Antioxidative, Anti-Inflammatory, Thiab Anti-aging Properties Ntawm Mycosporine-zoo li Amino Acids

Ntsiab lus:mycosporine zoo li amino acids; mycosporine-2-glycine; UV-absorbing compound;tshuaj pleev thaiv hnub;anti-aging; tiv thaiv oxidation; tiv thaiv kab mob; anti-protein-glycation ua haujlwm

Nyem qhov no Kom Tau Txais Cov Lus Qhia Ntxiv Txog Cistanche Rau Kev Tiv Thaiv Kev Laus

1. Taw qhia

Cov tawv nqaij, qhov loj tshaj plaws ntawm tib neeg lub cev, yog tas li raug rau sab nraud ib puag ncig. Kev nphav raug rauntau yam ntawm ib puag ncig kev ntxhov siab, tshwj xeeb tshaj yog ultraviolet (UV) hluav taws xob hauv tshav ntuj, tuaj yeem ua rau puas tsuajtawv nqaij. Hnub ci tuaj yeem tawg ua peb hom nonionizing electromagnetic hluav taws xob-infrared(IR) (780–3000 nm), pom (400–780 nm), thiab UV (100–400 nm). Cov feem pua ​​ntawm lub zog radiatedrau lub ntiaj teb, nyob rau hauv tag nrho lub zog tawm los ntawm lub hnub, yog 53 feem pua ​​​​IR, 39 feem pua ​​​​pom, thiab 8 feem pua ​​UV [1]. Nyob ntawmlub hauv paus ntawm nws physiological thiab biological effff uaects, UV hluav taws xob tuaj yeem muab faib ua peb lub ntsiabbands - 315-400 nm band (tsim yog UV-A), 280-315 nm band (tsim yog UV-B),thiab 100-280 nm band (tsim yog UV-C) [2]. Hnub ci UV hluav taws xob tsawg tsawgraws li nws dhau los ntawm ozone txheej thiab huab cua; Yog li ntawd, qhov kev faib ua feem ntawm UV rays nyob rau hauvLub hnub ci mus txog lub ntiaj teb nto, yog ua los ntawm 95 feem pua ​​UV-A thiab 5 feem pua ​​UV-B [1]. Txawm tias nws tsuas yog ib feem me me ntawm tag nrho cov hluav taws xob UV, UV-B xav tias yuav ua rau muaj kev phom sij ntau duaUV-A, vim UV-B feem ntau ua rau ua rau daim tawv nqaij thiab qhov muag [3]. UV-A thiab UV-B kuj paublos ua genotoxic, txhais tau tias lawv tuaj yeem tsim kev puas tsuaj photochemical hauv cellular DNA thiab proteins [4,5]. Yog li ntawd, raug rau UV-A thiab UV-B, txhawb nqa kev yees duab ntawm daim tawv nqaij thiab tuaj yeem ua lub luag haujlwm rauinduction ntawm daim tawv nqaij mob cancer [6]. Daim tawv nqaij photoaging yog tus cwj pwm los ntawm kev loj hlob ntawm pigmentarycov teeb meem xws li hnub ci lentigines, fifine thiab coarse wrinkles, thiab benign, premalignant, thiab malignantdaim tawv nqaij hlav ntawm daim tawv nqaij uas raug tshav ntuj [7]. Cov hluav taws xob muaj zog heev UV-C tsis muaj qhov tseem ceeb ntawm kev lom neeg,vim nws tsis ncav cuag lub ntiaj teb nto, vim nws ua tiav nqus los ntawm ozone txheej thiabhuab cua [1,3]. Lub depletion ntawm ozone txheej, nyob rau hauv ob peb lub xyoo dhau los, tau nce lubtus nqi ntawm hnub ci UV hluav taws xob mus txog lub ntiaj teb nto [8], tshwj xeeb tshaj yog UV-B qib, txij li UV-A yogtsis absorbed los ntawm ozone txheej [9]. Ntau cov kab mob hauv hiav txwv uas raug UV hluav taws xob tau tsim kev tiv thaiv photoprotectivemechanisms [10]. Piv txwv li, nyob rau hauv cyanobacteria, uas dominate lub marine ib puag ncig, UVCov txheej txheem tiv thaiv tau hloov zuj zus ntawm molecular, cellular, thiab kev coj cwj pwm [11]. Cyanobacteriatuaj yeem tsim ntau hom "tsim tshuaj pleev thaiv hnub", uas tuaj yeem tiv thaiv kev tiv thaiv UV hluav taws xob.Mycosporine-zoo li amino acids (MAAs), scytonemin, thiab carotenoids paub tias yog cov ntsiab lus tseem ceeb.nyob rau hauv cyanobacteria uas yuav nqus tau wavelengths nyob rau hauv lub UV ntau yam. Cov khoom ntuj no tau cog lus tsegCov neeg sib tw molecules nyob rau hauv lub fifield ntawm cosmeceutical compounds discovery [12]. Qhov tseeb, MAAs muajtwb tau ua lag luam ua Helioguard®365. Cov tshuaj pleev ib ce no muaj cov liposomalMAAs, Shinorine (SHI), thiab porphyra-334 (P334), uas yog Ameslikas muab rho tawm los ntawm liab algaPorphyra umbilicalis, thiab tau ua tiav kev lag luam raws li cov tshuaj tiv thaiv ntuj thiab nyab xeebcompound [12]. Tsis tas li ntawd, MAAs tau xav tias yog multifunctional secondary metabolites, hauvcell ntawm producers [13]. Ntau tus MAAs paub tias ua raws li antioxidants [14], thaum ob peb tsab ntawv ceeb toom tsis ntev los notau tawm tswv yim tias MAAs muaj peev xwm kho tau daim ntawv thov los txo cov txheej txheem ntawm daim tawv nqaij.Los ntawm qhov kev pom no, tsis ntev los no, ntau qhov kev tshuaj xyuas cov ntawv ceeb toom nrog tshwj xeeb tshwj xeeb rau kev siv tauntawm MAAs hauv cov khoom siv tshuaj pleev ib ce, tau luam tawm [15–17]. Hauv daim ntawv no, peb tshuaj xyuas MAAs thiablawv lub peev xwm los tiv thaiv daim tawv nqaij cov khoom xyaw, los ntawm kev piav qhia txog cov ntsiab lus tseem ceeb ntawm lawv cov qauv, ua ntejtsiv mus rau cov ncauj lus kom ntxaws txog kev soj ntsuam kev soj ntsuam tsis ntev los no, tau sau ua li nonyob deb. Cov txheej txheem uas MAAs tuaj yeem ua los tiv thaiv daim tawv nqaij los ntawm kev laus yog tham txog ntawm, ob qho tib si,cellular thiab qib molecular. Hauv particular, qhov tseem ceeb muaj peev xwm tiv thaiv kev laus ntawm covMAA mycosporine-2-glycine (M2G), uas yog biosynthesized los ntawm halotolerant cyanobacteriumAphanothece halophytica, yog highlighted.

2. Mechanisms ntawm UV-Induced Skin Aging

UV hluav taws xob yog qhov tseem ceeb rau peb txoj kev noj qab haus huv vim tias UV-B raug tuaj yeem ua rau muaj qhov tseem ceebcov zaub mov, vitamin D, hauv peb cov tawv nqaij [18]. Txawm li cas los xij, ntev ntev thiab rov raug UV tuaj yeem txhawb nqadaim tawv nqaij photoaging txheej txheem, nrog rau daim tawv nqaij mob cancer tsim [19]. Cov mechanisms uas UV-mediatedcellular puas yog induced yog luv luv piav nyob rau hauv nqe lus no.2.1. Cellular DNA puasDirect thiab indirect toxic effff uaects ntawm UV hluav taws xob ntawm DNA molecule, kho kom zoo nkauj photoaging.Kev nqus ncaj qha ntawm UV-B photons los ntawm DNA, tuaj yeem ua rau tsim cov pyrimidine dimers,ua rau muaj qhov tsis xws luag hauv DNA strand [20]. UV-B hluav taws xob feem ntau ua rau kev tsim ntawmcis-syncyclobutadipyrimidines (CPDs) thiab pyrimidine ({0}}) pyrimidone photoproducts (6-4PPs). 6-4PPstuaj yeem hloov mus rau lwm yam Dewar valence isomers (DewPPs), thaum UV-excitation ntawm 314 nm.Xws li DNA puas cuam tshuam nrog DNA replication thiab transcription, thiab coj ntau yam teeb meemeffff uaects rau lub cell, xws li kev hloov, instability ntawm chromosome, thiab cell tuag. UV-A tsisncaj qha hloov cov qauv ntawm DNA vim DNA tsis muaj zog nqus hluav taws xob hauv UV-A ntau [21]. Txawm li cas los xij, UV-A tuaj yeem ua rau DNA tsis ncaj, los ntawm cov tshuaj tiv thaiv photosensitized los ntawm kev tsimradical singlet oxygen (1O2), uas ua rau purine puag hloov kho [20]. Lub singlet oxygen anion oxidizes guanine moiety, ua raws li tiam ntawm 8-oxo-7, 8-dihydroguanine (8-oxo-G) thiab8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxo-dG). Raws li 8-oxo-G thiab 8-oxo-dG tuaj yeem koom nrog adeninees tsis txhob cytosine, kev hloov pauv yuav tshwm sim.2.2. Reactive Oxygen Hom GenerationReactive oxygen hom (ROS), pib ntawm oxidative kev nyuaj siab, yog cov pa oxygen reactiveCov tshuaj muaj xws li hydrogen peroxide (H2O2), hydroxyl radicals (·OH), superoxide anionradicals (·O2 −), thiab1O2. Nyob rau hauv peb cov tawv nqaij, raug rau UV hluav taws xob yog paub tias muaj feem xyuam nrog covtiam ROS. Cov ROS no tuaj yeem qhib cov tawv nqaij-laus cascades, xws li matrix metalloproteinase(MMP)-1-kev laus nruab nrab thiab NF-κB-TNF- -mediated, inflammation-induced aging [22]. Qhov ntau yamntawm ROS tiam mechanism los ntawm UV, nyob ntawm UV hluav taws xob wavelength ntau yam. Ntxiv rau1O2 tiam, raws li tau hais los saum no, nws tau raug tshaj tawm tias UV-A hluav taws xob tuaj yeem ua rau tiam neegntawm·O2 − los ntawm kev ua kom cov nicotinamide adenine dinucleotide phosphate intracellular (NADPH)oxidase, NOX [23], thiab koom nrog cov khoom siv qib siab glycation kawg (AGEs) [24]. Sakurai et al.elucidated tias ob leeg1O2 thiab·O2 - tau tsim nyob rau hauv daim tawv nqaij ntawm nas raug UV-A [25]. H2O2, ·O2 −, thiab·OH hom yuav raug tsim tawm hauv AGEs, thaum raug UV-A [24]. UV-B kuj tseem paub txogcoj mus rau kev tsim H2O2, ·O2 −, thiab·OH [26]. Txawm hais tias lub hauv paus ntawm cov UV-B-induced ROStseem tsis tau paub meej, tsis ntev los no tau tshaj tawm tias NADPH oxidase, NOX1, cuam tshuam nrog UV-B-inducedp38/MAPK activation thiab cytotoxicity, ntawm ROS tiam hauv keratinocytes [26]. Txhawm rau tiv thaiv kev puas tsuaj ntawm daim tawv nqaij los ntawm ntau dhau UV-induced ROS thiab tswj cov epidermal homeostasis,Cov hlwb ntawm daim tawv nqaij muaj cov tshuaj tiv thaiv oxidative uas ua raws li kev tiv thaiv endogenous [20]. Qhov no systemFeem ntau muaj rau enzymes-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase(GPX), glutathione reductase (GR), thioredoxin oxidase (TRXR), thiab peroxiredoxin (PRDX) (Daim duab1). SOD thiab CAT tshem tawm·O2 − thiab H2O2, ntsig txog, thiab thaum kawg hloov·O2 − rau H2O, hosGPX, GR, TRXR, thiab PRDX tshem tawm H2O2, los ntawm kev cai ntawm redox tej yam kev mob ntawm glutathionethiab thioredoxin. Ntxiv rau qhov no enzymatic system, non-enzymatic molecules, xws li vitamin Cascorbic acid (vitamin E), -tocopherol), glutathione, thiab ureic acid, ua lub luag haujlwm tseem ceeb ua antioxidantshauv daim tawv nqaij [27]. Cov molecules me no tshem tawm thiab tshem tawm cov dawb radicals, los ntawm kev muab ib qho ntxivelectron los ua ib khub electron.

Daim duab 1.Kev tshem tawm ntawm cov pa oxygen reactive (ROS) los ntawm kev tiv thaiv antioxidant muaj xws lisuperoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase(GR), thioredoxin oxidase (TRXR), thiab peroxiredoxin (PRDX). GSHred thiab GSSGox qhia tias txo qisglutathione thiab oxidized glutathione, feem. TRXred thiab TRXox qhia tias txo thioredoxinthiab oxidized thioredoxin, feem.

2.3. Inflammatory teb

Kev raug UV hluav taws xob ua rau muaj kev mob tshwm sim los ntawm kev ua rau muaj tshuaj lom neeg hauv daim tawv nqaij. Qhov txawvCov qauv ntawm o yog tshwm sim los ntawm kev raug rau cov wavelengths ntawm lub teeb.Peb pawg, UV-A,UV-B, thiab UV-C, tau raug cais tawm, raws li cov diffff uaerent qauv ntawm o [28]. Erythemainduced nyob rau hauv daim tawv nqaij, tom qab raug rau UV-B hluav taws xob yog yus muaj los ntawm sunburn. InflammatoryCov lus teb cuam tshuam los ntawm UV-B feem ntau ua tiav los ntawm ntau tus neeg nruab nrab, suav nrog nitricoxide (NO), inducible NO synthase (iNOS), prostaglandin E2 (PGE)2), cyclooxygenase-2 (COX-2),qog necrosis factor- (TNF- ), thiab lwm yam cytokines, xws li interleukin-1 (IL-1) thiab interleukin-6(IL-6) (Daim duab2). Cov molecules no feem ntau tswj los ntawm nuclear factor-kappa B (NF-κB), thiab feem ntau tsim nyob rau hauv keratinocytes, uas yog cov hom cell predominant nyob rau hauv lub epidermis [29]. Nws muajtau tshaj tawm tias qhov kev qhia ntawm COX-2 protein, uas yog lub luag haujlwm rau PGE2 production, yogupregulated, tom qab raug UV-B, nyob rau hauv tib neeg daim tawv nqaij thiab nyob rau hauv kab lis kev cai tib neeg keratinocytes [30]. ROS tseem paub tias muaj feem cuam tshuam nrog cov lus teb ua rau mob, raws li nws tau pom tiasCOX-2 kev qhia tau raug ntxias los ntawm ROS hauv diffff uaerent cell hom [31]

Daim duab 2.UV-B-induced inflammatory teb. Nitric oxide (NO), inducible NO synthase (iNOS),prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), qog necrosis factor- (TNF- ), thiab lwm yamcytokines, xws li interleukin-1 (IL-1) thiab interleukin-6 (IL-6), tau qhia tias yog tus neeg nruab nrab.

2.4. Induction ntawm Matrix Metalloproteinases

UV hluav taws xob upregulates kev qhia ntawm matrix metalloproteinases (MMPs) nyob rau hauv daim tawv nqaij. MMPs,uas paub tias yog lub luag haujlwm rau kev puas tsuaj ntawm extracellular matrix (ECM) proteins, xws liraws li collagen, ua lub luag haujlwm tseem ceeb hauv kev tswj cov tawv nqaij homeostasis thiab tawv nqaij laus [32]. MMPs yogsecreted los ntawm keratinocytes thiab dermal fifibroblasts, teb rau ntau yam stimuli, nrog rau oxidativekev nyuaj siab thiab cytokines, ntxiv rau UV hluav taws xob. Rov qab induction ntawm cov collagen-degradingenzymes, dhau mus ntev, xav tias yuav ua rau collagen puas tsuaj, uas yog ib qho ntawm cov laj thawj raukev yees duab. Txawm hais tias ob peb MMPs tau qhia nyob rau hauv cov tawv nqaij mammalian, nws tau raug pom zoouas MMP-1 yog qhov loj collagen-degrading enzyme lub luag haujlwm rau kev puas tsuaj collagen, hauv qhov hnyavdaim duab puas daim tawv nqaij [33]. Kev tswj hwm ntawm MMP kev qhia yog txhawb los ntawm activator protein-1(AP-1), uas paub tias yog UV-inducible transcription factor [34]. Qhov tseeb, AP -1 cov cai tswj hwmmuaj nyob rau hauv 5 'flflanking cheeb tsam ntawm MMP noob. Transforming growth factor-beta (TGF- ) thiab NF-κB kuj paub tias muaj kev koom tes hauv induction ntawm MMPs hauv daim tawv nqaij [34].

2.5. Induction ntawm Protein Glycation

Protein glycation (non-enzymatic glycosylation), tseem hu ua thawj kauj ruam ntawm Maillard cov tshuaj tiv thaiv,Nws suav nrog kev tsim covalent bonds ntawm cov proteins thiab txo cov suab thaj. Cov tshuaj tiv thaiv condensationnruab nrab ntawm cov amino pawg dawb ntawm cov proteins thiab cov pawg carbonyl ntawm cov suab thaj, ua rau muaj kev tsim ntawm aSchiff puag, ua raws li cov khoom Amadori. Cov khoom siv ntau dhau yog oxidized thiab lub cev qhuav dej los tsimruaj khov, molecular, cross-linking khoom, hu ua advanced glycation end-products (AGEs) [35]. Proteinglycation cuam tshuam lub cev thiab kev ua haujlwm ntawm cov protein, vim nws ua rau muaj kev sib haum xeebhloov pauv hauv cov qauv protein [36]. Hauv daim tawv nqaij, nws tau raug tshaj tawm tias glycation ntawm collagen hom kuv yogcuam ​​tshuam nrog kev txhim kho ntawm daim tawv nqaij dullness thiab txo cov tawv nqaij elasticity [37]. AGEs kuj yogkoom nrog rau tiam ntawm ROS. Masaki et al. qhia tias raug AGEs rau UV-A irradiationhauv vitro, ua rau tiam ntawm ROS, xws li·O2 −, H2O2, thiab·OH, raws li tau hais los saum toj no [24]. Hauv tib neeg, daim tawv nqaij autoflfluorescence, biomarker rau AGEs, tuaj yeem ua haujlwm raws li cov khoom siv hluav taws xob endogenous.uas induces ROS tiam, tom qab raug UV-A hluav taws xob [35]. Yog li, glycation tshwm simua raws li AGE tsim yog xav tias yog ib qho ntawm cov txheej txheem tseem ceeb cuam tshuam nrog daim tawv nqaijKev laus, nyob rau hauv ib puag ncig, tshwj xeeb tshaj yog UV hluav taws xob [24].

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