测定后用Western Blot法检测小鼠皮肤中核转录因子kappa-B(NF-κB)IκB蛋白(kappaB抑制蛋白)及IKK蛋白(κB抑制蛋白激酶)的表达.结果(1)UVB照射组的小鼠表皮中IκB蛋白水平与其它组相比明显减低,而IKK蛋白与其它组相比表达较高;(2)应用1.5%绞股蓝皂甙霜组及6%绞股蓝皂甙霜组IκB蛋白表达明显高于UVB照射组;IKK蛋白表达明显低于UVB照射组,与阳性对照VitE组小鼠皮肤中IκB蛋白、IKK蛋白的表达结果相似;(3)预先使用VitE霜组,1.5%绞股蓝皂甙霜组Balb/C小鼠皮肤组织中IκB蛋白表达高于先照紫外线UVB后用VitE霜组及1.5%绞股蓝皂甙霜组;(4)预先使用VitE霜组,1.5%绞股蓝皂甙霜组其IKK蛋白表达低于先照紫外线UVB后用VitE霜组及1.5%绞股蓝皂甙霜组.结论UVB辐射可以显著抑制Balb/C光损伤小鼠皮肤组织中抑制蛋白IκB蛋白的表达,促使IKK蛋白高表达,促使NF-κB(核转录因子-kappaB)活化;1.5%绞股蓝皂甙霜及6%绞股蓝皂甙霜可使UVB照射后光损伤Balb/C小鼠皮肤组织中IkB蛋白表达升高,恢复IκB抑制蛋白的活性;IKK蛋白表达活性受到抑制,进而抑制NF-κB通路的激活.
Objective To observe the effects of gypenosides（GP） on photo-damaged skin of mice and to explore the possible mechanisms.Methods We established Blab/C mouse skin photo-damage model by 7 times of UVB intermissive irradiation（every other day）.The concentration of protein was detected with Brad-Ford,then the nuclear NF-κB Inhibitor（IκB） protein as well as IκB kinase（IKK） expression were detected by western blot.Results（1） In UVB irradiation group,the expression of IκB was significantly decreased compared to other groups,while IKK protein expression was higher than other groups;（2） In 1.5% gypenosides group and 6% gypenosides group the protein expression of IκB was significantly higher than that of UVB irradiation group,whereas IKK protein expression was significantly lower than that of UVB irradiation group,similar with the positive control group of vitamin E;（3） In pre-treated vitamin E group and 1.5% gypenosides group,IκB protein expression was higher than that of treatment with vitamin E and 1.5% gypenosides after UVB exposure ;（4） In pre-treated VitE group and 1.5% gypenosides group,IKK protein expression was lower than that of treatment with vitamin E and 1.5% gypenosides after UVB exposure.Conclusions UVB can significantly inhibit IκB protein and increase IKK protein expression in the Balb/C mouse skin tissue,thus activate of NF-κB（NF-kappa B）.1.5% gypenosides and 6% gypenosides cream can enhance IκB protein expression in the Balb/C mouse skin tissue damaged by UVB exposure,reactivate IκB,and inhibit IKK protein activity,thereby inhibit the activity of NF-κB
出处
《昆明医学院学报》
2010年第2期53-56,60,共5页
Journal of Kunming Medical College
作者简介
邓丹琪（1963～），女，贵州盘县人，医学博士，主任医师，主要从事光线性皮肤病及自身免疫疾病的临床及研究工作．
[通讯作者]刘流．E-mail：liuliu@ydyy．cn
