CAJ | 학술논문

目的探讨绞股蓝皂苷(GP)抗光损伤的作用机制.方法 80只雌性BALB/c小鼠随机分为8组,每组10只,分别为:空白对照组(未加任何处理)、UVB模型组、GP组Ⅰ(先涂GP后照UVB)、GP组Ⅱ(先照UVB后涂GP)、维生素E组Ⅰ(先涂维生素E乳膏后照UVB)、维生素E组Ⅱ(先照UVB后涂维生素E乳膏)、基质组Ⅰ(先涂基质后照UVB)、基质组Ⅱ(先照UVB后涂基质).中波紫外线(UVB)照射BALB/c小鼠建立光损伤模型,根据以上分组对光损伤小鼠皮肤进行干预.运用蛋白Western印迹法检测各组小鼠表皮中p53蛋白、p21蛋白的表达.结果 BALB/c小鼠表皮p53蛋白的表达:空白组p53蛋白(0.11±0.08)与UVB模型组(0.22 ±0.12)相比低表达,GP组Ⅰ(0.44±0.23)高于空白组(P<0.01),GP组Ⅱ(0.48±0.24)高于空白组(P<0.01)及UVB模型组(P<0.05),维生素E组Ⅰ(0.49±0.29)及维生素E组Ⅱ(0.50±0.27)均与GP组作用相似.小鼠表皮p21蛋白的表达各组间差异无统计学意义.结论 1.5%GP乳膏抗光损伤的作用机制之一可能与上调表皮细胞中p53蛋白表达量有关.
목적 탐토교고람조감(GP)항광손상적작용궤제.방법 80지자성BALB/c소서수궤분위8조,매조10지,분별위:공백대조조(미가임하처리)、UVB모형조、GP조Ⅰ(선도GP후조UVB)、GP조Ⅱ(선조UVB후도GP)、유생소E조Ⅰ(선도유생소E유고후조UVB)、유생소E조Ⅱ(선조UVB후도유생소E유고)、기질조Ⅰ(선도기질후조UVB)、기질조Ⅱ(선조UVB후도기질).중파자외선(UVB)조사BALB/c소서건립광손상모형,근거이상분조대광손상소서피부진행간예.운용단백Western인적법검측각조소서표피중p53단백、p21단백적표체.결과 BALB/c소서표피p53단백적표체:공백조p53단백(0.11±0.08)여UVB모형조(0.22 ±0.12)상비저표체,GP조Ⅰ(0.44±0.23)고우공백조(P<0.01),GP조Ⅱ(0.48±0.24)고우공백조(P<0.01)급UVB모형조(P<0.05),유생소E조Ⅰ(0.49±0.29)급유생소E조Ⅱ(0.50±0.27)균여GP조작용상사.소서표피p21단백적표체각조간차이무통계학의의.결론 1.5%GP유고항광손상적작용궤제지일가능여상조표피세포중p53단백표체량유관.
Objective To explore the mechanism underlying the effects of gypenosides (GP) against photodamage. Methods Eighty BALB/c mice were equally divided into 8 groups, i.e., blank control group (untreated), UVB model group (irradiated with UVB), GP I group (irradiated with UVB before topical application of GP), GPⅡ group (irradiated with UVB followed by topical application of GP), VitE I group (irradiated with UVB after topical application of Vitamine E cream), VitE Ⅱ group (irradiated with UVB followed by topical application of Vitamine E cream), Vehicle group Ⅰ (irradiated with UVB after application of the drug vehicle),and Vehicle group Ⅱ (irradiated with UVB before application of the drug vehicle). UVB irradiation was performed once every other day for 14 days. Mice were sacrificed after the last irradiation and skin specimens were obtained from the irradiated sites, and the levels of p53 and p21 protein were measured by Western blot in the specimens. Results The expression level of p53 protein was significantly lower in the blank control group than in the UVB model group (0.11 ± 0.08 vs. 0.22 ± 0.12) and GP Ⅰ group (0.44 ± 0.23, P < 0.01),in the blank control group and UVB model group than in the GP Ⅱ group (0.48 ± 0.24, P < 0.01, 0.05). VitE Ⅰ group (0.49 ± 0.29) and VitE II group (0.50 ± 0.27) were similar to the GP groups in the expression of p53 protein. No statistical difference was observed in the expression of p21 protein between the eight groups. Conclusion The upregulation of p53 protein expression in epidermal cells may be related to the mechanisms underlying the protective effect of 1.5% GP cream against photodamage.