活性磷脂抗皮肤老化的实验研究

目的探讨活性磷脂延缓小鼠皮肤老化的作用及其机理。方法小鼠每日颈背部皮下注射D-半乳糖(1 000 mg/kg)造成小鼠老化模型,同时灌胃活性磷脂42 d后,去背部皮肤,用分光光度法测定小鼠皮肤中胶原蛋白的含量。结果活性磷脂使D-半乳糖所致的小鼠皮肤老化模型中各剂量组胶原蛋白含量均显著增加。结论活性磷脂可提高皮肤中胶原蛋白含量,提示活性磷脂具有延缓皮肤老化的作用。     

大豆磷脂对小鼠皮肤胶原蛋白含量的影响

目的 研究大豆磷脂对小鼠皮肤胶原蛋白含量的影响。方法 小鼠用不同剂量的大豆磷脂2.5g/(kg.d)(低剂量组)、5.0 g/(kg.d)(中剂量组)和10.0 g/(kg.d)(高剂量组)灌胃30d后,取背部皮肤,用分光光度法测定小鼠皮肤中胶原蛋白的含量。结果 与对照组小鼠皮肤胶原蛋白含量[(31.70±5.00)mg/g]比较,中剂量组小鼠皮肤胶原蛋白含量[(36.80±5.50)mg/g]显著增加(P<0.05),高剂量组小鼠皮肤胶原蛋白含量[(41.23±7.54)mg/g]极显著增加(P<0.01)。结论 大豆磷脂可提高皮肤中胶原蛋白含量,具有延缓皮肤衰老作用。     

正交实验法优选榛子叶中鞣质的超声提取工艺

目的：优选榛子叶中鞣质的最佳工艺。方法：采用正交实验法优选榛子叶中鞣质的最佳条件,以含量为指标确定,采用EDTA络合滴定法测定含量。结果：最佳工艺为60%丙酮,8倍溶剂量,超声提取60min。结论：该工艺提取榛子叶总鞣质是可行的。     

胶原蛋白及复方抗氧化美白补水功效研究

目的 检验胶原蛋白及复方样品是否具有抗氧化及美白补水活性.方法 通过豚鼠酪氨酸酶及黑色素测定、D-半乳糖衰老模型小鼠的抗氧化作用研究、小鼠皮肤羟脯氨酸及水分含量测定,统计各个指标结果.结果 胶原蛋白及复方样品均可以显著地抑制豚鼠血液中酪氨酸酶含量;减少豚鼠皮肤毛囊内含有黑色素颗粒细胞的数量;能够降低D-半乳糖亚急性衰老模型小鼠血清中MDA含量,升高机体SOD水平;还能够显著增加D-半乳糖亚急性衰老模型小鼠皮肤羟脯氨酸和水分含量.结论 胶原蛋白及复方样品具有一定抗氧化作用,具有减少皮肤黑色素,增加皮肤羟脯氨酸和水分的功效.     

虾青素-胶原蛋白耦合物改善小鼠皮肤光老化作用研究

目的 在制备虾青素-胶原蛋白耦合物的基础上,探讨耦合物对小鼠皮肤光老化的改善作用。方法 将来源于雨生红球藻的虾青素单体和均一分子量胶原蛋白多肽在一定条件下反应后生成耦合物,将耦合物与适当基质混合后制成外用乳膏。采用UV灯照射Balb/c小鼠背部裸露皮肤,建立动物光老化模型,随机分为正常对照组、模型对照组、基质对照组、虾青素组、胶原蛋白多肽组、耦合物组和维生素E组,每天UV照射前进行药物涂抹。6周后观察小鼠皮肤形态、测定皮肤厚度变化及进行皮肤组织病理学检测等。结果 虾青素和胶原蛋白可结合生成具有特征吸收波长的水溶性耦合物,耦合物可有效缓解皮肤厚度增生,修复皮肤胶原纤维和弹性纤维网状结构。结论 虾青素-胶原蛋白多肽耦合物可有效改善UV引起的皮肤光老化损伤。     

枸杞多糖与丹参酮延缓小鼠皮肤衰老的实验研究

目的比较枸杞多糖与丹参酮对衰老小鼠皮肤的抗衰老作用。方法60只雌性昆明种小鼠,随机分为4组（n=15）：正常对照组皮下注射生理盐水;其余3组每日颈背部皮下注射D-半乳糖[1000mg/（kg·d）]造成小鼠衰老模型,同时各组分别灌胃生理盐水（衰老模型组）、枸杞多糖[200mg/（kg·d）]、丹参酮[1500mg/（kg·d）]。42d后,测定小鼠背部皮肤组织匀浆中超氧化物歧化酶（SOD）活力、过氧化脂质代谢产物丙二醛（MDA）含量和皮肤羟脯氨酸（Hyp）含量。结果枸杞多糖可使衰老模型小鼠皮肤中MDA含量显著降低,较丹参酮组明显;但SOD活力显著升高,不及丹参酮组改变显著;枸杞多糖和丹参酮均可使羟脯氨酸含量升高,且效果相当。结论枸杞多糖与丹参酮都有显著的抗小鼠皮肤衰老作用,枸杞多糖清除皮肤中脂质过氧化代谢产物方面较丹参酮明显,而提高皮肤抗氧化酶活力则不及丹参酮显著,在增强成纤维细胞活性方面两者效果相当。     

鱿鱼皮胶原蛋白水解肽抗氧化活性研究

目的探讨秘鲁鱿鱼(Dosidicus eschrichitiiSteenstrup)皮胶原蛋白多肽组分对自由基的清除作用以及水解产物的体内抗氧化作用,为鱿鱼加工废弃物的高值化利用探索一条新途径。方法采用化学发光法研究胶原蛋白活性多肽体外对超氧阴离子自由基(O2.-)和羟自由基(.OH)的清除作用,并筛选出体外清除自由基活性最好的组分;灌胃于D-半乳糖致衰老的模型小鼠,测定小鼠血液及皮肤中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)及羟脯氨酸(Hyp)含量。结果与结论鱿鱼皮胶原蛋白多肽分子量小于2000D组分对O2.-和.OH具有较好的清除效果,该活性多肽组分可以提高小鼠血液及皮肤中SOD和GSH-Px的活力,降低MDA含量,并能提高小鼠皮肤组织中Hyp的含量。     

牛蒡叶多酚对DSS诱导小鼠急性结肠炎的缓解作用

目的 本研究探讨牛蒡叶多酚提取物干预对葡聚糖硫酸钠诱导的急性溃疡性结肠炎小鼠的改善作用。方法 连续7 d饮用3%DSS水构建急性结肠炎模型,通过测量小鼠的结肠长度、疾病指数评分、结肠HE染色、结肠组织中炎症因子TNF-α与IL-6的含量和抗氧化指标SOD、CAT、 GSH-PX和MDA的活性,评价在牛蒡叶多酚的干预下,其对小鼠急性结肠炎的保护效果。结果 10 mg·kg^-1·d^-1牛蒡叶多酚干预可以有效降低急性结肠炎小鼠的DAI评分,改善结肠缩短情况,增强结肠组织的完成性和抗氧化酶的活性,减少促炎细胞因子的分泌。结论 结果证明,牛蒡叶多酚提取物可以通过抗氧化,减少氧化损伤,减轻炎症反应,有效缓解小鼠急性结肠炎症状。     

温泉矿物泥抗皮肤衰老作用的实验研究

目的 观察温泉矿物泥对皮肤的抗衰老作用. 方法 60只雌性昆明种小鼠, 随机分为6组(n＝10)：正常对照组皮下注射0.9%氯化钠溶液, 其余5组每日颈背部皮下注射D 半乳糖(1 000 mg.kg 1&#8226;d 1)造成小鼠衰老模型, 同时每只小鼠分别涂抹纯化水(衰老模型组)、空白基质(基质对照组)、温泉矿物泥200 mg(低剂量矿物泥组)、温泉矿物泥500 mg(高剂量矿物泥组)、大宝SOD蜜(阳性对照组). 42 d后, 测定小鼠背部皮肤组织匀浆中超氧化物歧化酶(SOD)活力、过氧化脂质代谢产物丙二醛(MDA)和皮肤羟脯氨酸含量. 结果温泉矿物泥低、高剂量均能明显增加小鼠皮肤羟脯氨酸含量(P<0.05), 升高小鼠皮肤SOD活性(P<0.05), 使其MDA含量下降(P<0.05). 结论温泉矿物泥对皮肤具有一定的抗衰老作用.     

没食子酰表没食子儿茶素对TPA促癌的抑制作用

目的 从绿茶中提取的多酚成分,具有很强的抗氧化作用。沿食子酰表没食子儿茶互(EGCG)是该提取物的主要成分。本实验旨在证明EGCG对TPA的促癌作用具有抑制效应。方法 采用BALB／3T3细胞转化试验、诱导小鼠耳部炎性水肿试验和小鼠背部皮肤增生试验,以观察EGCG对TPA的抑制作用。结果 体外试验、EGCG具有抑制TPA的促细胞转化作用;在整体实验,EGCG可以抑制TPA诱导的小鼠耳部水肿。其最大抑制率为43．51％;EGCG对TPA所诱导的小鼠背部皮肤增生的最大抑制率为46．60％。结论 EGGC对癌症预防具有某些实用价值。     

河豚鱼皮胶原寡肽的护肤美白功效研究

目的 探究河豚鱼皮胶原寡肽的护肤美白功效。方法 以3个月的雄性豚鼠为试验对象,在豚鼠的背部一侧脱毛处,每天涂抹1次受试物,连续30天。在试验后分别测定豚鼠血清的酪氨酸酶含量,受试皮肤的含水量和羟脯氨酸含量,观察受试皮肤组织形态及黑色素毛囊数,对河豚鱼皮胶原寡肽的护肤美白功效进行评价。 结果 在本试验条件下,受试豚鼠的皮肤无病变现象。河豚鱼皮胶原寡肽能够提高受试豚鼠皮肤的胶原蛋白含量,而且具有抑制皮肤黑色素表达的作用。结论 河豚鱼皮胶原寡肽具有一定的延缓皮肤衰老和美白的功效。     

罗仙子油精制工艺优化及其对D-半乳糖致小鼠皮肤衰老的作用研究

目的:优化罗仙子油的精炼工艺,研究罗仙子精油对D-半乳糖致小鼠皮肤衰老的干预作用。方法:分别考察不同因素对罗仙子油的水化脱胶、碱炼脱酸精炼效果的影响,分析比较罗仙子油精制前后的理化值。将昆明种雌性小鼠随机分为正常组、模型组、基质组、维生素E组、罗仙子精油低剂量组和高剂量组。除正常组外,其余各组均每日颈背部皮下注射3%D-半乳糖连续42 d,建立小鼠亚急性衰老模型;各给药组于小鼠颈背部涂抹相应药物qd,持续32 d,HE染色观察皮肤组织形态,检测皮肤含水量、超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活力、羟脯氨酸(HYP)及丙二醛(MDA)的含量。采用家兔对罗仙子精油进行皮肤刺激性实验,将12只家兔分为正常组、完整皮肤组、破损皮肤组。在家兔背部左侧给予0.5 m L罗仙子精油,右侧给予同体积基质,qd,连续7 d。观察药物对家兔皮肤的刺激性,对皮肤红斑和水肿进行评分,于末次给药后72 h对给药部位皮肤进行HE染色,并观察皮肤组织形态。结果:罗仙子油精炼后,碘值(18.714±0.116) g·100 g^-1、酸值(0.465±0.006) mg·g^-1、过氧化值(0.016±0.001) g·100 g^-1和皂化值(130.212±1.623) mg·g^-1,符合按摩精油及润肤油的国家标准。与模型组比较,罗仙子精油组小鼠皮肤真皮层增厚,毛囊数明显增加且胶原纤维增多,皮肤含水量、HYP含量、SOD及GSH-PX活力明显提高(P<0.05,P<0.01),MDA含量显著降低(P<0.01)。在家兔皮肤刺激实验中,各组家兔的红斑和水肿评分均为0分,皮肤刺激性均评价为无刺激。结论:罗仙子精油具有延缓D-半乳糖致小鼠皮肤衰老的作用,且无刺激性,具有潜在应用价值。精炼后罗仙子油的色泽、气味、澄明度和流动性均得到改善,为罗仙子精油的抗衰老产品开发提供依据。     

芦荟胶外涂对大鼠背部创面愈合和疤痕形成的影响

目的：研究芦荟胶外涂对大鼠背部创面愈合及疤痕形成的影响。方法：36只健康雄性大鼠随机分为空白组、实验组和对照组,建立大鼠背部切创伤模型,外涂创面给药后,以创伤面积愈合率和皮肤组织中毛囊、皮脂腺、胶原纤维等的生成情况来评价愈合效果。结果：与空白组相比,实验组上皮出现时间早,创面愈合时间较短,伤口愈合率明显提高(P<0.05),皮肤组织中毛囊、皮脂腺等附属器官及Ⅲ型胶原纤维的生成较多,胶原蛋白束排列较为有序;实验组各项指标与对照组接近。结论：芦荟胶对于皮肤创伤有着较好的治疗效果,并且可以抑制疤痕的形成。     

Possible involvement of mast cells in collagen remodeling in the late phase of cutaneous wound healing in mice

We examined possible roles of mast cells in cutaneous wound healing using mast cell deficient (W/Wv) mice and their normal littermates (+/+). A round full-thickness wound was made on the back skin of these mice. The wounds closed completely within 20 days, and there was no difference in wound contraction between +/+ and W/Wv mice during the wound healing. While either chymase or tryptase activities were hardly detectable in W/Wv mice, chymase activities decreased at the impaired sites and recovered to the control level within 20 days in +/+ mice. Tryptase activities were higher than the control level on day 15 and day 20 in +/+ mice. Histological observations on day 15 and day 20 in +/+ mice revealed that mast cells were abundant at the wound edges but absent at the center. The latent and the active forms of MMP-2 and MMP-9 increased on day 10 and day 15 but recovered nearly to control levels on day 20 in both mice groups. The hydroxyproline contents in W/Wv mice were significantly higher than those in +/+ mice on day 15 and day 20. Furthermore, histological observations revealed that the collagen aggregation at the wound edges was tighter and less interwoven in W/Wv mice compared with +/+ mice. These results suggest that mast cells accumulated at the wound edge may participate in tissue remodeling in the late phase of wound healing.     

Photocarcinogenesis study of aloe vera [CAS NO. 481-72-1(Aloe-emodin)] in SKH-1 mice (simulated solar light and topical application study)

The popular recognition of the Aloe barbadensis Miller (Aloe vera) plant as a therapeutic dermatologic agent has led to the widespread incorporation of Aloe vera leaf extracts in skincare products. Studies have suggested that Aloe vera in skincare preparations may enhance the induction of skin cancer by ultraviolet radiation. A 1-year study was conducted in mice to determine whether the topical application of creams containing Aloe vera plant extracts (aloe gel, whole leaf, or decolorized whole leaf) or creams containing aloe-emodin would enhance the photocarcinogenicity of simulated solar light (SSL). 1-YEAR STUDY: groups of 36 male and 36 female Crl:SKH-1 (hr -/hr -) hairless mice received topical applications of control cream or creams containing 3% or 6% (w/w) aloe gel, whole leaf, or decolorized whole leaf or 7.46 or 74.6 μg/g aloe-emodin to the dorsal skin region each weekday morning. The mice were irradiated with SSL emitted from filtered 6 kW xenon arc lamps each weekday afternoon. The topical applications of creams and irradiance exposures were conducted 5 days per week for a period of 40 weeks. A 12-week recovery/observation period followed the 40-week treatment/exposure period. Additional groups of 36 male and 36 female mice received no cream and were exposed to 0.00, 6.85, 13.70, or 20.55 mJ?CIE/cm2 SSL per day. Mice that received no cream treatment and were exposed to increasing levels of SSL showed significant SSL exposure-dependent decreases in survival and significant increases in the in-life observations of skin lesion onset, incidence, and multiplicity, and significant SSL exposure-dependent increases in the incidences and multiplicities of histopathology-determined squamous cell nonneoplastic skin lesions (squamous hyperplasia and focal atypical hyperplasia) and squamous cell neoplasms (papilloma, carcinoma in situ, and/or carcinoma). Squamous cell neoplasms were not detected in mice that received no SSL exposure. The topical treatment with the control cream of mice that were exposed to SSL did not impart a measurable effect when compared with comparable measurements in mice that received no cream treatment and were exposed to the same level of SSL, suggesting that the control cream used in these studies did not alter the efficiency of the SSL delivered to mice or the tolerability of mice to SSL. The application of aloe gel creams to mice had no effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. The administration of aloe gel creams to male mice had no effect on the incidences or multiplicities of histopathology-determined squamous cell nonneoplastic skin lesions or neoplasms. Female mice treated with aloe gel creams (3% and 6%) had significantly increased multiplicities of squamous cell neoplasms. There were no treatment-related effects on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity in mice treated with the whole leaf creams. In male mice exposed to SSL and treated with the 6% whole leaf cream, a significant increase was observed in the multiplicity of squamous cell neoplasms. Female mice exposed to SSL and treated with the 3% whole leaf creams had significantly decreased multiplicity of squamous cell nonneoplastic lesions and significantly increased multiplicity of squamous cell neoplasms. Female mice exposed to SSL and treated with the 6% whole leaf cream had significantly decreased multiplicity of squamous cell nonneoplastic lesions. The application of decolorized whole leaf creams to mice had no effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. Male mice administered the 3% decolorized whole leaf cream had significantly increased multiplicity of squamous cell neoplasms. Female mice administered the 3% decolorized whole leaf cream had significantly decreased multiplicity of squamous cell nonneoplastic skin lesions and significantly increased multiplicity of squamous cell neoplasms. In female mice that received the 6% decolorized whole leaf cream, there was a significant increase in the multiplicity of squamous cell neoplasms. As with the Aloe vera plant extracts, the application of aloe-emodin creams to mice had no measurable effect on body weights, survival, or the in-life observations of skin lesion onset, incidence, or multiplicity. The administration of aloe-emodin creams to male mice had no effect on the incidence or multiplicity of histopathology-determined nonneoplastic skin lesions or squamous cell neoplasms. Female mice treated with the 74.6 μg/g aloe-emodin cream had significantly decreased multiplicity of histopathology-determined squamous cell nonneoplastic skin lesions and significantly increased multiplicity of squamous cell neoplasms. CONCLUSIONS: these experiments investigated the potential of topical application of creams containing extracts of Aloe barbadensis Miller plant (aloe gel, whole leaf, or decolorized whole leaf) or aloe-emodin to alter the photocarcinogenic activity of filtered xenon arc simulated solar light (SSL) in male and female SKH-1 hairless mice. Data on skin lesions were collected both on digital images during the in-life phase and by histopathologic evaluation at necropsy. No effects of creams upon SSL-induced skin lesions were identified from data collected during the in-life phase. ALOE GEL OR ALOE-EMODIN: under the conditions of these studies, there was a weak enhancing effect of aloe gel or aloe-emodin on the photocarcinogenic activity of SSL in female but not in male SKH-1 mice based on an increase in the multiplicity of histopathologically-determined squamous cell neoplasms. ALOE WHOLE LEAF OR DECOLORIZED WHOLE LEAF: under the conditions of these studies, there was a weak enhancing effect of aloe whole leaf or decolorized whole leaf on the photocarcinogenic activity of SSL in both male and female SKH-1 mice based on an increase in the multiplicity of histopathologically-determined squamous cell neoplasms.     

紫外线的皮肤损伤机制及具有紫外线防护作用的天然产物的研究进展

皮肤长期暴露在紫外线下可以引起皮肤损伤,出现皮肤光老化甚至出现皮肤癌变和其他皮肤病变。紫外线引起的皮肤光老化的主要机制有:氧化应激、炎症反应、细胞凋亡、胶原和弹性蛋白的降解等。目前国内外关注的焦点是开发紫外线防护剂,目前主要研究的有黄酮类化合物、萜类化合物、鞣质类、香豆素类等。该文主要对紫外线的皮肤损伤机制及天然来源紫外线防护剂的研究进展进行综述。