Inflammatory Molecules Associated With Ultraviolet Radiation-Mediated Skin Aging Part 1

Thov hu rauoscar.xiao@wecistanche.comyog xav paub ntxiv

Abstract:Daim tawv nqaij yog lub cev loj tshaj plaws thiab nyuaj tshaj plaws hauv tib neeg lub cev uas muaj ntau txheej txheej nrog ntau hom cell. Ntau hom kev ntxhov siab ib puag ncig, piv txwv li, hluav taws xob ultraviolet (UVR), qhov kub thiab txias, huab cua paug, haus luam yeeb, thiab noj zaub mov, ua kom cov tawv nqaij laus zuj zus los ntawm kev ua kom cov kab mob inflammatory molecules. Kev laus ntawm daim tawv nqaij tshwm sim los ntawm UJVR yog tus cwj pwm los ntawm kev poob ntawm elasticity, cov kab zoo, wrinkles, txo cov epidermal thiab dermal Cheebtsam, nce epidermal permeability, ncua qhov txhab kho, thiab kwv yees li 90 feem pua ​​ntawm cov tawv nqaij laus. Cov txheej txheem sab nraud tuaj yeem ua rau kev laus los ntawm cov kab mob oxygen reactive (ROS) - kho mob o, nrog rau cov tawv nqaij laus yog ib qho ntawm cov kab mob inflammatory molecules uas ua rau cov tawv nqaij laus zuj zus thiab ua rau cov kab mob aging. Tsab ntawv tshuaj xyuas no tsom mus rau txoj hauv kev uas cuam tshuam nrog UVR-mediated tawv nqaij laus.

Ntsiab lus:mob; ultraviolet hluav taws xob (UVR); tawv nqaij laus

Thov nias ntawm no kom paub ntxiv

1. Taw qhia

Tib neeg daim tawv nqaij yog lub cev loj tshaj plaws nyob rau hauv lub cev thiab tiv thaiv peb cov kabmob sab hauv los ntawm lub ntiaj teb sab nraud thiab yog li raug rau ntau hom kev phom sij ib puag ncig. Kev laus ntawm daim tawv nqaij yog ib qho ntawm cov cim pom ntawm tib neeg kev laus nyob ntawm qhov tshwm sim ntawm lub sijhawm (kev laus hauv nruab nrab) thiab lwm yam (extrinsic aging lossis photoaging). Intrinsic aging yog ib qho txheej txheem physiological uas tshwm sim los ntawm kev txo cov cell proliferation nyob rau hauv basal khaubncaws sab nraud povtseg thiab tsub zuj zuj ntawm senescent hlwb nyob rau hauv lub epidermis thiab dermis ua rau cov tawv nqaij dryness, thinning, nplua wrinkles, khaus [], thiab susceptibility rau ntau daim tawv nqaij mob, xws li kab mob, kab mob autoimmune, thiab malignancy [2]. Lwm yam tseem ceeb, suav nrog cov pa phem, haus luam yeeb, noj zaub mov, kub, thiab tshwj xeeb tshaj yog ultraviolet thiab infrared hluav taws xob muaj kev cuam tshuam loj dua rau kev ua rau mob hnyav thiab kev laus phenotypes xws li wrinkles, pigmentation tsis tu ncua, tawv nqaij qhuav, thiab txo qis dermal thiab epidermal thickness [3]. Cov hluav taws xob ultraviolet (UVR) yog tawm los ntawm lub hnub thiab cov khoom siv dag zog tuaj yeem ua rau muaj kev puas tsuaj loj rau daim tawv nqaij, hu ua sunburn. Cov khoom siv hluav taws xob tseem ceeb ntawm UVR yog mercury vapor teeb, cov teeb dej txias, thiab cov teeb cua txias feem ntau yog siv rau kev kuaj mob thiab kho lub hom phiaj.suab puam hyacinthKev cuam tshuam rau UVR nrog cov tshuaj tsawg dua ua rau lub hnub ci ci thiab ua kom tawv nqaij laus, hu ua photoaging. UVR los ntawm lub hnub ci tuaj yeem faib ua peb hom los ntawm lawv qhov wavelength: UVA ({0}} nm), UVB (280-320 nm), thiab UVC (100-280 nm)[4]. Ntawm lawv, yuav luag tag nrho UVC thiab qee qhov UVB yog absorbed los ntawm ozone txheej thiab tsis muaj kev cuam tshuam rau peb cov tawv nqaij [5,6]. Tus so ntawm UVB tuaj yeem nkag mus rau ntawm daim tawv nqaij epidermis thiab ua rau erythema (sunburn), thaum UVA tuaj yeem cuam tshuam lub dermis thiab yog li 98 feem pua ​​​​ntawm cov tawv nqaij laus [7] (Daim duab 1).

UVB absorbed los ntawm cov epidermal hlwb ua rau DNA puas, ua rau oxidative kev nyuaj siab, thiab reactive oxygen hom (ROS), thiab ua rau cov laus ntxov ntxov [8,9]. UVA, ntawm qhov tsis sib xws, muaj lub wavelength siab dua uas tuaj yeem ua rau tsis ncaj qha DNA puas nrog rau collagen thiab elastin fiber ntau degradation los ntawm oxidative stress pathways [4]. Ua ke, kev raug UVR ntev ua rau muaj kev nce hauv nicotinamide adenine dinucleotide phosphate (NADPH) oxidase thiab tsim ROS, uas ua rau o, cytokines, chemokines, thiab tawv nqaij laus [10]. Kev mob ntev thiab mob tshwm sim los ntawm UVR tuaj yeem ua rau cov tawv nqaij tiv thaiv tsis muaj zog thiab ua rau cov collagen thiab elastin fibers, thiab thaum kawg ua rau kev laus ntxov ntxov. Lub hom phiaj ntawm qhov kev tshuaj xyuas no yog los tham txog cov inflammatory molecules txuam nrog UVR-mediated tawv nqaij laus.Flavonoid extraction method pdfHauv qhov kev tshuaj xyuas no, peb lub hom phiaj tseem ceeb yog los piav qhia txog cov teebmeem ntawm UVR ntawm epidermal keratinocytes thiab dermal fibroblast hauv cov txheej txheem ntawm daim tawv nqaij laus.

2. Inflammatory Response Los ntawm UVR

Nws yog qhov nkag siab zoo tias qhov mob hnyav ntawm daim tawv nqaij rau UVR yog o, xws li erythema thiab edema, thiab DNA thiab mitochondrial puas los ntawm ROS [11]. Hom ROS loj koom nrog hauv cov txheej txheem no yog superoxide radical anion (O,-), hydroxyl radical (OH), hydrogen peroxide (H, O,), thiab singlet oxygen hom (O,) [12]. Nws tau raug tshaj tawm tias UVB (290-320 nm) raug tshwm sim ua rau muaj kev nce ntxiv hauv ROS ntau lawm hauv tib neeg epidermal keratinocytes (HaCaT) cell nrog rau kev txo qis hauv cell viability [13]. ROS yog cov khoom lag luam ntawm cov pa oxygen tsis tu ncua thiab koom nrog ntau lub zog ntawm lub cev, xws li kev taw qhia ntawm tes, ua kom muaj kev tiv thaiv kev tiv thaiv kab mob, thiab kev loj hlob ntawm tes. Txawm li cas los xij, UVR raug rau ntawm daim tawv nqaij tuaj yeem tsim cov nyiaj ntau ntawm ROS, uas ua rau muaj qhov tsis sib xws ntawm ROS ntau lawm thiab cov tshuaj tiv thaiv antioxidant, uas ua rau muaj kev ntxhov siab oxidative [10,14]. Nyob rau hauv lub voj voog tsis zoo, qhov kev ntxhov siab oxidative no tuaj yeem ua rau ROS ntau lawm thiab tuaj yeem pib ob qho tib si o thiab pro-inflammatory cytokine activation, xws li interleukin-2(IL-2), interleukin-6(IL{ {12}}), thiab qog necrosis factor (TNF- ), uas muaj ntau txoj hauv kev nrog rau cov teeb meem nuclear kappa lub teeb saw txuas ntxiv ntawm cov tshuab ua kom B(NF-kB), hypoxia-inducible factor 1-alpha(HIF{{17}) }a), nuclear factor erythroid 2-related factor 2 (Nrf-2), thiab activator protein 1(AP-1)[15,16]. UVR-txog o tuaj yeem cuam tshuam nrog klotho deficiency. Klotho yog transmembrane protein uas tseem hu ua cov tshuaj tiv thaiv kev laus tiv thaiv kev ntxhov siab sib txawv [17]. Ntau qhov kev tshawb fawb tau lees paub tias klotho txoj haujlwm yog kho los ntawm NF-kB txoj hauv kev. UV irradiation ua rau txo qis hauv klotho mRNA thiab cov protein qhia nrog rau kev nthuav qhia pro-inflammatory cytokine, xws li interleukin -1 (IL-1), interleukin-6(IL-6) ), thiab TNF- hauv HaCaT hlwb. Ntxiv mus, klotho overexpression nyob rau hauv tib neeg keratinocytes txo UV-induced cell puas thiab o los ntawm inhibiting NF-kB nuclear translocation thiab nws kuj txo H2O2-induced o los ntawm inhibiting tus xov tooj-zoo li Receptor 4 qhia [18,19]. Sirtuins, nicotinamide adenine dinucleotide (NAD (ntxiv rau))-nyob ntawm histone deacetylase, kuj tau txais kev saib xyuas rau lawv lub peev xwm los ua kom muaj sia nyob raws li lawv tuaj yeem ncua kev cellular senescence thiab txhawb kev kho DNA puas. Nws tau pom tias SIRT1, ib tug tswv cuab ntawm tsev neeg Sirtuins, qhia txog kev tiv thaiv kab mob los ntawm inhibiting NF-kB signaling. UVR tuaj yeem ua rau mob ntev los ntawm kev txo qis SIRT1 qhia hauv tib neeg keratinocytes [20,21] (Daim duab 2).

2.1.Major Inflammatory Responses nyob rau hauv Epidermis thaum raug UV

Cov txheej txheem ntawm daim tawv nqaij sab nraud yog cov epidermis, thiab nws txuas ntxiv txuas ntxiv thiab sib txawv. Nws kuj ua haujlwm raws li kev thaiv kev tiv thaiv lub ntiaj teb sab nrauv thiab cuam tshuam ncaj qha los ntawm ib puag ncig ib puag ncig, feem ntau yog UVR. Lub epidermis feem ntau muaj plaub hom hlwb: feem ntau keratinocytes (~ 90 feem pua), melanocytes, Langerhans Cells, thiab Merkel Cells [22]. Keratinocytes tsim cov dej thaiv los ntawm txoj kev ntawm stratum corneum (SC), uas yog tsim nyob rau hauv lub epidermal basal txheej, thiab cov junctions nruj nreem tsim ib tug barrier nyob rau hauv lub stratum granulosum [23]. Yuav luag tag nrho UVB yog absorbed los ntawm SC, txheej txheej ntawm daim tawv nqaij. Ntau cov ntaub ntawv tau tshawb xyuas qhov cuam tshuam ntawm UVR hauv cov epidermis [24-26]. Qhov loj SC kev puas tsuaj los ntawm UV raug suav nrog kev ntxhib los mos thiab lub cev qhuav dej, txo qis desquamation thiab thaiv kev ua haujlwm, thiab cuam tshuam rau kev sib koom tes ntawm tes [27]. Cov kab mob UV-irradiated epidermis yog tus cwj pwm los ntawm thinning ntawm epidermis, zoo wrinkles, dryness, thiab cuam tshuam epidermal barrier muaj nuj nqi [26,28].flavonoidsCov kev tshawb fawb hauv vitro pom tau tias muaj qhov nce ntawm cov epidermal thickness raws li UV irradiation nyob rau hauv tib neeg cov qauv, whereas, nyob rau hauv kev tshawb fawb soj ntsuam, ib tug maj mam txo nyob rau hauv epidermal thickness nyob rau hauv cov cheeb tsam raug tshav ntuj tsawg heev tau tshaj tawm [29-32]. Qhov sib txawv no nyob ntawm qhov ntev ntawm qhov raug UV. Kev mob hnyav nrog UV txhim kho keratinocyte proliferation los ntawm activating epidermal growth factor receptor (EGFR), thaum lub sij hawm ntev raug rau lub hnub ci accelerates cov txheej txheem kev laus, uas ua rau cov epidermis thinner nrog flattening ntawm rete ridges (Daim duab 3). Ntawm qhov tod tes, qhov chaw uas tsis muaj hnub ci tawm ntawm cov neeg laus pom qhov sib piv rau cov tub ntxhais hluas [33].

Nws tau raug pom tias UVB raug cuam tshuam rau cov kab mob epidermal barrier muaj nuj nqi nyob rau hauv cov txiv neej hairless Balb / c nas nyob rau hauv ib tug npaum li cas ntawm koob tshuaj [34,35], thiab daim tawv nqaij barrier cuam tshuam yuav ua rau mob inflammatory teb los yog exacerbation ntawm cov kab mob inflammatory ntawm daim tawv nqaij, xws li raws li atopic dermatitis [36] Transepidermal dej poob (TEWL) feem ntau hu ua qhov ntsuas ntsuas ntawm daim tawv nqaij cuam tshuam kev cuam tshuam thiab ntau cov ntawv ceeb toom tau lees tias qhov sib txawv ntawm UV tuaj yeem ua rau nce TEWL hauv murine thiab tib neeg cov qauv [37-40]. Nyob rau hauv lub epidermis, muaj ob peb inflammatory signaling txoj kev txuas mus rau txawv nto receptors, xws li EGFR [41, transforming growth factor receptors(TGFR)[42,A43], hu-like receptors(TLRs)[44], IL{{ 10}} receptor, thiab TNF receptor (TNFR)[{11}}]. Lub hauv paus tseem ceeb ntawm cytokines nyob rau hauv lub epidermis yog keratinocytes, thiab loj cytokines secreted los ntawm keratinocytes thaum UVR irradiation yog Interleukins (IL-1, IL-3, IL-6, IL-8 , IL-33), colony-stimulating factor (GM-CSF, M-CSF, G-CSF), thiab transforming growth factor (TGF-), transforming growth factor (TGF- ), TNF-c, high- Mobility group box1 (HMGB1), thiab platelet-derived growth factor (PDGF)[48-50]. UVR tuaj yeem qhib qhov taw qhia ncaj qha los ntawm ROS ntau lawm lossis tsis ncaj qha los ntawm DNA lossis mitochondrial puas thiab tom qab ntawd ua rau mob. Cov kev tshawb fawb yav dhau los hais txog UVR-mediated o yog sau tseg hauv Table 1.

EGFR signaling plays lub luag haujlwm tseem ceeb hauv keratinocyte proliferation, sib txawv, cell adhesion, tsiv teb tsaws, thiab ciaj sia taus. Txawm li cas los xij, lub luag haujlwm ntawm EGFR ntawm inflammatory teb rau UVR yog qhov nyuaj heev. Ib daim ntawv tshaj tawm qhia tau tias UV-irradiated nas thiab keratinocytes kho nrog EGFR inhibitor tau pom muaj kev cuam tshuam cov lus teb, xws li txo qis hauv lub cev tiv thaiv kab mob thiab txo qis ntawm cov kab mob cytokines (TNF-, IL-8, IL-1a, Cyclooxygenases (COX2)) [77]. Cov txiaj ntsig kuj tau pom tias EGFR yog ib feem ntawm lub luag haujlwm rau p38 mitogen-activated protein kinase (MAPK)-activated inflammatory teb [77]. Nws yog qhov paub zoo tias p38 MAPK signaling yog koom nrog ntau yam pro-inflammatory cytokine ntau lawm, ua rau ntau yam kab mob ntawm daim tawv nqaij, suav nrog kev yees duab. UV-induced COX-2 qhia feem ntau yog nyob ntawm p38 MAPK signaling pathway[78] thiab tswj cov prostaglandin 2(PGE2)secretion, uas yog loj pro-inflammatory cytokines lub luag hauj lwm rau kev tiv thaiv cell infiltration, o, thiab edema [79 ].hesperidin sivTxawm li cas los xij, qee cov ntawv tshaj tawm tsis ntev los no tau qhia tias kev kho mob ntev EGFR inhibitor tuaj yeem ua rau cov tawv nqaij laus ntxov ntxov los ntawm ROS-induced oxidative stress lossis cellular senescence induced by cell cycle capture [80]. Yog li ntawd, lub luag hauj lwm ntawm EGFR ntawm UVR-mediated tawv nqaij laus yog heev complex thiab tseem tsis tau elucidated. NF-kB yog ib qho ntawm cov neeg kho mob tseem ceeb ntawm cov txheej txheem inflammatory ntawm tes thiab nws tau tsim tau zoo tias UV irradiation tuaj yeem ua rau NF-kB transcriptional kev ua haujlwm, ua rau muaj teeb meem mob ntev [81]. Tib neeg keratinocytes irradiated nrog UV pom tau hais tias muaj zog cytokines IL-1 , IL-6, IL-8, thiab TNF- los ntawm NF-kB txoj kev [82,83]. TLRs tau qhia nyob rau hauv epidermal keratinocytes thiab Langerhans hlwb thiab tseem ceeb heev hauv kev txheeb xyuas kab mob thiab kev tiv thaiv kab mob. Nws tau pom tias TLRs muaj lub luag haujlwm tseem ceeb hauv UV-mediated o los ntawm nws txoj kev taw qhia nqes mus rau NF-kB. Tshwj xeeb, UV-kev puas tsuaj keratinocytes secrete noncoding RNA uas tuaj yeem qhib TLR3 thiab ua rau cov lus teb inflammatory, xws li TNF- thiab kuv -6 [84]. Daim tawv nqaij epidermis muaj qhov nthuav qhia ntawm TNFR, thiab TNF- tuaj yeem qhib ntau txoj hauv kev los ntawm NF-kB thiab MAPK. Nws tau raug tshaj tawm tias UV irradiation tau nce ntxiv rau ob qho tib si soluble thiab tag nrho-ntev TNF- hauv epidermal keratinocytes [85]. Txawm hais tias cov kab mob epidermis txuas ntxiv mus tas li thiab cov cell apoptosis yog qhov tseem ceeb rau cov epidermis homeostasis, nws tseem ceeb heev uas yuav tsum nco ntsoov tias kev ua tsis taus, ntxov ntxov, los yog ntau dhau apoptosis tuaj yeem ua rau epidermal homeostasis dysregulation thiab txhawb kev laus phenotypes, xws li sunburn cells.poob teb chaws Ottoman cistancheNws tau raug pov thawj tias TNF- tuaj yeem ua rau keratinocyte apoptosis los ntawm UV-induced TNFR-1 lossis p55 receptor pathway [86,87]. Qhov kev qhia ntawm TGF- yog qhov sib piv qis dua hauv tib neeg cov kab mob epidermis, uas feem ntau qhia nyob rau hauv cov txheej txheem epidermal basal thiab lub luag hauj lwm rau epithelial homeostasis, qhov txhab kho, thiab cov lus teb los tiv thaiv kab mob [88]. UV irradiation ntev tuaj yeem txo TGF- 2 synthesis los ntawm kev txo TGF-hom II receptor (T RII) mRNA qhia [89,90].

Cistanche tuaj yeem tiv thaiv kev laus

2.2.Major Inflammatory Responses in Dermis upon UV Exposure

Lub dermis feem ntau yog tsim los ntawm collagen, elastic fibers, paj hlwb, cov hlab ntsha, cov hauv paus plaub hau, thiab qog, qhov twg cov khoom tseem ceeb ntawm lub dermis yog collagen [91]. Cov cell loj hauv dermis yog fibroblasts, vascular du leeg cell, macrophages, adipocytes, mast hlwb, Schwann hlwb, thiab follicular qia hlwb [91,92]. Fibroblasts muab cov dermis nrog cov collagen-nplua nuj extracellular matrix (ECM) thiab kev tiv thaiv kab mob hauv lub cev yog tswj los ntawm cov hlab ntsha thiab cov hlab ntsha lymphatic [93,94]. Lub photoaged dermis feem ntau yog tus cwj pwm los ntawm nyias dermis, txo cov ntsiab lus collagen, disorganized thiab fragmented collagen fibers, elastic fiber degradation, thiab loj dermal connective cov ntaub so ntswg puas, uas ua rau pom feem ntau pom ntawm daim tawv nqaij laus, xws li wrinkle tsim, fragile atrophic daim tawv nqaij. , ncua qhov txhab kho, thiab sagging [95]. Muaj ntau qhov kev tshawb fawb hauv vivo thiab hauv vitro uas tau tshawb pom qhov cuam tshuam ntawm UVR ntawm lub dermis (Table 1).

Kev puas tsuaj collagen fibrils thiab elastin fibers yog qhov pom tseeb tshaj plaws ntawm UVR-mediated aged dermis, feem ntau tshwm sim los ntawm matrix-degrading metalloproteinases (MMPs) synthesis los ntawm MAP kinase signaling [14]. MMPs yog ib tsev neeg ntawm ubiquitous endopeptidases thiab koom nrog cov txheej txheem inflammatory los ntawm kev tswj cov tshuaj chemokine [96,97]. Nws tau raug tshaj tawm tias MMPs yog lub luag haujlwm rau collagen degradation, feem ntau los ntawm collagenase-1 (MMP-1), stromelysin-1(MMP-3), thiab gelatinase B (MMP{ {9}}), uas ncaj qha thiab tag nrho degrade collagen [98]. Ib daim ntawv tshaj tawm qhia tau hais tias muaj kev qhia ntau ntxiv ntawm MMP-1, MMP-2, MMP-3, MMP-9, MMP-11, MMP-17, thiab MMP -27 nyob rau hauv ib tug photoaged tib neeg forearm correlated nrog txo hom I procollagen qhia [99]. Hom I collagen yog cov protein ntau tshaj plaws nyob rau hauv ECM, thiab collagen fibrils yog synthesized los ntawm cov procollagens (collagen precursor molecules) los ntawm ib tug series ntawm cov tshuaj [100]. Lwm daim ntawv tshaj tawm qhia tias MMP-1 qhia tau nce hauv tib neeg UV-irradiated daim tawv nqaij nrog rau collagen degradation [101]. UVR tseem tuaj yeem pib ua kom cov collagen degradation los ntawm kev txo qis procollagen synthesis, thiab nws tau raug tshaj tawm tias UVR tuaj yeem txo qhov kev sib txuas ntawm procollagen los ntawm kev txo qis TGF- / Smad signaling pathway [102]. TGF- pib taw qhia los ntawm kev khi nrog cov cell nto receptors (TGF- hom I thiab hom II receptors), tom qab ntawd hloov pauv ntawm TGF- -cov noob sib txuas los ntawm phosphorylating Smad2 / Smad3 complex. Nws tau raug tshaj tawm tias TGF- tuaj yeem qhib kev txhawb nqa kev ua haujlwm ntawm Hom I collagen gene (COL1A2) los ntawm Smad signaling pathway [103]. Ib daim ntawv tshaj tawm qhia tias UV irradiation inhibits Smad2 / Smad3 nuclear translocation, ua rau txo qis TGF-type II receptor transcription thiab protein synthesis thiab procollagen hom I qhia hauv cov nas tsis muaj plaub hau thiab hauv tib neeg dermal fibroblasts [76,102,104] (Daim duab 4).

Ntau yam kev ntxhov siab suav nrog UV hluav taws xob tuaj yeem ua kom DNA puas cov lus teb uas tuaj yeem pib lub voj voog ntawm tes los ntawm p53 / p21 txoj hauv kev uas cuam tshuam nrog P38 / MAPK cascade thiab NF-kB [105] txoj hauv kev. Nws tau raug pom tias UV-tshuaj rau tib neeg cov tawv nqaij muaj qhov sib txuam ntawm cov hlwb loj heev [106]. Kev sib sau ntawm senescent fibroblasts tuaj yeem ua kom cov tawv nqaij laus zuj zus los ntawm kev zais cov senescence-associated secretory phenotype (SASP), xws li IL-1a, IL-1 , IL-6, IL-8, thiab MMPs.SASP yam secreted los ntawm senescent fibroblasts yog lub luag hauj lwm rau mob o thiab ECM degradation, uas ua rau photoaging[107]. Daim duab 5 piav qhia txog cov kev taw qhia tseem ceeb uas cuam tshuam nrog UV-mediated photoaging.

3. Cov lus xaus

Qhov kev tshuaj xyuas no tau sau tseg txog kev sib koom ua ke ntawm cov molecules inflammatory thiab tawv nqaij laus kho los ntawm UVR. Kev laus ntuj tuaj yeem ua kom nrawm los ntawm lwm yam, feem ntau yog UVR, uas ua rau muaj kev puas tsuaj ncaj qha rau DNA lossis tsis ncaj los ntawm kev tsim cov radicals. Nyob rau hauv daim tawv nqaij, epidermal keratinocytes yog lub hauv paus loj ntawm cytokines ntau lawm thiab dermal fibroblasts yog lub hauv paus loj ntawm MMPs, thiab nws tau pom tias DNA puas ua rau tso tawm inflammatory molecules los ntawm epidermal keratinocytes (IL-1, IL{ {1}}, IL-6, IL-8, GM-CSF, M-CSF, G-CSF, TGF-, TGF-, TNF- , thiab PDGF) thiab los ntawm dermal fibroblasts (MMP{ {10}}, MMP-2, MMP-3, MMP-9, MMP-11, MMP-17, thiab MMP-27) [48 ]. Kev mob ntev tuaj yeem ua rau muaj kev laus zuj zus ntxiv thiab ua rau muaj kev tso tawm ntawm SASP yam hauv dermal fibroblasts thiab melanocytes [108,109]. Cov kab mob SASP tsis ntev los no yog lub luag haujlwm rau ntau lub hnub nyoog ntsig txog pathologies, piv txwv li, atherosclerosis, ntshav qab zib hom 2, rog rog, kab mob plawv, sarcopenia, kab mob neurodegenerative, thiab Alzheimer's disease [110-113]. Txij li thaum nws tau raug tsim los hais tias cov lus teb inflammatory tom qab UV raug tuaj yeem ua rau cov txheej txheem laus zuj zus ntxiv nrog rau cov hnub nyoog cuam tshuam txog kev mob ntshav qab zib, cov txheej txheem tshiab tsom rau cov inflammatory molecules yuav tsum tau tsim.

Kab lus no yog muab rho tawm los ntawm Int. J. Mol. Sci. 2021, 22, 3974. https://doi.org/10.3390/ijms22083974 https://www.mdpi.com/journal/ijms