中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2012年
3期
195-198
,共4页
邓丹琪%李杨%王医林%袁李梅%刘流
鄧丹琪%李楊%王醫林%袁李梅%劉流
산단기%리양%왕의림%원리매%류류
绞股蓝皂甙%NF-κB%I-κB激酶%p38丝裂原活化蛋白激酶类%辐射损伤,实验性
絞股藍皂甙%NF-κB%I-κB激酶%p38絲裂原活化蛋白激酶類%輻射損傷,實驗性
교고람조대%NF-κB%I-κB격매%p38사렬원활화단백격매류%복사손상,실험성
GYPENOSIDE%NF-kappa B%I-kappa B kinase%p38 Mitogen-activated protein kinases%Radiation injuries,experimental
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-κB)、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；②UVB模型组:UVB照射60 s；③GP乳膏Ⅰ组；④GP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,30 min后照射UVB 60 s；Ⅱ组均先用UVB照射60 s,30 min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-κB抑制蛋白(IκB蛋白)、κB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IκB、IKK蛋白未见表达.UVB模型组小鼠表皮中IκB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IκB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IκB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-κB活化,激活磷酸化p38MAPK; 1.5％GP乳膏能抑制UVB诱导的NF-κB通路及p38MAPK的激活,可能是其抗炎、抗光损伤的作用机理之一.
目的 觀察絞股藍皂苷(GP)對光損傷Balb/C小鼠皮膚中覈轉錄因子kappa-B(NF-κB)、p38絲裂原活化蛋白激酶(p38MAPK)的影響,進一步探討GP抗皮膚光損傷的可能機製.方法 將80隻雌性Balb/C小鼠隨機分為8組,每組10隻.①空白對照組:不做任何處理；②UVB模型組:UVB照射60 s；③GP乳膏Ⅰ組；④GP乳膏Ⅱ組；⑤維生素E乳膏Ⅰ組；⑥維生素E乳膏Ⅱ組；⑦基質Ⅰ組；⑧基質Ⅱ組.Ⅰ組均先外塗相應的乳膏或基質,30 min後照射UVB 60 s；Ⅱ組均先用UVB照射60 s,30 min後外塗相應的乳膏或基質.採用隔日UVB照射7次Balb/C小鼠建立皮膚光損傷動物模型,應用Western印跡法檢測小鼠皮膚中NF-κB抑製蛋白(IκB蛋白)、κB抑製蛋白激酶(IKK蛋白)及p38MAPK、燐痠化p38MAPK(pp38)的錶達.結果 空白對照組小鼠錶皮中IκB、IKK蛋白未見錶達.UVB模型組小鼠錶皮中IκB蛋白水平為0.40±0.07,IKK蛋白為2.01±1.75.GP乳膏Ⅰ組與Ⅱ組IκB蛋白錶達(分彆為1.63±0.85和0.90±0.40)明顯高于UVB模型組(P值均＜0.05),IKK蛋白錶達(分彆為0.23±0.12和0.45±0.29)明顯低于UVB模型組(P值均＜0.05),與維生素E組小鼠皮膚中IκB蛋白、IKK蛋白的錶達結果相似.各組p38MAPK錶達量沒有明顯差異.GP乳膏Ⅰ組與Ⅱ組燐痠化p38MAPK錶達水平(分彆為0.425±0.054和0.571±0.090)明顯低于UVB模型組(0.835±0.049),與維生素E組相似.結論 UVB照射能促使NF-κB活化,激活燐痠化p38MAPK; 1.5％GP乳膏能抑製UVB誘導的NF-κB通路及p38MAPK的激活,可能是其抗炎、抗光損傷的作用機理之一.
목적 관찰교고람조감(GP)대광손상Balb/C소서피부중핵전록인자kappa-B(NF-κB)、p38사렬원활화단백격매(p38MAPK)적영향,진일보탐토GP항피부광손상적가능궤제.방법 장80지자성Balb/C소서수궤분위8조,매조10지.①공백대조조:불주임하처리；②UVB모형조:UVB조사60 s；③GP유고Ⅰ조；④GP유고Ⅱ조；⑤유생소E유고Ⅰ조；⑥유생소E유고Ⅱ조；⑦기질Ⅰ조；⑧기질Ⅱ조.Ⅰ조균선외도상응적유고혹기질,30 min후조사UVB 60 s；Ⅱ조균선용UVB조사60 s,30 min후외도상응적유고혹기질.채용격일UVB조사7차Balb/C소서건립피부광손상동물모형,응용Western인적법검측소서피부중NF-κB억제단백(IκB단백)、κB억제단백격매(IKK단백)급p38MAPK、린산화p38MAPK(pp38)적표체.결과 공백대조조소서표피중IκB、IKK단백미견표체.UVB모형조소서표피중IκB단백수평위0.40±0.07,IKK단백위2.01±1.75.GP유고Ⅰ조여Ⅱ조IκB단백표체(분별위1.63±0.85화0.90±0.40)명현고우UVB모형조(P치균＜0.05),IKK단백표체(분별위0.23±0.12화0.45±0.29)명현저우UVB모형조(P치균＜0.05),여유생소E조소서피부중IκB단백、IKK단백적표체결과상사.각조p38MAPK표체량몰유명현차이.GP유고Ⅰ조여Ⅱ조린산화p38MAPK표체수평(분별위0.425±0.054화0.571±0.090)명현저우UVB모형조(0.835±0.049),여유생소E조상사.결론 UVB조사능촉사NF-κB활화,격활린산화p38MAPK; 1.5％GP유고능억제UVB유도적NF-κB통로급p38MAPK적격활,가능시기항염、항광손상적작용궤리지일.
Objective To observe the effects of gypenosides (GP) on nuclear factor κB (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 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-κB(IκB),inhibitor of NF-κB kinase (IKK),p38MAPK as well as phosphorylated p38MAPK (pp38) in skin tissue from the mice.Results No expressions of IκB or IKK were observed in the blank control group.The expression level of IκB 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 ± 1.75vs.0.23 ± 0.12 and 0.45 ± 0.29,both P ＜ 0.05).No significant difference was observed in the expression of IκB 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.
