中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2011年
6期
437-440
,共4页
李燃%陈斌%闫宁%陈刚%李双凤%毕志刚%张银娣
李燃%陳斌%閆寧%陳剛%李雙鳳%畢誌剛%張銀娣
리연%진빈%염저%진강%리쌍봉%필지강%장은제
黄芪甲苷%皮肤衰老%模型,动物%转化生长因子β%Smad7蛋白质
黃芪甲苷%皮膚衰老%模型,動物%轉化生長因子β%Smad7蛋白質
황기갑감%피부쇠로%모형,동물%전화생장인자β%Smad7단백질
Astragaloside%Skin aging%Models,animal%Transforming growth factor beta%Smad 7 protein
目的 探讨黄芪甲苷对皮肤光老化的保护机制.方法 BALB/c小鼠分为模型组、模型+基质组、模型+黄芪甲苷组、正常对照组.RT-PCR测定转化生长因子β受体Ⅱ(TGF-βRⅡ)、Smad 7的mRNA表达水平,免疫组化观察TGF-βR Ⅱ、Smad 7在小鼠皮肤组织中的蛋白表达情况.结果 正常对照组中,TGF-βR Ⅱ、Smad 7的灰度值比值分别为0.5688±0.0439、0.5900 ±0.0585,阳性表达率分别为(53.00 ±4.72)%、(47.50±3.81)%;模型组中,TGF-βR Ⅱ、Smad 7的灰度值比值分别为0.2588±0.0283、0.8637±0.0514,阳性表达率分别为(28.20±5.24)%、(82.06±2.18)%;模型+基质组中,TGF-βR Ⅱ、Smad 7的灰度值比值分别为0.2653±0.0456、0.8553±0.0575,阳性表达率分别为(28.74±2.28)%、(82.62±4.02)%;模型+黄芪甲苷组中TGF-βRⅡ、Smad 7的灰度值比值分别为0.3767±0.0374、0.7131±0.0410,阳性表达率分别为:(41.64±2.59)%、(64.36±2.62)%.皮肤组织中TGF-βRⅡ和Smad灰度值比值4组小鼠间比较,F值分别为80.98和736.80,TGF-βRⅡ和Smad 7的阳性表达率4组小鼠间比较,F值分别为45.36和132.25,P值均<0.01.与正常对照组相比,模型组TGF-βR Ⅱ mRNA和蛋白表达明显降低,Smad 7 mRNA和蛋白表达显著升高(P值均<0.01).与模型组和模型+基质组比较,模型+黄芪甲苷组TGF-βRⅡ mRNA和蛋白表达明显升高,Smad 7 mRNA和蛋白表达显著下调(P值均<0.01).模型+基质组TGF-βR Ⅱ、Smad 7的mRNA和蛋白表达与模型组相比差异无统计学意义(P值均>0.01).结论 黄芪甲苷可以通过上调TGF-βRⅡ表达和下调Smad 7表达而改变TGF-β通路的信号转导参与抗光老化.
目的 探討黃芪甲苷對皮膚光老化的保護機製.方法 BALB/c小鼠分為模型組、模型+基質組、模型+黃芪甲苷組、正常對照組.RT-PCR測定轉化生長因子β受體Ⅱ(TGF-βRⅡ)、Smad 7的mRNA錶達水平,免疫組化觀察TGF-βR Ⅱ、Smad 7在小鼠皮膚組織中的蛋白錶達情況.結果 正常對照組中,TGF-βR Ⅱ、Smad 7的灰度值比值分彆為0.5688±0.0439、0.5900 ±0.0585,暘性錶達率分彆為(53.00 ±4.72)%、(47.50±3.81)%;模型組中,TGF-βR Ⅱ、Smad 7的灰度值比值分彆為0.2588±0.0283、0.8637±0.0514,暘性錶達率分彆為(28.20±5.24)%、(82.06±2.18)%;模型+基質組中,TGF-βR Ⅱ、Smad 7的灰度值比值分彆為0.2653±0.0456、0.8553±0.0575,暘性錶達率分彆為(28.74±2.28)%、(82.62±4.02)%;模型+黃芪甲苷組中TGF-βRⅡ、Smad 7的灰度值比值分彆為0.3767±0.0374、0.7131±0.0410,暘性錶達率分彆為:(41.64±2.59)%、(64.36±2.62)%.皮膚組織中TGF-βRⅡ和Smad灰度值比值4組小鼠間比較,F值分彆為80.98和736.80,TGF-βRⅡ和Smad 7的暘性錶達率4組小鼠間比較,F值分彆為45.36和132.25,P值均<0.01.與正常對照組相比,模型組TGF-βR Ⅱ mRNA和蛋白錶達明顯降低,Smad 7 mRNA和蛋白錶達顯著升高(P值均<0.01).與模型組和模型+基質組比較,模型+黃芪甲苷組TGF-βRⅡ mRNA和蛋白錶達明顯升高,Smad 7 mRNA和蛋白錶達顯著下調(P值均<0.01).模型+基質組TGF-βR Ⅱ、Smad 7的mRNA和蛋白錶達與模型組相比差異無統計學意義(P值均>0.01).結論 黃芪甲苷可以通過上調TGF-βRⅡ錶達和下調Smad 7錶達而改變TGF-β通路的信號轉導參與抗光老化.
목적 탐토황기갑감대피부광노화적보호궤제.방법 BALB/c소서분위모형조、모형+기질조、모형+황기갑감조、정상대조조.RT-PCR측정전화생장인자β수체Ⅱ(TGF-βRⅡ)、Smad 7적mRNA표체수평,면역조화관찰TGF-βR Ⅱ、Smad 7재소서피부조직중적단백표체정황.결과 정상대조조중,TGF-βR Ⅱ、Smad 7적회도치비치분별위0.5688±0.0439、0.5900 ±0.0585,양성표체솔분별위(53.00 ±4.72)%、(47.50±3.81)%;모형조중,TGF-βR Ⅱ、Smad 7적회도치비치분별위0.2588±0.0283、0.8637±0.0514,양성표체솔분별위(28.20±5.24)%、(82.06±2.18)%;모형+기질조중,TGF-βR Ⅱ、Smad 7적회도치비치분별위0.2653±0.0456、0.8553±0.0575,양성표체솔분별위(28.74±2.28)%、(82.62±4.02)%;모형+황기갑감조중TGF-βRⅡ、Smad 7적회도치비치분별위0.3767±0.0374、0.7131±0.0410,양성표체솔분별위:(41.64±2.59)%、(64.36±2.62)%.피부조직중TGF-βRⅡ화Smad회도치비치4조소서간비교,F치분별위80.98화736.80,TGF-βRⅡ화Smad 7적양성표체솔4조소서간비교,F치분별위45.36화132.25,P치균<0.01.여정상대조조상비,모형조TGF-βR Ⅱ mRNA화단백표체명현강저,Smad 7 mRNA화단백표체현저승고(P치균<0.01).여모형조화모형+기질조비교,모형+황기갑감조TGF-βRⅡ mRNA화단백표체명현승고,Smad 7 mRNA화단백표체현저하조(P치균<0.01).모형+기질조TGF-βR Ⅱ、Smad 7적mRNA화단백표체여모형조상비차이무통계학의의(P치균>0.01).결론 황기갑감가이통과상조TGF-βRⅡ표체화하조Smad 7표체이개변TGF-β통로적신호전도삼여항광노화.
Objective To study the protective mechanism of astragaloside on skin photoaging. Methods BALB/c mice were randomly divided into four groups: model group irradiated with ultraviolet rays (UV), model plus matrix group pretreated with the matrix before UV irradiation, model plus astragaloside group pretreated with astragaloside 0.08% cream before UV irradiation, normal control group received no irradiation or pretreatment. After 4-week irradiation, the mice were sacrificed, and skin tissues were resected from the back of these mice. Then, reverse transeription PCR (RT-PCR) and immunohistochemistry were performed to detect the mRNA and protein expression of TGF-βR Ⅱ and Smad 7, respectively. Gray scale ratio was used to represent the mRNA levels of TGF-βR Ⅱ and Smad 7. Results There was a significant difference in the mRNA level (F = 80.98, 736.80, respectively, both P < 0.01) and protein positivity rate (F = 45.36,132.25, respectively,both P < 0.01) of TGF-βR Ⅱ and Smad 7 among the 4 groups. The mRNA level and protein positivity rate of TGF-βR Ⅱwere 0.2588±0.0283 and (28.20 ± 5.24)% respectively in the model group, significantly lower than those in the normal control group[0.5688 ± 0.0439, (53.00 ± 4.72)%, both P < 0.01] and model plus astragaloside group [0.3767 ± 0.0374, (41.64 ± 2.59)%, both P< 0.01]; on the contrary, the mRNA level and protein positivity rate of Smad 7 in the model group [0.8637 ± 0.0514, (82.06 ± 2.18)%] were significantly higher than those in the normal control group [0.5900 ± 0.0585, (47.50±3.81)%, both P < 0.01] and model plus astragaloside group [0.7131 ± 0.0410, (64.36 ± 2.62)%, both P< 0.01]. In the model plus astragaloside group, the mRNA level and protein positivity rate of TGF-βR Ⅱ were significantly higher than in the model plus matrix group [0.2653 ± 0.0456, (28.74 ± 2.28)%, both P < 0.01], while those of Smad 7 were statistically lower than in the model plus matrix group [0.8553 ± 0.0575, (82.62 ± 4.02)%, both P < 0.01]. However,no significant difference was observed in the mRNA level or protein positivity rate of TGF-βR Ⅱ or Smad 7 between the model group and model plus matrix group (all P > 0.01). Conclusion Astragaloside can prevent skin photoaging by the alteration of TGF-β pathway via up-regulating TGF-βR Ⅱ expression and down-regulating Smad 7 expression.