1、精選優(yōu)質(zhì)文檔-傾情為你奉上皮膚光老化及其防治吳景東 周鴻波遼寧中醫(yī)學(xué)院 皮老化是機(jī)體衰老的一部分，機(jī)體的衰老在皮膚上表現(xiàn)最清楚。皮膚老化分為有遺傳因素及不可抗力因素（如重力，機(jī)體內(nèi)分泌及免疫功能隨機(jī)體衰老的改變）引起的固有老化又稱自然老化或內(nèi)源性老化；及有環(huán)境因素如紫外線，吸煙，風(fēng)吹，接觸化學(xué)物質(zhì)引起的外源性老化，由于日光中紫外線長(zhǎng)期反復(fù)照射是環(huán)境中影響皮膚老化的最重要因素，故外源性老化又指光老化。1 紫外線與皮膚大量研究表明日光中的紫外線（UVR）與皮膚老化有著密切的關(guān)系，是“光老化”中的最重要因素。根據(jù)UVR的波長(zhǎng)和不同的生物學(xué)作用，分成三段：長(zhǎng)波紫外線（UVA）波長(zhǎng)320nm400n；中

2、波紫外線UVB波長(zhǎng)280nm320nm;短波紫外線UVC波180nm280nm。波長(zhǎng)短于160nm的紫外線被空氣完全吸收,天然環(huán)境中幾乎不存在。在自然界中，UVR約占太陽(yáng)光、的13%,到達(dá)地面時(shí)，大部分UVB和幾乎全部的UVC被大氣平留層的臭氧層所吸收，因此，自然界的UVA約占97%UVB只占3%。對(duì)于地區(qū)上的生物來(lái)說(shuō)，主要作用的是UVA和少量UVB。UVB照射皮膚可達(dá)表皮基地層，它可產(chǎn)生紅斑效應(yīng)，DNA損傷甚至誘發(fā)皮膚癌,UVA盡管能量底穿透力較強(qiáng)，可達(dá)真皮深部，UVA UVB在皮膚老化中起著重要作用。先進(jìn)認(rèn)為UVA對(duì)皮膚DNA的損傷能力是UVB的30倍，且由于UVA比UVB更多，更容易達(dá)到

3、真皮層，UVA是導(dǎo)致皮膚結(jié)締組織重要損傷的主要因素。.2 光老化的臨床表現(xiàn)多表現(xiàn)為暴露皮膚松弛，粗深皺皮，結(jié)節(jié)皮革樣外觀，色素斑增多毛細(xì)血管擴(kuò)張，原有幾何外觀明顯改變或消失，膚色呈灰黃色，可發(fā)生各種良性，癌前期或惡性腫瘤。3 光老化的組織形態(tài)學(xué)在組織形態(tài)學(xué)上，光損傷的表皮早期反映是過(guò)度增殖樣修復(fù)，表皮增厚，細(xì)胞異質(zhì)性增強(qiáng)角質(zhì)形成細(xì)胞急性消失晚期表現(xiàn)為表皮急性畏縮，照射部位皮膚黑素細(xì)胞增多，色素分布不均，郎葛罕細(xì)胞數(shù)量減少50%使得抗原體提升及加工能力下降，免疫功能受到限制，可使靜止的腫瘤細(xì)胞逃避或超越機(jī)體的防御能力引起皮膚癌或癌性改變。還有研究表明，光老化部位皮膚電鏡下可見葛罕細(xì)胞中birbe

4、ckds顆粒(郎葛罕細(xì)胞中的特殊細(xì)胞)明顯少于自然老化的皮膚光老化皮膚真皮改變明顯。膠原減少，增粗，可溶性下降。彈力纖維增粗，卷曲，變性，絳解為顆?；虿欢ㄐ螆F(tuán)塊，氨基多糖的結(jié)構(gòu)種類均發(fā)生改變，功能異常，水合能力下降，過(guò)多的日曬使真皮附屬器也有改變，小血管減少，血管壁變薄，汗腺數(shù)量減少，分泌汗腺能力下降，皮脂腺增生，但總皮脂分泌量減少。上述真皮結(jié)構(gòu)的改變引發(fā)光暴露部位皮膚干燥、皺紋較粗、較深、松弛及皮革樣變。4 光老化的發(fā)生機(jī)制4.1光老化與非酶糖基化反應(yīng)：糖基化終末產(chǎn)物（AGEs）在體內(nèi)積累，使相鄰的大分子交聯(lián)，尤其是引起膠原分子間交聯(lián)。不但降低了結(jié)締組織的通透性，使養(yǎng)料及廢物的擴(kuò)散性能減弱，

5、組織硬度增加，而且難以被膠原酶水解，從而造成皮膚彈性下降，皺紋不易平復(fù)而不斷加深。Wondrak等通過(guò)體外實(shí)驗(yàn)驗(yàn)證了，在UVA引起的光老化皮膚過(guò)氧化反應(yīng)中，非酶糖基化蛋白質(zhì)是體內(nèi)皮膚細(xì)胞紫外線過(guò)氧化損傷的光感物這一假說(shuō)。 4.2光化與皮膚免疫系統(tǒng)，紫外線照射通過(guò)多種途徑引起免疫抑制造成皮膚感染性疾病惡化、皮膚衰老，甚至皮膚癌。UV抑制抗原的表達(dá)，刺激有免疫抑制作用的細(xì)胞因子的釋放并引起有抑制表型的淋巴細(xì)胞產(chǎn)生。在光老化皮膚中，表皮郎格罕細(xì)胞的特征性改變使細(xì)胞數(shù)量減少、形態(tài)萎縮、缺乏樹突形成和缺少Birbeck顆粒。 4.3 光老化與自由基學(xué)說(shuō)：1956年，Harman提出了衰老的自由基學(xué)說(shuō)。自

6、由基具有極強(qiáng)的氧化能力，可使生物膜中不飽和脂類發(fā)生過(guò)氧化，形成過(guò)氧化脂質(zhì)，其中產(chǎn)物丙二醛（MDA）是強(qiáng)膠聯(lián)劑。與蛋白質(zhì)、核酸或脂類結(jié)成難溶性物質(zhì)使生物膜硬化導(dǎo)致通透性降低，影響細(xì)胞物質(zhì)交換，繼而使之破裂死亡。自由基可改變膠原分子，使其易受酶的作用，使透明脂酸解聚，減少蛋白聚糖合成，降解基底膜等。UV的照射產(chǎn)生的自由基對(duì)機(jī)體內(nèi)各種大分子都有損傷作用。它們可引起皮膚細(xì)胞過(guò)氧化，產(chǎn)生的自由基增多，并在皮膚中產(chǎn)生過(guò)氧化脂質(zhì)，與皮膚中的膠原蛋白作用使皮膚角質(zhì)化過(guò)度，使皮膚變的粗糙，松弛，出現(xiàn)皺紋等老化現(xiàn)象。但健康機(jī)體同時(shí)還存在著強(qiáng)大的防護(hù)機(jī)制對(duì)抗自由基的損害。隨年齡增長(zhǎng)及各種外界環(huán)境的刺激，尤其是日光中

7、的紫外線作用的損害，使體內(nèi)抗氧化酶類減少。防護(hù)功能減退或發(fā)生障礙，自由基累積性增加，造成體內(nèi)各種大分子損傷，導(dǎo)致機(jī)體、皮膚的病變和衰老。 4.4 線粒體突變學(xué)說(shuō)：線粒體DNA（mtDNA）是哺乳動(dòng)物細(xì)胞內(nèi)唯一的核外遺傳物質(zhì)，由于缺乏組蛋白保護(hù)及相應(yīng)的修復(fù)系統(tǒng)，易受外界因素誘發(fā)突變并累積。線粒體DNA突變?cè)谌祟愃ダ霞霸S多退行性疾病中的作用已被廣泛證實(shí)，線粒體DNA突變及累積被認(rèn)為是人類皮膚老化尤其是皮膚光老化的重要因素。甚至有研究表明，氧自由基對(duì)生物膜及mtDNA的損害，使DNA的損害，使DNA突變和破裂，從而導(dǎo)致線粒體結(jié)構(gòu)的改變和功能的退化，最終影響ATP的生成，能量供應(yīng)不足而使機(jī)體代謝能力下

8、降，發(fā)生一系列衰老變化。 4.5 細(xì)胞凋亡與皮膚光老化：細(xì)胞凋亡時(shí)最突出的特征是細(xì)胞DNA的有控裂解。有許多研究資料顯示這種有控裂程序的啟動(dòng)與“細(xì)胞凋亡相關(guān)基因”有關(guān)研究發(fā)現(xiàn)bcl-2多位于細(xì)胞內(nèi)氧自由基產(chǎn)生較多的位置和線粒體、內(nèi)質(zhì)網(wǎng)和核膜等，這與細(xì)胞的抗氧化自我保護(hù)不無(wú)關(guān)系。已經(jīng)發(fā)現(xiàn)bcl-2基因是細(xì)胞凋亡研究中最受重視的癌基因之一，它不同于其他癌基因，是延長(zhǎng)細(xì)胞的生命期限，通過(guò)阻斷細(xì)胞凋亡信號(hào)傳遞系統(tǒng)的最后的共同通道抑制細(xì)胞凋亡從而促進(jìn)細(xì)胞存活，是一種重要的細(xì)胞生存基因。Bax與bcl-2有高度的同源性，Bax過(guò)表達(dá)可以拮抗bcl-2的促進(jìn)細(xì)胞生存的代表，二者表達(dá)水平之間的平衡結(jié)果，決定了

9、細(xì)胞生存死亡。機(jī)體受到過(guò)量的紫外線的照射不僅是光老化的直接原因，也可使體內(nèi)的酶性的抗脂質(zhì)過(guò)氧化機(jī)制遭到破壞，進(jìn)一步導(dǎo)致和加劇光老化的進(jìn)展。皮膚細(xì)胞在接觸到過(guò)量的紫外線后形成的所謂“曬傷細(xì)胞”就是凋亡的角質(zhì)形成細(xì)胞。其中活性氧、脂質(zhì)過(guò)氧化和原癌基因等的表達(dá)與調(diào)控起到非常重要的作用。4.6光老化的其它學(xué)說(shuō)：基質(zhì)合成與降解等。5 光老化治療的方法 光老化的最好治療方法是預(yù)防，即應(yīng)該避免過(guò)度的日曬。我國(guó)人群的皮膚特點(diǎn)是易曬黑不易曬傷，因此對(duì)我們而言，防止紫外線危害很重要的防治UVA的危害。兒童期就應(yīng)該開始重視避免過(guò)度的日光暴曬。最有效的方法就是適當(dāng)?shù)拇┲?、戴帽、打傘，并正?guī)的使用廣譜防曬劑。主要分為兩

10、大類一是非手術(shù)療法：包括藥物療法、化學(xué)剝脫術(shù)、微波療法、激光療法等。一是手術(shù)療法：包括擦皮術(shù)、皮下填充術(shù)、面部整形術(shù)等（后兩者主要與皮膚自然老化的治療）。5.1抗氧化劑：抗氧化劑可以通過(guò)抑制紫外線所致DNA損傷，達(dá)到防止皮膚光老化的目的。主要的抗氧化劑為：谷胱甘肽，B-胡蘿卜素，過(guò)氧化氫酶，SOD，其中以B-胡蘿卜素和SOD的作用要顯著。此外，還有一些抗氧化劑如三羥基苯乙烯多酚、生姜提取物、黃芩甘、黃氏提取物、蘆薈等均可抗皮膚光老化。5.2內(nèi)用防光劑：營(yíng)養(yǎng)缺乏時(shí)易發(fā)生皮膚損傷，而補(bǔ)充維生素、類胡蘿卜素和不飽和脂肪酸等營(yíng)養(yǎng)素具有保護(hù)皮膚少受紫外線的作用。防曬劑5.3外用防光劑：紫外線吸收劑，以及

11、使紫外線射的散射劑，或散射作用和吸收作用相結(jié)合的方法。紫外線散射劑主要是利用某些無(wú)機(jī)物質(zhì)對(duì)紫外線的散射或減少紫外線對(duì)皮膚的侵害。如高嶺土、氧化鋅、滑石粉、氧化鈦及新型有機(jī)粉等。氧化鈦及新型有機(jī)粉等。他們主要是在皮膚表面形成阻擋層，以防紫外線直接照射到皮膚上，但這種物質(zhì)具有用量大，防曬效果差等缺點(diǎn)，過(guò)多使用易阻塞毛孔，造成皮膚的新疾病等不良后果。目前所說(shuō)的防曬劑是指對(duì)紫外線具有吸收作用的紫外光吸收劑。它們的分子從紫外線中吸收的光能與引起分子“光化學(xué)激發(fā)”所需要的能量相等，這樣就可以把光能轉(zhuǎn)化成熱能或無(wú)害的可見光放射出來(lái)，從而有效地防止紫外線對(duì)皮膚的曬黑和曬傷作用。5.4 化學(xué)剝脫術(shù)：化學(xué)剝脫也叫

12、化學(xué)剝蝕，是將具有剝脫作用的化學(xué)涂劑于治療區(qū)域，使之立即發(fā)生角質(zhì)層的的分離和蛋白凝固，而使表皮和真皮乳頭不同程度的壞死而引起剝脫?；准?xì)胞層和真皮網(wǎng)狀層以上受損，可通過(guò)上皮細(xì)胞的再生而自然愈合。皮膚剝脫術(shù)就是運(yùn)用這一原理，除去病變皮膚的表層，包括皮膚癌前病變，軟化痤瘡瘢痕?？刂起畀彛龠M(jìn)新生的健康上皮覆蓋病變區(qū)，同時(shí)刺激皮膚彈力纖維收縮，使皮膚收緊，促進(jìn)表淺皺紋消失。目前人們經(jīng)常采用的化學(xué)剝脫劑按照剝脫創(chuàng)傷的程度分為3類，即表淺性、中度和深度。5.5 微波療法：原理是不同波長(zhǎng)的微波作用與皮膚和皮下層次，可促進(jìn)恢復(fù)皮彈性活力，刺激膠原纖維增生修復(fù)，此外，還可通過(guò)電離滲透作用，促進(jìn)皮膚吸收水分營(yíng)養(yǎng)

13、，促進(jìn)腺體活動(dòng)，微循環(huán)和新陳代謝。5.6 其他療法：激光療法、擦皮術(shù)等。參考文獻(xiàn)1. Gichrest BA. A review of skin ageing and its medical therapy J .Br J Deramatol, 1996:13(6):867-8752. Castanet J, Ortonne JP. Pigmentary changes in aged and photoaged skin J.Arch Dermatol,1997:133(10):1296-12993. Laker RM,Gerbreick GF, Veres d,et alCumulativ

14、e effects from repeated exposures tosuberythe mal does for UVB and UVA in hu man skinJ.J Am acad dermatol , 1995,32:53-62.4. wondrak GT et,al. Photosensitized growth inhibition of cultured human skincells: mechanism and suppression of oxidative syress from solar irradiation of glycated proteins.J In

15、vest Dermatol 2002 Aug;119(2):489-985. Schwarz T.Photoinmiunosuppression.Photodermatal Photoinhunol Photomed 2002Jun;18(3):141-56. GreweM.Chronological ageing and Photoageing of dendritic cells. Clin Exp Dermatol 2001Oct;26(7):608-127. 劉承煌。皮膚病理生理學(xué)M.北京：中國(guó)醫(yī)藥科技出版社，1991.37-338. Miquel J. Can Antioxidant

16、 drite supplemention protect against age-related mitochondrialdaamage?J. Ann N Y Acad Sci,2002,959:508.9. Fryer M. Evidence for the photoprotect ive effects of Vitamin E J. Photochem Photobiol,1993,58:304.10. 劉仲榮 等.線粒體DNA突變與皮膚老化.國(guó)外醫(yī)學(xué)皮膚性病學(xué)分冊(cè)，2003： 29（3）：173-17611. Brirch-Machin MA et al. J Invest Der

17、matol,1998:110(2):149-15212. 曾昭惠 等.自由基氧化致線粒體DNA損傷與細(xì)胞凋亡.國(guó)外醫(yī)學(xué)臨床生物與檢驗(yàn)學(xué)分冊(cè)，1999：20. （4）：167-168皮膚光老化及其防治一文，對(duì)皮膚光老化的發(fā)病機(jī)理，從生理、生化、組織學(xué)與胚胎學(xué)等方面，進(jìn)行了詳盡專業(yè)科學(xué)的陳述，參考文獻(xiàn)、資料真實(shí)可靠，具有很強(qiáng)的專業(yè)性，對(duì)皮膚光老化的治療方法的闡述也十分全面、可行、收效良好。 The Aging of the Skin and its Prevention and Cure Wu Jingdong, ZhouHongbo Liaoning College of Traditional

18、 Chinese Medicine The aging of the skin is a part of organism senile and the senile of the organism appears most clearly on the skin. The aging of the skin can be divided in two categories , one is intrinsic aging also called natural aging or endogenous aging caused by heredity factor and the factor

19、 that can not be avoid ( such as gravity ,endocrine of the organism and immunity function change with Organism senile ) . The other is exogenous aging caused environment factor such as ultraviolet ray, smoking, wind blowing, chemical substance contacting. Because the long-term and repeat shinning of

20、 ultraviolet ray in sunlight is the most important factor that affects the aging of the skin, so exogenous aging is also called sunlight aging.1. Ultraviolet Ray ad Skin: Lots of research have made clearly that the ultraviolet ray (UVR) in light has close relationship with aging of skin, which is th

21、e most important element in “l(fā)ight aging”. According the length of UVR and different biological function, It can be divided into three wave bands， they are long wave ultraviolet ray ( UVA ) which wavelength is 320nm400mn ,medium wave ultraviolet ray (UVA ) which wavelength is 280nm320nm and short wa

22、ve ultraviolet ray (UVC ) which wavelength is 180nm28nm.The ultraviolet ray whose wavelength is shorter than 160nm will be adsorbed by air completely, which almost cant be found in natural environment. In natural environment, UVR takes up about 13% of the light .When reaching the earth, most of the

23、UVR and almost all the UVC is absorbed by O3. In the stratosphere of the air, so, there is about 97% UVA, while there is only 3% UVB in the nature .As for the creatures on the earth, which mainly have affection on them is UVA and a little UVB, UVB can reach the basal lamina of the epidermis when it

24、irradiate the skin, and it can produce erythrism effect, DNA damaging even inducing carcinoma cutis. Although UVA is low in energy and has strong penetrating power can reach basal lamina of the corium lesion, VVB has great important function in skin aging, It is believed that the damage power of UVR

25、 to the DNA of the skin is 30 times as much as that of the UVB, and because UVA can reach the corium layer more in amount easier than UVB, UVA is the main factor which leads to the severe damage of connective tissue of the skin.2. Clinical Manifestations of Aging of Skin: It usually appears as the d

26、ermatolysis of exposure part, wide and deep wrinkle, tuberculum parchment-like outward appearance, increasing pigmented spots, capillare ctasia, obvious changing or disappearing of the original geometrical figure, the skin usually appears yellow and grey, also it can produce all kinds of benign , pr

27、ecancerous injury or malignant tumor. 3. Histomorphology Change of Skin Aging: In his to morphology, the premature reaction of light injured skin is over proliferous, renovation, the epidern becoming thicker, cell heterogeneity increasing cut ion taking-shape and cell polarity, it appears as the sev

28、ere atrophy of the epidern. skin melancyte increases in the part that is irradiated, pigment misdistribution, the amount causes antigen increasing and processing ability descending, restraining immunologic function and making quiescent cell tumour and leading to skin precancer pathologic changing po

29、wer and leading to skin precancer pathologic changing or carcinous pathologic changing, also making clear that we can see Birbecks granule in langerhans cell (special cell organ in langerhans cell ) less than these of natural aging skin obviously. Corium changes apparently on light aging skin. Colla

30、gen reduces and became thicker and solubility descending. Elastic fibers will become thicker, crimping, clenaturating, degradating into granular ball or unsetting ball. The structure of amino-group poly saccharide (GAGS), types all changes, and dysfunction appears, hydrate descending, and dysfunctio

31、n appear, hydrate descending excess sunlight makes corium accessory organ have some changes, such as small vessels reduce, vascular become thinner, the number of sweat gland decrease, the power of secreting sweat descending and sebaceous glands proliferating which the total amount of sebum secreting

32、 descending. Above-mentioned changes of corium structure can initiate the region of the skin that exposing below the sunlight to be dry, flabbily parchment-like and have thick and deep wrinkle.4. Occurrence Mechanism of Light Aging4.1 Light aging and non-ferment glycosylation reaction: the product o

33、f glycosylation, which accumulates in human body makes adjacent macromolecular crosslink with each other, especially makes collagen molecule crosslink with each other. Not only does it make the permeability descend but also make the spreading nature of trash and nutriment descend, enhance the tissue

34、 hardness to make it hard be hydrolysised collagenase which causing skin resiliency to descend, the wrinkle hard to be smoothed and became deep continuously. Wondrak and others proved the hypothesis by experiment that non-glycosylation protein is the photophil product of the per oxidation injury of

35、the skin cell ultraviolet ray in the peroxidation of light aging skin caused by UVA.4.2 Light Aging and Skin Immunologic System: Ultraviolet ray causes immunologic restrained which leading to exacerbation of skin infective illness of the skin even carcinoma cutis through many ways .Uv can retrain th

36、e expression of the skin and stimulate the releasing of the cell factor which has immunsuppression function and causes the producing of the lymphocytes which have antigenic phenotypic. In the light aging skin, the characteristic lesions of the epidermis Lange Hanss cell makes the amount of cells red

37、uce, its figure atrophies, deficits the forming of the dendrite and be lack of Birbeck granule.4.3 Light Aging and Free Radical Theory: In 1956, Harman put forward senile free radical theory. Free radical has extremely strong oxidation powers, which can oxidated the lipid in biological membranes and

38、 form into oxidated ester which terminal product (MDA) is strong cement, and it can mix with protein, nucleic acid forming into dysubstance making biological merebrane leading into the descending of its permeability and affecting the cell exchanges of substance then making it rapture and die. Free r

39、adical can change collagen molecule, making it to be affected by ferment and hyaluronic acid degradated, reducing the producing of the albumen polysugar, depredating basement membrane and so on. The free radical is produce by the irradiation of the UV can damage all kinds of macromolecular in the hu

40、man body. They can cause the skin cell to be oxidated, the free radical produced by to be excess, and produces per oxidation lipid in the skin and makes the skin lose its resiliency with the function of the collagen albumen In the skin, also the tree radical can make elastic fibers cross link and po

41、lymerize which causing the degradation of elastin and collagen leading to the excess cornification of the skin, making the skin rough, relaxing and wrinkle, aging phenomenon appearance. But there is the damage of the resistive free radical caused by the powerful protection system exists in the healt

42、h organism at the same time with the increasing of the age and all kinds of outside stimulatation especially the damage caused by the action of the ultraviolet ray in the sunlight makes the resistive oxidation ferment reduce in human body, protection power go down or occurrence of the disturbance, a

43、ccumulate action of free radical increase which causing the damage of the macromolecular in human body leading to the pathological changes and senility of the skin and organsm.4.4. Mitochondrion Mutation Theory: mitochondrion DNA (mtDNA) is the only extra nuclear in mammal cell. It is easy to be ind

44、icted to mutate by outer sphere factor, because of lacking of tissue protection and homologues re notation system. The function of mitochondrion mutation in human being senile and many retrograde illnesses is diffusely proved, mitochondrion DNA mutation and accumulating is also considered as the imp

45、ortant factor in aging of the skin especially light aging of the skin. Even research shows clearly that the incidence of the Mito chondrion DNA mutation has nothing to do with age but has close relation with the degree of light aging of the skin. The experiment has also proved that the damage of the

46、 oxygen free radical to biological membrane and mitDNA makes DNA mutate and split, which cause the change of the structure and do generation of the function of the mitochondrion and finally affect the producing of ATP, lacking of energy supply leading to the descending of organism super session abil

47、ity and accruing a serials of senile changes reveal.4.5 The Wither of the Cell and Light ageing of the Skin: the most out-standing feature of the cell is the controlled splitting of the cell DNA .many research materials reveal that the start of this controlled splitting has something to do with “the

48、 correlation gene of the withering and death of the cell. The research found that bcl-2 usually locates in the place where can produce more oxygen free radical such as mitochondrion, endoplasmic, reticulum and so on, which have some relation with the protection of the cell. We have already found tha

49、t bcl-2 gene is one oncogene in the reassert of withering of the cell which is different with the other gene and can extend the life term of the cell, it restrain the cell withering by blocking the common thoroughfare of the delivering system of the withering signal to advance the survival of the ce

50、ll and is a important cell existing gene. Bax and bcl-2 have highly autophoidy. The excess expression of the Bax can resist the function of bel-2 which can advance the generation of the cell and restrain of the withering of the cell. Bax/balx which acts as the representation of the death gene of the

51、 cell while bcl-2 acts as the representation of the cell, the result of their balance between their level of expression determines the cell should exist or be dead . The excess ultraviolet ray irradiating to the organsm is not only the direct reason for light aging but also can damage the peroxidati

52、on mechanism of the resistive ester quality of the ferment quality or non-ferment quality which causes and exacerbate the advance of the light aging .The cell of the skin can form into what is called “sunburned cell” that is withered cutin forming cell when contacting with excess ultraviolet ray. Th

53、e expression and regulation of the oxidation primitive cancer and so on in it have extremely important function. 4.6 The Other Theory Of Light Aging: the compounding and degradation of the radical. 5. The Treatment for the Photoaged Skin: The best treatment for light aging is to prevent, that is to

54、avoid over-basked. The trait for the skin of Chinese is that it is easy to be sun-banned but not sun-burned. So it is more important for us to prevent the harmfulness of UVA when we are preventing and curing the danger of the ultraviolet ray. And we should pay more attraction to avoid over-basked in

55、 the sunbeam even in our childhood. Ti is reported that the most efficient method is to wear properly, apply sun-tan cream regularly, and take an umbrella with you when you are out. The treatment is mainly divided into two types: one is unoperational treatment such as pharmacotherapy, chemical denud

56、ation, Microwave therapy, laser therapy and so on. Another is operational treatment such as clermabrasion, subcutaneous enthesis facial plastic operation and so on.5.1 Anti-oxidant: Anti-oxidant can lead to damage of DNA by controlling ultraviolet ray; serve the purpose to prevent light aging of ski

57、n. The main anti-oxidant are: tathion,-carotene, permanganate, SOD , especially the-carotene and SOD, which function is remarkable. Furthermore, there are some others such as ginger-extract, scutellaria astragal us-extract, aloe and so on. All of them can prevent the light aging of skin.5.2 Light-pr

58、oof Agent for Internal Use: Malnutrition can easily cause skin injury, while supplying vitamin，carotenoid, unsaturated fatty acid and some other kinds of nutrient all can keep skin from ultraviolet ray injury. 5.3 Light-proof Agent for External Use: Ultraviolet ray absorbent, the scattering agent wh

59、ich can make sun-ray scatter, and some other medium which combines scattering function and absorption together. Ultraviolet ray scattering agent mainly makes use of the function of scattering or reflex of some inorganic substance to ultraviolet ray to reduce the skin injury form sun-ray, for instance, kaolin, zine oxide, talc