皮肤光老化及其防治

1、皮肤光老化及其防治吴景东周鸿波辽宁中医学院110023皮老化是机体衰老的一局部,机体的衰老在皮肤上表现最清楚.皮肤老化分为有遗传因素及不可抗力因素如重力,机体内分泌及免疫功能随机体衰老的改变引起的固有老化又称自然老化或内源性老化；及有环境因素如紫外线,吸烟,风吹,接触化学物质引起的外源性老化,由于日光中紫外线长期反复照射是环境中影响皮肤老化的最重要因素,故外源性老化又指光老化.1紫外线与皮肤大量研究说明日光中的紫外线UVR与皮肤老化有着密切的关系,是“光老化中的最重要因素.根据UVR的波长和不同的生物学作用,分成三段：长波紫外线UVA波长320nm400n;中波紫外线UVB波长280nm320

2、nm;短波紫外线UVC波180nm280nm.波长短于160nm的紫外线被空气完全吸收,天然环境中几乎不存在.在自然界中,UVR约占太阳光、的13%,到达地面时,大局部UVB和几乎全部的UVC被大气平留层的臭氧层所吸收,因此,自然界的UVA约占97%UVB只占3%.对于地区上的生物来说,主要作用的是UVA和少量UVB.UVB照射皮肤可达表皮基地层,它可产生红斑效应,DNA损伤甚至诱发皮肤癌,UVA尽管能量底穿透力较强,可达真皮深部,UVAUVB在皮肤老化中起着重要彳用.先进认为UVA对皮肤DNA的损伤水平是UVB的30倍,且由于UVA比UVB更多,更容易到达真皮层,UVA是导致皮肤结缔组织重要

3、损伤的主要因素.2光老化的临床表现多表现为暴露皮肤松弛,粗深皱皮,结节皮革样外观,色素斑增多毛细血管扩张,原有几何外观明显改变或消失,肤色呈灰黄色,可发生各种良性,癌前期或恶性肿瘤.3光老化的组织形态学在组织形态学上,光损伤的表皮早期反映是过度增殖样修复,表皮增厚,细胞1/10异质性增强角质形成细胞急性消失晚期表现为表皮急性畏缩,照射部位皮肤黑素细胞增多,色素分布不均,郎葛罕细胞数量减少50%使得抗原体提升及加工水平下降,免疫功能受到限制,可使静止的肿瘤细胞逃避或超越机体的防御水平引起皮肤癌或癌性改变.还有研究说明,光老化部位皮肤电镜下可见葛罕细胞中birbeckds颗粒郎葛罕细胞中的特殊细胞

4、明显少于自然老化的皮肤光老化皮肤真皮改变明显.胶原减少,增粗,可溶性下降.弹力纤维增粗,卷曲,变性,绛解为颗粒或不定形团块,氨基多糖的结构种类均发生改变,功能异常,水合水平下降,过多的日晒使真皮附属器也有改变,小血管减少,血管壁变薄,汗腺数量减少,分泌汗腺水平下降,皮脂腺增生,但总皮脂分泌量减少.上述真皮结构的改变引发光暴露部位皮肤枯燥、皱纹较粗、较深、松弛及皮革样变.4光老化的发生机制4.1光老化与非酶糖基化反响：糖基化终末产物AGEs在体内积累,使相邻的大分子交联,尤其是引起胶原分子间交联.不但降低了结缔组织的通透性,使养料及废物的扩散性能减弱,组织硬度增加,而且难以被胶原酶水解,从而造成

5、皮肤弹性下降,皱纹不易平复而不断加深.Wondrak等通过体外实验验证了,在UVA引起的光老化皮肤过氧化反响中,非酶糖基化蛋白质是体内皮肤细胞紫外线过氧化损伤的光感物这一假说.4.2光化与皮肤免疫系统,紫外线照射通过多种途径引起免疫抑制造成皮肤感染性疾病恶化、皮肤衰老,甚至皮肤癌.UV抑制抗原的表达,刺激有免疫抑制作用的细胞因子的释放并引起有抑制表型的淋巴细胞产生.在光老化皮肤中,表皮郎格罕细胞的特征性改变使细胞数量减少、形态萎缩、缺乏树突形成和缺少Birbeck颗粒.4.3光老化与自由基学说：1956年,Harman提出了衰老的自由基学说.自由基具有极强的氧化水平,可使生物膜中不饱和脂类发生

6、过氧化,形成过氧化脂质,其中产物丙二醛MDA是强胶联剂.与蛋白质、核酸或脂类结成难溶性物质使生物膜硬化导致通透性降低,影响细胞物质交换,继而使之破裂死亡.自由基可改变胶原分子,使其易受酶的作用,使透明脂酸解聚,减少蛋白聚糖合成,降解基底膜等.UV的照射产生的自由基对机体内各种大分子都有损伤作用.它们可引起皮肤细胞过氧化,产生的自由基增多,并在皮肤中产生过氧化脂质,与皮肤中的胶原蛋白作用使皮肤角质化过度,使皮肤变的粗糙,松弛,出现皱纹等老化现象.但健康机体同时还存在着强2/10大的防护机制对抗自由基的损害.随年龄增长及各种外界环境的刺激,尤其是日光中的紫外线作用的损害,使体内抗氧化酶类减少.防护

7、功能减退或发生障碍,自由基累积性增加,造成体内各种大分子损伤,导致机体、皮肤的病变和衰老.4.4线粒体突变学说：线粒体DNA(mtDNA)是哺乳动物细胞内唯一的核外遗传物质,由于缺乏组蛋白保护及相应的修复系统,易受外界因素诱发突变并累积.线粒体DNA突变在人类衰老及许多退行性疾病中的作用已被广泛证实,线粒体DNA突变及累积被认为是人类皮肤老化尤其是皮肤光老化的重要因素.甚至有研究说明,氧自由基对生物膜及mtDNA的损害,使DNA的损害,使DNA突变和破裂,从而导致线粒体结构的改变和功能的退化,最终影响ATP的生成,能量供给缺乏而使机体代谢水平下降,发生一系列衰老变化.4.5细胞凋亡与皮肤光老化

8、：细胞凋亡时最突出的特征是细胞DNA的有控裂解.有许多研究资料显示这种有控裂程序的启动与“细胞凋亡相关基因有关研究发现bcl-2多位于细胞内氧自由基产生较多的位置和线粒体、内质网和核膜等,这与细胞的抗氧化自我保护不无关系.已经发现bcl-2基因是细胞凋亡研究中最受重视的癌基因之一,它不同于其他癌基因,是延长细胞的生命期限,通过阻断细胞凋亡信号传递系统的最后的共同通道抑制细胞凋亡从而促进细胞存活,是一种重要的细胞生存基因.Bax与bcl-2有高度的同源性,Bax过表达可以拮抗bcl-2的促进细胞生存的代表,二者表达水平之间的平衡结果,决定了细胞生存死亡.机体受到过量的紫外线的照射不仅是光老化的直

9、接原因,也可使体内的酶性的抗脂质过氧化机制遭到破坏,进一步导致和加剧光老化的进展.皮肤细胞在接触到过量的紫外线后形成的所谓“晒伤细胞就是凋亡的角质形成细胞.其中活性氧、脂质过氧化和原癌基因等的表达与调控起到非常重要的作用.4.6光老化的其它学说：基质合成与降解等.5光老化治疗的方法光老化的最好治疗方法是预防,即应该预防过度的日晒.我国人群的皮肤特点是易晒黑不易晒伤,因此对我们而言,预防紫外线危害很重要的防治UVA的危害.儿童期就应该开始重视预防过度的日光暴晒.最有效的方法就是适当的穿着、戴帽、打伞,并正规的使用广谱防晒剂.主要分为两大类一是非手术疗法：包括药物疗法、化学剥脱术、微波疗法、激光疗

10、法等.一是手术疗法：包括擦皮术、皮下填充术、面部整形术等(后两者3/10主要与皮肤自然老化的治疗.5.1抗氧化剂：抗氧化剂可以通过抑制紫外线所致DNA损伤,到达预防皮肤光老化的目的.主要的抗氧化剂为：谷胱甘肽,B-胡萝卜素,过氧化氢酶,SOD,其中以B-胡萝卜素和SOD的作用要显著.此外,还有一些抗氧化剂如三羟基苯乙烯多酚、 生姜提取物、 黄苓甘、黄氏提取物、芦荟等均可抗皮肤光老化.5.2内用防光剂：营养缺乏时易发生皮肤损伤,而补充维生素、类胡萝卜素和不饱和脂肪酸等营养素具有保护皮肤少受紫外线的作用.防晒剂5.3外用防光剂：紫外线吸收剂,以及使紫外线射的散射剂,或散射作用和吸收作用相结合的方法

11、.紫外线散射剂主要是利用某些无机物质对紫外线的散射或减少紫外线对皮肤的侵害.如高岭土、氧化锌、滑石粉、氧化钛及新型有机粉等.氧化钛及新型有机粉等.他们主要是在皮肤外表形成阻挡层,以防紫外线直接照射到皮肤上,但这种物质具有用量大,防晒效果差等缺点,过多使用易阻塞毛孔,造成皮肤的新疾病等不良后果.目前所说的防晒剂是指对紫外线具有吸收作用的紫外光吸收剂.它们的分子从紫外线中吸收的光能与引起分子“光化学激发所需要的能量相等,这样就可以把光能转化成热能或无害的可见光放射出来,从而有效地预防紫外线对皮肤的晒黑和晒伤作用.5.4化学剥脱术：化学剥脱也叫化学剥蚀,是将具有剥脱作用的化学涂剂于治疗区域,使之立即

12、发生角质层的的别离和蛋白凝固,而使表皮和真皮乳头不同程度的坏死而引起剥脱.基内幕胞层和真皮网状层以上受损,可通过上皮细胞的再生而自然愈合.皮肤剥脱术就是运用这一原理,除去病变皮肤的表层,包括皮肤癌前病变,软化瘗疮瘢痕.限制瘗疮,促进新生的健康上皮覆盖病变区,同时刺激皮肤弹力纤维收缩,使皮肤收紧,促进表浅皱纹消失.目前人们经常采用的化学剥脱剂根据剥脱创伤的程度分为3类,即表浅性、中度和深度.5.5微波疗法：原理是不同波长的微波作用与皮肤和皮下层次,可促进恢复皮弹性活力,刺激胶原纤维增生修复,此外,还可通过电离渗透作用,促进皮肤吸收水分营养,促进腺体活动,微循环和新陈代谢.5.6其他疗法：激光疗法

13、、擦皮术等.参考文献1.GichrestBA.AreviewofskinageinganditsmedicaltherapyJ.BrJ4/10Deramatol,1996:13(6):867-8752.CastanetJ,OrtonneJP.PigmentarychangesinagedandphotoagedskinJ.ArchDermatol,1997:133(10):1296-12993.LakerRM,GerbreickGF,Veresd,etalCumulativeeffectsfromrepeatedexposurestosuberythemaldoesforUVBandUVAin

14、humanskinJ.JAmacaddermatol,1995,32:53-62.4.wondrakGTet,al.Photosensitizedgrowthinhibitionofculturedhumanskincells:mechanismandsuppressionofoxidativesyressfromsolarirradiationofglycatedproteins.JInvestDermatol2022Aug;119(2):489-985.SchwarzT.Photoinmiunosuppression.PhotodermatalPhotoinhunolPhotomed202

15、2Jun;18(3):141-56.GreweM.ChronologicalageingandPhotoageingofdendriticcells.ClinExpDermatol2001Oct;26(7):608-127.刘承煌.皮肤病理生理学M.北京：中国医药科技出版社,1991.37-338.MiquelJ.CanAntioxidantdritesupplementionprotectagainstage-relatedmitochondrialdaamage?J.AnnNYAcadSci,2022,959:508.9.FryerM.Evidenceforthephotoprotecti

16、veeffectsofVitaminEJ.PhotochemPhotobiol,1993,58:304.10.刘仲荣等.线粒体DNA突变与皮肤老化.国外医学皮肤性病学分册,2022:29(3):173-17611.Brirch-MachinMAetal.JInvestDermatol,1998:110(2):149-15212.曾昭惠等.自由基氧化致线粒体DNA损伤与细胞凋亡.国外医学临床生物与检验学分册,1999:20.(4):167-168?皮肤光老化及其防治?一文,对皮肤光老化的发病机理,从生理、生化、组织学与胚胎学等方面,进行了详尽专业科学的陈述,参考文献、资料真实可靠,具有很强的专业

17、性,对皮肤光老化的治疗方法的阐述也十分全面、可行、收效良好.TheAgingoftheSkinanditsPreventionandCure5/10WuJingdong,ZhouHongboLiaoningCollegeofTraditionalChineseMedicine110023Theagingoftheskinisapartoforganismsenileandthesenileoftheorganismappearsmostclearlyontheskin.Theagingoftheskincanbedividedintwocategories,oneisintrinsicagin

18、galsocallednaturalagingorendogenousagingcausedbyheredityfactorandthefactorthatcannotbeavoid(suchasgravity,endocrineoftheorganismandimmunityfunctionchangewithOrganismsenile).Theotherisexogenousagingcausedenvironmentfactorsuchasultravioletray,smoking,windblowing,chemicalsubstancecontacting.Becausethel

19、ong-termandrepeatshinningofultravioletrayinsunlightisthemostimportantfactorthataffectstheagingoftheskin,soexogenousagingisalsocalledsunlightaging.1. UltravioletRayadSkin:Lotsofresearchhavemadeclearlythattheultravioletray(UVR)inlighthascloserelationshipwithagingofskin,whichisthemostimportantelementin

20、lightaging.AccordinthelengthofUVRanddifferentbiologicalfunction,Itcanbedividedintothreewavebands,theyarelongwaveultravioletray(UVA)whichwavelengthis320nm400mn,mediumwaveultravioletray(UVA)whichwavelengthis280nm320nmandshortwaveultravioletray(UVC)whichwavelengthis180nm28nm.Theultravioletraywhosewavel

21、engthisshorterthan160nmwillbeadsorbedbyaircompletely,whichalmostcantbefoundinnaturalenvironment.Innaturalenvironment,UVRtakesupabout13%ofthelight.Whenreachingtheearth,mostoftheUVRandalmostalltheUVCisabsorbedbyO3.Inthestratosphereoftheair,so,thereisabout97%UVA,whilethereisonly3%UVBinthenature.Asforth

22、ecreaturesontheearth,whichmainlyhaveaffectiononthemisUVAandalittleUVB,UVBcanreachthebasallaminaoftheepidermiswhenitirradiatetheskin,anditcanproduceerythrismeffect,DNAdamagingeveninducingcarcinomacutis.AlthoughUVAislowinenergyandhasstrongpenetratingpowercanreachbasallaminaofthecoriumlesion,VVBhasgrea

23、timportantfunctioninskinaging,ItisbelievedthatthedamagepowerofUVRtotheDNAoftheskinis30timesasmuchasthatoftheUVB,andbecauseUVAcanreachthecoriumlayermoreinamounteasierthanUVB,UVAisthemainfactorwhichleadstotheseveredamageofconnectivetissueoftheskin.2. ClinicalManifestationsofAgingofSkin:Itusuallyappear

24、sasthedermatolysisofexposurepart,wideanddeepwrinkle,tuberculumparchment-likeoutwardappearance,increasingpigmentedspots,capillarectasia,obviouschangingordisappearingoftheoriginalgeometricalfigure,theskinusuallyappearsyellowandgrey,alsoitcanproduceallkindsofbenign,precancerousinjuryormalignanttumor.3.

25、 HistomorphologyChangeofSkinAging:Inhistomorphology,theprematurereactionoflightinjuredskinisoverproliferous,renovation,theepidernbecomingthicker,cellheterogeneityincreasingcutiontaking-shapeandcellpolarity,itappearsasthesevereatrophyoftheepidern.skinmelancyteincreasesinthepartthatisirradiated,pigmen

26、tmisdistribution,theamountcausesantigenincreasingandprocessingabilitydescending,restrainingimmunologicfunctionandmakingquiescentcelltumourandleadingtoskinprecancerpathologicchangingpowerandleadingtoskinprecancerpathologicchangingorcarcinouspathologicchanging,alsomakingclearthatwecanseeBirbecksgranul

27、einlangerhanscell(specialcellorganinlangerhanscell)lessthantheseofnaturalagingskinobviously.Coriumchangesapparentlyonlightagingskin.Collagenreducesandbecamethickerandsolubilitydescending.Elasticfiberswillbecomethicker,crimping,clenaturating,degradatingintogranularballorunsettingball.Thestructure6/10

28、ofamino-grouppolysaccharide(GAGS),typesallchanges,anddysfunctionappears,hydratedescending,anddysfunctionappear,hydratedescendingexcesssunlightmakescoriumaccessoryorganhavesomechanges,suchassmallvesselsreduce,vascularbecomethinner,thenumberofsweatglanddecrease,thepowerofsecretingsweatdescendingandseb

29、aceousglandsproliferatingwhichthetotalamountofsebumsecretingdescending.Above-mentionedchangesofcoriumstructurecaninitiatetheregionoftheskinthatexposingbelowthesunlighttobedry,flabbilyparchment-likeandhavethickanddeepwrinkle.4. OccurrenceMechanismofLightAging4.1Lightagingandnon-fermentglycosylationre

30、action:theproductofglycosylation,whichaccumulatesinhumanbodymakesadjacentmacromolecularcrosslinkwitheachother,especiallymakescollagenmoleculecrosslinkwitheachother.Notonlydoesitmakethepermeabilitydescendbutalsomakethespreadingnatureoftrashandnutrimentdescend,enhancethetissuehardnesstomakeithardbehyd

31、rolysisedcollagenasewhichcausingskinresiliencytodescend,thewrinklehardtobesmoothedandbecamedeepcontinuously.Wondrakandothersprovedthehypothesisbyexperimentthatnon-glycosylationproteinisthephotophilproductoftheperoxidationinjuryoftheskincellultravioletrayintheperoxidationoflightagingskincausedbyUVA.4

32、.2LightAgingandSkinImmunologicSystem:Ultravioletraycausesimmunologicrestrainedwhichleadingtoexacerbationofskininfectiveillnessoftheskinevencarcinomacutisthroughmanyways.Uvcanretraintheexpressionoftheskinandstimulatethereleasingofthecellfactorwhichhasimmunsuppressionfunctionandcausestheproducingofthe

33、lymphocyteswhichhaveantigenicphenotypic.Inthelightagingskin,thecharacteristiclesionsoftheepidermisLangeHanscellmakestheamountofcellsreduce,itsfigureatrophies,deficitstheformingofthedendriteandbelackofBirbeckgranule.4.3LightAgingandFreeRadicalTheory:In1956,Harmanputforwardsenilefreeradicaltheory.Free

34、radicalhasextremelystrongoxidationpowers,whichcanoxidatedthelipidinbiologicalmembranesandformintooxidatedesterwhichterminalproduct(MDA)isstrongcement,anditcanmixwithprotein,nucleicacidformingintodysubstancemakingbiologicalmerebraneleadingintothedescendingofitspermeabilityandaffectingthecellexchanges

35、ofsubstancethenmakingitraptureanddie.Freeradicalcanchangecollagenmolecule,makingittobeaffectedbyfermentandhyaluronicaciddegradated,reducingtheproducingofthealbumenpolysugar,depredatingbasementmembraneandsoon.ThefreeradicalisproducebytheirradiationoftheUVcandamageallkindsofmacromolecularinthehumanbod

36、y.Theycancausetheskincelltobeoxidated,thefreeradicalproducedbytobeexcess,andproducesperoxidationlipidintheskinandmakestheskinloseitsresiliencywiththefunctionofthecollagenalbumenIntheskin,alsothetreeradicalcanmakeelasticfiberscrosslinkandpolymerizewhichcausingthedegradationofelastinandcollagenleading

37、totheexcesscornificationoftheskin,makingtheskinrough,relaxingandwrinkle,agingphenomenonappearance.Butthereisthedamageoftheresistivefreeradicalcausedbythepowerfulprotectionsystemexistsinthehealthorganismatthesametimewiththeincreasingoftheageandallkindsofoutsidestimulatationespeciallythedamagecausedby

38、theactionoftheultravioletrayinthesunlightmakestheresistiveoxidationfermentreduceinhumanbody,protectionpowergodownoroccurrenceofthedisturbance,accumulateactionoffreeradicalincreasewhichcausingthedamageofthemacromolecularinhumanbodyleadingtothe7/10pathologicalchangesandsenilityoftheskinandorgansm.4.4.

39、MitochondrionMutationTheory:mitochondrionDNA(mtDNA)istheonlyextranuclearinmammalcell.Itiseasytobeindictedtomutatebyouterspherefactor,becauseoflackingoftissueprotectionandhomologuesrenotationsystem.Thefunctionofmitochondrionmutationinhumanbeingsenileandmanyretrogradeillnessesisdiffuselyproved,mitocho

40、ndrionDNAmutationandaccumulatingisalsoconsideredastheimportantfactorinagingoftheskinespeciallylightagingoftheskin.EvenresearchshowsclearlythattheincidenceoftheMitochondrionDNAmutationhasnothingtodowithagebuthascloserelationwiththedegreeoflightagingoftheskin.Theexperimenthasalsoprovedthatthedamageoft

41、heoxygenfreeradicaltobiologicalmembraneandmitDNAmakesDNAmutateandsplit,whichcausethechangeofthestructureanddogenerationofthefunctionofthemitochondrionandfinallyaffecttheproducingofATP,lackingofenergysupplyleadingtothedescendingoforganismsupersessionabilityandaccruingaserialsofsenilechangesreveal.4.5

42、TheWitheroftheCellandLightageingoftheSkin:themostout-standingfeatureofthecellisthecontrolledsplittingofthecellDNA.manyresearchmaterialsrevealthatthestartofthiscontrolledsplittinghassomethingtodowiththecorrelationgeneofthewitheringanddeathofthecell.Theresearchfoundthatbcl-2usuallylocatesintheplacewhe

43、recanproducemoreoxygenfreeradicalsuchasmitochondrion,endoplasmic,reticulumandsoon,whichhavesomerelationwiththeprotectionofthecell.Wehavealreadyfoundthatbcl-2geneisoneoncogeneinthereassertofwitheringofthecellwhichisdifferentwiththeothergeneandcanextendthelifetermofthecell,itrestrainthecellwitheringby

44、blockingthecommonthoroughfareofthedeliveringsystemofthewitheringsignaltoadvancethesurvivalofthecellandisaimportantcellexistinggene.Baxandbcl-2havehighlyautophoidy.TheexcessexpressionoftheBaxcanresistthefunctionofbel-2whichcanadvancethegenerationofthecellandrestrainofthewitheringofthecell.Bax/bal*whi

45、chactsastherepresentationofthedeathgeneofthecellwhilebcl-2actsastherepresentationofthecell,theresultoftheirbalancebetweentheirlevelofexpressiondeterminesthecellshouldexistorbedead.Theexcessultravioletrayirradiatingtotheorgansmisnotonlythedirectreasonforlightagingbutalsocandamagetheperoxidationmechan

46、ismoftheresistiveesterqualityofthefermentqualityornon-fermentqualitywhichcausesandexacerbatetheadvanceofthelightaging.Thecelloftheskincanformintowhatiscalledsunburnedcellthatiswitheredcutinformingcellwhencontactingwithexcessultravioletray.Theexpressionandregulationoftheoxidationprimitivecancerandsoo

47、ninithaveextremelyimportantfunction.4.6TheOtherTheoryOfLightAging:thecompoundinganddegradationoftheradical.5. TheTreatmentforthePhotoagedSkin:Thebesttreatmentforlightagingistoprevent,thatistoavoidover-basked.ThetraitfortheskinofChineseisthatitiseasytobesun-bannedbutnotsun-burned.Soitismoreimportantf

48、orustopreventtheharmfulnessofUVAwhenwearepreventingandcuringthedangeroftheultravioletray.Andweshouldpaymoreattractiontoavoidover-baskedinthesunbeameveninourchildhood.Tiisreportedthatthemostefficientmethodistowearproperly,applysun-tancreamregularly,andtakeanumbrellawithyouwhenyouareout.Thetreatmentis

49、mainlydividedintotwotypes:oneisunoperationaltreatmentsuchas8/10pharmacotherapy,chemicaldenudation,Microwavetherapy,lasertherapyandsoon.Anotherisoperationaltreatmentsuchasclermabrasion,subcutaneousenthesisfacialplasticoperationandsoon.5.1 Anti-oxidant:Anti-oxidantcanleadtodamageofDNAbycontrollingultr

50、avioletray;servethepurposetopreventlightagingofskin.Themainanti-oxidantare:tathion,3-carotene,permanganate,SOD,especiallythe-caroteneandSOD,whichfunctionisremarkable.Furthermore,therearesomeotherssuchasginger-extract,scutellariaastragalus-extract,aloeandsoon.Allofthemcanpreventthelightagingofskin.5.

51、2 Light-proofAgentforInternalUse:Malnutritioncaneasilycauseskininjury,whilesupplyingvitamin,carotenoid,unsaturatedfattyacidandsomeotherkindsofnutrientallcankeepskinfromultravioletrayinjury.5.3 Light-proofAgentforExternalUse:Ultravioletrayabsorbent,thescatteringagentwhichcanmakesun-rayscatter,andsome

52、othermediumwhichcombinesscatteringfunctionandabsorptiontogether.Ultravioletrayscatteringagentmainlymakesuseofthefunctionofscatteringorreflexofsomeinorganicsubstancetoultravioletraytoreducetheskininjuryformsun-ray,forinstance,kaolin,zineoxide,talcumpowder,titaniumoxide,neworganicpowderandsoon.Theycou

53、ldformaresistantlayertopreventultravioletrayirradiatetheskindirectly,butitalsohasmanydisadvantages,suchaslargedosage,beinglessinsun-tanfunction,excessusingcaneasilycausesomeharmfulresultssuchasmakingporeclogged,newdiseaseoftheskinandsoon.Sofar,thesun-tanmediumweoftenmentionistheultravioletlightabsor

54、bentwhichcanabsorbultravioletray.Andthelightenergywhichgetsformsun-raybyitsmoleculesisequaltotheenergythePhotochemicalExcitation“needed.Sointhisway,itcanconvertlightenergyintothermalenergyorvisiblelightandsendthemouttopreventskinfromsun-tannedorsun-burntbysun-rayefficiently.5.4 ChemicalDenudation:Ch

55、emicaldenudationalsonamedChemicaldecollement.Itreferstoapplytheexfoliatingchemicalinunctumonthetherapeuticregionevenly,andthenitcanseparatefromstratumcorneumandsolidifytheproteinimmediately,causingepidermisanddermalpapillaetodieatdifferentdegreewhichleadingdenudation.Iftheregionabovethestratumbasale

56、andthedermalreticularlayergetdamaged,itcanhealnaturallybythenewbornepitheliumcells.Skindenudationjustapplythistenet,strippingoffthesurfacelayerofthepathologicchangesoftheskin,likethediseaseasskincanceration,makingtheacheandscarsoft,controllingtheache,advancingthehealthnewbornepitheliumtocoverthetherapeuticarea,andstimulatingtheelasticfibertosystole,tighteninguptheskin,makingthewrinklesdisappear.TheChemicaldenudationwhichisadoptedatpresen