Influence Of The Mediterranean Diet On Healthy Aging Part 1

Abstract: Lub neej expectancy ntawm cov pejxeem thoob ntiaj teb tau nce. Kev laus yog ib qho txheej txheem physiological uas tsim teeb meem loj hauv cov neeg nyob ntev thiab tsis muaj zog. Ob peb molecular mechanisms koom nrog hauv kev laus. Ib yam li ntawd, lub plab microbiota, uas cuam tshuam los ntawm ib puag ncig yam xws li kev noj haus, ua lub luag haujlwm tseem ceeb hauv kev hloov pauv ntawm cov txheej txheem no. Cov zaub mov Mediterranean, nrog rau cov khoom muaj nyob hauv nws, muaj qee qhov pov thawj ntawm qhov no. Ua kom muaj kev noj qab haus huv kev laus yuav tsum tau tsom mus rau kev txhawb nqa kev noj qab haus huv ntawm kev noj qab haus huv uas txo qis kev loj hlob ntawm pathologies uas cuam tshuam nrog kev laus, txhawm rau txhim kho lub neej zoo ntawm cov neeg laus. Hauv qhov kev tshuaj xyuas no, peb txheeb xyuas qhov cuam tshuam ntawm Mediterranean noj zaub mov ntawm txoj hauv kev molecular thiab microbiota cuam tshuam nrog cov qauv kev laus zoo dua, nrog rau nws lub luag haujlwm ua haujlwm los tiv thaiv kev laus.

Glycoside ntawm cistanche tuaj yeem ua rau muaj kev ua haujlwm ntawm SOD hauv plawv thiab daim siab cov ntaub so ntswg, thiab txo cov ntsiab lus ntawm lipofuscin thiab MDA hauv txhua cov ntaub so ntswg, tshem tawm ntau yam reactive oxygen radicals (OH-, H₂O₂, thiab lwm yam) thiab tiv thaiv DNA puas. los ntawm OH-radicals. Cistanche phenylethanoid glycosides muaj peev xwm tshem tawm cov dawb radicals, muaj peev xwm txo tau ntau dua li cov vitamin C, txhim kho cov haujlwm ntawm SOD hauv cov phev ncua, txo cov ntsiab lus ntawm MDA, thiab muaj qee yam kev tiv thaiv ntawm cov phev ua haujlwm. Cistanche polysaccharides tuaj yeem txhim kho kev ua haujlwm ntawm SOD thiab GSH-Px hauv erythrocytes thiab ntsws cov ntaub so ntswg ntawm cov nas senescent sim los ntawm D-galactose, nrog rau txo cov ntsiab lus ntawm MDA thiab collagen hauv lub ntsws thiab ntshav, thiab nce cov ntsiab lus ntawm elastin, muaj Cov nyhuv scavenging zoo ntawm DPPH, ncua lub sijhawm ntawm hypoxia hauv cov nas senescent, txhim kho cov haujlwm ntawm SOD hauv cov ntshav, thiab ncua lub physiological degeneration ntawm lub ntsws hauv kev sim cov nas nrog cellular morphological degeneration, kev sim tau pom tias Cistanche muaj peev xwm antioxidant zoo. thiab muaj peev xwm los ua ib qho tshuaj tiv thaiv thiab kho cov kab mob ntawm daim tawv nqaij laus. Nyob rau tib lub sijhawm, echinacoside hauv Cistanche muaj lub peev xwm tseem ceeb txhawm rau txhawm rau DPPH dawb radicals thiab muaj peev xwm tshem tawm cov pa oxygen reactive thiab tiv thaiv dawb radical-induced collagen degradation, thiab kuj muaj kev kho zoo ntawm thymine dawb radical anion puas.

Nyem rau Cistanche ntsiav tshuaj Cov txiaj ntsig

【Yog xav paub ntxiv:george.deng@wecistanche.com / WhatApp:86 13632399501 】

1. Taw qhia

Tam sim no, cov pej xeem thoob ntiaj teb muaj qhov tseem ceeb nce lub neej expectancy piv rau ntau xyoo dhau los, ntau tshaj 60 xyoo ntawm cov neeg mob. Raws li Lub Koom Haum Ntiaj Teb Kev Noj Qab Haus Huv (WHO), feem pua ​​​​ntawm cov neeg muaj hnub nyoog tshaj 60 xyoo yuav ob npaug thoob ntiaj teb los ntawm 2050 [1]. Txawm li cas los xij, lub neej ntev dua ua rau peb rov xav txog tsis yog kev noj qab haus huv ntawm cov neeg laus xwb tab sis kuj muaj qhov cuam tshuam txog kev laus li cas [2].

Kev laus yog cov txheej txheem physiological uas ua rau muaj kev loj hlob ntawm cov cellular functionality, nrog rau cov kev tshwm sim uas predispose tib neeg mus rau ib qho kev pheej hmoo ntawm frailty, morbidity, thiab tuag [3]. Lub luag haujlwm ntawm kev ua neej thiab kev noj haus tuaj yeem txhawb "kev laus noj qab haus huv", uas lub neej zoo ua ntej. Raws li WHO, lub tswv yim no hais txog cov txheej txheem ntawm kev txhim kho thiab tswj lub peev xwm ua haujlwm uas ua rau muaj kev noj qab haus huv hauv cov laus [1,4].

Ntau lub cellular thiab molecular cov cim qhia tau koom nrog hauv cov txheej txheem kev laus. Tshwj xeeb, cuaj lub cim tseem ceeb yog qhov txiav txim siab hauv cov txheej txheem kev laus: genomic instability, telomere attrition, epigenetic alterations, poob ntawm proteostasis, dysregulation ntawm nutrient sensing, mitochondrial dysfunction, cellular senescence, qia cell depletion, thiab al. Cov txheej txheem molecular no koom nrog hauv kev tsim cov kab mob uas muaj hnub nyoog xws li mob qog noj ntshav, rog rog, ntshav qab zib, kab mob plawv (CVD), thiab kab mob neurodegenerative [3]. Cov kab mob muaj hnub nyoog no tau cuam tshuam nrog kev pheej hmoo uas tuaj yeem hloov kho feem ntau los ntawm kev noj zaub mov, uas yog ib qho tseem ceeb ntawm kev noj qab haus huv [6]. Tsis tas li ntawd, microbiota, uas tau hloov kho los ntawm kev noj haus, kuj tau koom nrog kev laus [6]. Nws tau raug pom tias muaj hnub nyoog txog kev poob qis hauv lub cev tsis muaj zog (immunosenescence) thiab mob qis qis tuaj yeem ua rau muaj kev cuam tshuam microbiota uas cuam tshuam nrog ntau lub hnub nyoog ntsig txog pathologies. Yog li, nws tau raug sib cav tias kev noj zaub mov kom zoo tuaj yeem hloov kho qhov kev loj hlob ntawm cov kab mob tshwj xeeb hauv plab microbiota. Qhov no tau cuam tshuam nrog kev txhim kho kev noj qab haus huv hauv cov neeg laus [7].

Nyob rau hauv lub teeb ntawm cov saum toj no, peb kev tshuaj xyuas tsom los tshuaj xyuas cov ntaub ntawv muaj txog qhov muaj feem cuam tshuam ntawm Mediterranean noj zaub mov (MedDiet) tag nrho, lossis ntawm tus kheej cov ntsiab lus ntawm nws, ntawm cuaj lub cim ntawm kev laus, los muab pov thawj ntxiv ntawm nws txoj kev noj qab haus huv. cov txiaj ntsig. Ntxiv mus, peb kuj tau tshuaj xyuas cov txiaj ntsig ntawm MedDiet ntawm microbiota thiab nws txoj kev sib raug zoo rau kev laus.

2. Kev laus thiab Frailty: Kev sib txuas lom neeg

Los ntawm kev xav txog kev lom neeg, kev laus tuaj yeem txhais tau tias yog lub cev nqaij daim tawv thiab kev loj hlob ntawm cov hlwb hauv cov kabmob thiab cov ntaub so ntswg, uas tshwm sim thaum lub neej ntawm ib tug neeg thiab ua rau kev ua haujlwm qeeb lossis tag nrho cov haujlwm poob [8-10] .

Pleiotropic antagonist noob muaj xws li ib pawg ntawm cov noob uas tswj cov cellular senescence, ua lub luag haujlwm tseem ceeb hauv kev tiv thaiv kev degeneration ntawm malignant hlwb hauv lub voj voog ntawm tes [11,12]. Cov noob no tseem koom nrog hauv kev tiv thaiv cov txheej txheem hauv lub cev ntawm cov cellular senescence txheej txheem thiab cov kab mob uas muaj hnub nyoog. Txawm li cas los xij, cov hlwb laus tsim cov proinflammatory thiab lytic extracellular matrix molecules nyob rau hauv cov txheej txheem hu ua senescence-associated complex secretory phenotype (SASP), uas ua rau degeneration thiab pathological senescence. Ntxiv mus, cov txheej txheem kev laus muaj kev tiv thaiv kab mob; tshwj xeeb, cell-mediated tiv thaiv mechanism yog qeeb. Senescent hlwb tsis tsim cov teeb liab txaus los qhib lub cev tiv thaiv kab mob. Ib yam li ntawd, senescence yog induced los ntawm tsub zuj zuj ntawm ntau yam ntawm cov cellular theem uas yog lub luag hauj lwm rau macromolecular puas, xws li theem nrab DNA alterations vim oxidative puas, telomere shortening, thiab endoplasmic reticulum (ER) degeneration [13]. Yog li, kev laus yog qhov tshwm sim ntawm kev sib cuam tshuam ntawm ntau qhov sib txawv ntawm cov hauv zos thiab cov kab ke ib puag ncig thiab cov xwm txheej cuam tshuam vim yog cellular senescence. Yog li ntawd, tus naj npawb ntawm senescent hlwb nyob rau hauv ib tug neeg lub cev nce nrog lub hnub nyoog raws li cov laus tiv thaiv kab mob yuav ua tsis tau zoo thiab senescent hlwb accumulates. Qhov no ua rau cov tib neeg muaj kev cuam tshuam rau kev puas tsuaj ntxiv tom qab raug rau ib puag ncig kev ntxhov siab [13]. Tus kab mob no tshwm sim thaum ib puag ncig kev ntxhov siab tawm tsam cov ntaub so ntswg uas twb muaj nyob rau hauv lub xub ntiag ntawm senescent hlwb nrog tsawg resilience [14,15].

Frailty tshwm sim vim qhov kev poob qis feem ntau txuas nrog lub hnub nyoog, kev puas tsuaj loj, thiab qhov pib ntawm cov xeev pathological. Qhov no ua rau muaj qhov ua rau muaj kev pheej hmoo ntau ntxiv thiab txo qhov muaj peev xwm hloov tau, thiab thaum kawg, kev hloov pauv kev noj qab haus huv tsis zoo tshwm sim los ntawm kev ntxhov siab me ntsis. Nws yog pom zoo kom hais txog "frailty syndrome": ib tug mob pathological mob tshwm sim los ntawm kev sib cuam tshuam ntawm ob peb yam, nrog rau kev laus-txog kev hloov ntawm lub cev, neuropathology, kev noj haus tsis txaus mus txog rau kev tsis txaus noj haus, thiab kev cuam tshuam tsis zoo ntawm kev noj qab haus huv. [16]. Feem ntau ntawm cov neeg tsis muaj zaub mov tsis txaus yog qhov tsis txaus, thiab kev noj zaub mov tsis zoo ua rau poob phaus, uas tuaj yeem ua rau lub cev tsis muaj zog [17]. Ntawm lwm yam, kev rog rog ua rau muaj kev pheej hmoo ntawm frailty [18]. Nyob rau hauv cov nqe lus ntawm lub cev muaj pes tsawg leeg, frailty tau txuam nrog ib tug ntau dua lub cev rog loj thiab rog feem pua ​​thiab nrog ib tug tsawg leeg nqaij thiab yog feem ntau tsis koom nrog lub cev loj Performance index [19-21].

Tag nrho cov no tuaj yeem ua rau cov neeg laus tsis muaj zog poob tag nrho nws tus kheej txaus, ua rau muaj kev pheej hmoo ntawm kev poob, thiab tuaj yeem ua rau muaj kev tsis sib haum xeeb nrog kev puas tsuaj loj ntawm kev txawj ntse uas thaum kawg ua rau muaj kev pheej hmoo ntawm kev loj hlob ntawm cov kab mob [22].

3. Kev Noj Qab Haus Huv Mediterranean

Lub sij hawm MedDiet yog thawj zaug los ntawm Ancel Keys hauv 1960s [23]. Lub MedDiet qhia txog cov qauv kev noj haus uas zoo ib yam ntawm kev vam meej nyob ib ncig ntawm Hiav Txwv Mediterranean, tshwj xeeb tshaj yog tim Nkij teb chaws, cov kob ntawm Crete, thiab yav qab teb Ltalis thaum ntxov 1960s [24]. Lub MedDiet yog qhov sib txuas nrog cov txiv ntseej loj hlob hauv thaj tsam Mediterranean thiab tau cuam tshuam nrog cov kab mob qis (qis dua ntawm CVD thiab cov kab mob metabolic cuam tshuam nrog qhov hnyav tshaj) thiab, yog li ntawd, lub neej expectancy [24,25].

MedDiet yog tus cwj pwm los ntawm kev noj cov roj txiv roj ntau (OO) ua cov roj tseem ceeb - tshwj xeeb tshaj yog nkauj xwb (VOO) thiab cov nkauj xwb (EVOO) - thiab kev noj zaub mov ntau ( zaub, txiv hmab txiv ntoo, legumes, qos yaj ywm, qhob cij. , thiab lwm yam cereals (tsawg kawg refined), txiv ntseej thiab noob), raws li zoo raws li tshiab raws caij nyoog, zus nyob rau hauv lub zos, thiab cov zaub mov ua tiav tsawg kawg nkaus. Cov mis nyuj noj yog nruab nrab (tsuas yog cheeses thiab yogurts), thiab ntses (qhov zoo tshaj plaws ntawm cov saw hlau ntev polyunsaturated fatty acids (PUFAs), tshwj xeeb tshaj yog omega-3) thiab nqaij qaib tau noj tsawg lossis nruab nrab. MetDiet suav nrog kev noj tsawg ntawm cov nqaij liab thiab khoom qab zib thiab haus cawv ntawm cov pluas noj. Tsis pub ntau tshaj plaub lub qe noj ib lub lis piam. Hauv cov ntsiab lus dav dav, caloric kom tsawg hauv daim ntawv ntawm cov rog tsis pub tshaj 30 feem pua ​​​​ntawm kev noj, nrog tsawg dua 8-10 feem pua ​​​​ntawm cov rog saturated. Qee cov tshuaj bioactive hauv MedDiet suav nrog cov vitamins, minerals, polyphenols, fiber, nitrates, PUFAs, thiab mono-unsaturated fatty acids (MUFAs) uas, ua ke los yog sib cais, muaj txiaj ntsig zoo rau kev noj qab haus huv [26–28]. Ntawm cov PUFAs, qhov tseem ceeb omega -6 fatty acid yog linoleic acid (LA). Tsis tas li ntawd, ntev omega -3 PUFAs, xws li eicosapentaenoic acid (EPA) thiab docosahexaenoic acid (DHA), yog derivatives ntawm alpha-linoleic acid. Cov no feem ntau muaj nyob rau hauv cov roj ntses [29]. Rau cov laj thawj no, MedDiet yog qhov tshwj xeeb thiab txawv ntawm lwm cov qauv kev noj qab haus huv [29].

4. Interplay ntawm Mediterranean noj zaub mov, Kev laus thiab Frailty

4.1. Mediterranean noj zaub mov thiab Hallmarks of Aging

Cov txheej txheem kev laus tau txuas rau cuaj qhov tshwj xeeb ntawm cov cellular thiab molecular nta [5] (Daim duab 1). Txhua yam ntawm no plays lub luag hauj lwm nyob rau hauv lub trajectory ntawm natural aging; lawv cov kev sim exacerbation accelerates tus txheej txheem, thiab lawv optimization slows nws, yog li nce lifespan [30]. Kev ua neej nyob sab nraud xws li kev noj haus tuaj yeem hloov kho txoj kev laus [31,32].

4.1.1. Genomic Instability

Kev laus ua rau muaj kev cuam tshuam rau DNA kev hloov pauv uas tshwm sim los ntawm kev sib xyaw ntawm oxidative kev nyuaj siab, kev hloov pauv ntawm epigenetic, puas DNA, thiab telomere attrition [33]. DNA tsis kho tuaj yeem ua rau muaj kev pheej hmoo ntawm kev hloov pauv thiab nyiam qhov pib lossis kev loj hlob ntawm cov kab mob muaj hnub nyoog [34,35]. MedDiet tuaj yeem ua lub luag haujlwm tiv thaiv kev hloov pauv genomic. Tseeb, bioactive compounds uas muaj nyob rau hauv lub MedDiet, xws li melatonin, phytosterols, carotenoids, polyphenols (xws li resveratrol thiab hydroxytyrosol (HT)), vitamins, thiab glucosinolates (nyob rau hauv cruciferous zaub), yuav txhawb DNA kho thiab attenuate telomere shortening [ 36, 37] ib. Cov txiaj ntsig zoo no tau piav qhia los ntawm cov tshuaj tiv thaiv kab mob ntawm MedDiet thiab kev hloov pauv ncaj qha thiab tsis ncaj (epigenetic) cuam tshuam los ntawm MedDiet ntawm cov noob qhia [38–41].

DNA kev puas tsuaj vim oxidative kev nyuaj siab yog tshwm sim los ntawm tsis ua hauj lwm ntawm oxidative kev puas tsuaj kho mechanisms raws li ib tug tshwm sim ntawm ntau reactive oxygen hom (ROS) [42]. Guanine yog lub hom phiaj tseem ceeb rau DNA oxidation, tsim oxidized metabolites. Ntawm lawv, 8-oxo- 2 0 -deoxyguanosine (8-OHdG) yog suav tias yog ib qho cim ntawm oxidative stress nrog mutagenic peev xwm [43–45]. Urquiaga et al. cuam ​​tshuam nrog MedDiet, suav nrog kev haus cawv liab me me, nrog rau kev txo qis hauv 8-OHdG qib hauv peripheral ntshav leukocyte DNA, uas cuam tshuam zoo rau kev tswj cov kev ntxhov siab oxidative [46]. Ib yam li ntawd, qis dua ntawm lwm tus cim ntawm oxidative kev nyuaj siab, deoxyguanosine adduct, tau cuam tshuam nrog kev ua raws li MedDiet hauv Italian pawg ntawm EPIC (European Kev Tshawb Fawb Txog Kev Kho Mob thiab Khoom Noj Khoom Haus) [47].

Cov txiv ntseej thiab cov txiv lws suav siav siv OO qhia txog lub luag haujlwm tiv thaiv oxidative DNA puas [48–50]. Qhov kev tiv thaiv no tau pom nyob rau hauv kev tshawb fawb txog kev cuam tshuam hauv tib neeg tom qab noj txiv lws suav [51,52], broccoli [53,54], spinach [55,56], thiab blueberries [57,58]. Tsis tas li ntawd, ib txoj kev tshawb fawb hauv nas noj nrog cov khoom noj uas muaj txiaj ntsig nrog VOO pom muaj kev sib koom ua ke nrog kev puas tsuaj tsawg hauv cov khoom siv caj ces hauv cov qe ntshav peripheral vs. nas noj nrog cov roj sunflower [59]. Hauv cov ntsiab lus no, MUFAs thiab PUFAs tau pom los ua lub luag haujlwm tiv thaiv oxidative kev nyuaj siab thiab DNA puas tsuaj [60–62]. Hauv kev soj ntsuam me me ntawm txoj kev tshawb fawb PREDIMED, pab pawg cuam tshuam nrog MedDiet nrog MUFA (EVOO) lossis PUFA (walnuts) piv rau kev tswj hwm (kev noj zaub mov tsis muaj rog) tau pom qhov kev txhim kho tseem ceeb hauv cov txiaj ntsig ntawm cov hlab plawv thiab qis dua ntawm cov cim oxidative. hauv cov zis [63] Ib yam li ntawd, lwm qhov kev sim tshuaj ntsuam pom tau zoo dua kev tswj xyuas cov cim atherosclerosis hauv cov tib neeg ntawm MedDiet noj OO; Txawm li cas los xij, tsuas yog cov pab pawg uas nws lub ntsiab rog yog VOO txo qis zis 8-OHdG qib [64]. Feem ntau, MedDiet thiab OO pab pawg cuam tshuam tau pom cov txiaj ntsig zoo hauv kev tswj hwm DNA kho cov noob. Ib qho kev qhia qis ntawm cov noob polymerase k, uas encodes cov protein uas yog lub luag haujlwm rau kev rov ua dua DNA puas, raug txheeb xyuas hauv MedDiet thiab OO pab pawg [64]. Yog li, cov qauv kev noj haus no tau pom muaj txiaj ntsig zoo rau ntshav siab, insulin rhiab heev, thiab qib lipid ua rau cov neeg muaj kev pheej hmoo siab plawv [65-69].

Kev hloov pauv hauv kev noj zaub mov zoo rau tus qauv Mediterranean tau raug npaj ua qhov zoo hauv kev txo qis oxidative DNA puas tsuaj rau cov neeg mob qog noj ntshav [70]. Tsis tas li ntawd, ntau qhov kev tshawb fawb qhia txog kev sib cuam tshuam ntawm kev ua raws li MedDiet thiab cov neoplasms uas muaj ntau heev xws li mob qog noj ntshav mis, mob qog noj ntshav (CRC), mob qog noj ntshav, lossis mob qog nqaij hlav prostate [71–73]. Tshwj xeeb, cov tib neeg uas muaj CRC thiab kev ua siab zoo rau MedDiet tau nthuav tawm cov qib histological qis thiab qis dua ntawm synchronous adenomas piv rau cov neeg mob oncologic uas tsis ua raws li MedDiet. Kev nce qib ntawm glutathione peroxidase (nrog rau cov khoom antioxidant) thiab txo qis 8-OHdG qhov tseem ceeb tau kuaj pom hauv cov neeg mob uas muaj kev ua raws li MedDiet [74].

Hais txog cov kab mob neurodegenerative, qhov txo qis ntawm Alzheimer's disease (AD) tau cuam tshuam nrog kev cuam tshuam ncaj qha ntawm MedDiet Cheebtsam ntawm pathogenesis ntawm AD [75,76]. Cov txiaj ntsig zoo ntawm qhov teeb meem neurodegenerative no feem ntau yog vim EVOO noj. Oleuropein (ib qho ntawm cov phenolic tseem ceeb ntawm cov txiv ntseej ntsuab) txo qis Poly ADP-ribose polymerase (PARP)-1 ua kom, tiv thaiv cov hlwb neuronal los ntawm kev puas tsuaj oxidative. Tsis tas li ntawd, Zhang et al. pom muaj hnub nyoog nce nyob rau hauv 8-OHdG hauv tib neeg lub hlwb cov ntaub so ntswg, tshwj xeeb tshaj yog nyob rau hauv cov neeg uas muaj AD [77]. Hauv cov neeg uas muaj kev puas siab puas ntsws me me, qhov nce hauv 8-OHdG tau kuaj pom hauv qee thaj chaw hauv hlwb, thiab qhov no tuaj yeem txhais tau tias yog biomarker kwv yees ntawm AD pathogenesis [78]. Yog li, thaum ntsuas oxidative DNA puas tsuaj raws li 8-OHdG qhov tseem ceeb hauv cov neeg mob uas muaj kev paub tsis meej me ntsis uas tau noj EVOO rau ib xyoos, 8-OHdG qib tau txo qis [79].

Zuag qhia tag nrho, nws zoo li tus qauv Mediterranean muaj qhov cuam tshuam zoo rau genomic instability.

4.1.2. Telomere Attrition

Telomeres yog nucleotide ib ntus ntawm qhov kawg ntawm chromosomes, uas ua rau luv luv nrog lub hnub nyoog. Lawv hu ua biomarkers ntawm kev laus. Mob oxidative kev nyuaj siab yog txuam nrog telomere attrition [80]. Tsis tas li ntawd, o ua rau telomere luv luv los ntawm kev nce tus nqi ntawm hematopoietic qia cell replication los muab cov leukocyte thov tsim nyob rau hauv cov txheej txheem inflammatory [81]. Txawm hais tias qhov ntev telomere tau txais txiaj ntsig, nws cuam tshuam los ntawm lwm yam xws li haus luam yeeb, rog rog, thiab kev ua neej nyob tsis muaj zog. Nyob rau hauv lem, telomere shortening ua rau muaj kev pheej hmoo ntawm CVD, mob qog noj ntshav, thiab kev tuag, tshwj xeeb tshaj yog thaum ntxov [82,83].

Kev ua raws li MedDiet ntau dua yog txuam nrog ntev telomeres thiab ntau dua telomerase kev ua haujlwm [84,85], uas tuaj yeem cuam tshuam rau qis qis ntawm qhov mob thiab oxidative stress [84,86]. Hauv lawv cov kev txheeb xyuas meta, Canudas et al. tsim kom muaj kev sib raug zoo ntawm MedDiet adherence thiab telomere ntev hauv cov qe ntshav tshwj tsis yog cov qauv coj los ntawm cov txiv neej [87]. Txawm li cas los xij, nws yuav tsum tau muab sau tseg tias cov kev tshawb fawb suav nrog yog ntu ntu thiab, yog li ntawd, tsis tsim kom muaj kev sib haum xeeb. Txawm li cas los xij, qhov txiaj ntsig no tuaj yeem sib txawv nrog ob txoj kev tshawb fawb yav tom ntej tau ua rau hnub tim [88,89]. Kev ua haujlwm ntawm Meinilä et al. yav tom ntej tau kawm 1046 Dutch cov ntsiab lus nrog lub hnub nyoog nruab nrab ntawm 61 xyoo tshaj 10 xyoo thiab tsis tau tsim kev koom tes ntawm cov txiv neej pw ua ke thiab ua raws li MedDiet. Hauv tib txoj kev tshawb fawb, cov poj niam tau ceev telomere luv luv [89]. Ntawm cov ntsiab lus no, tib qhov kev sim tshuaj pom los txog niaj hnub no yog los ntawm García-Calzón li al.; Qhov no yog ib qho kev soj ntsuam me me ntawm txoj kev tshawb fawb PREDIMED-Navarra, uas tau soj ntsuam 520 tus neeg, suav nrog 55 feem pua ​​​​cov poj niam hnub nyoog 55-80 xyoo. Peb pawg kev cuam tshuam tau muab tso rau hauv kev tswj hwm lossis kev noj zaub mov tsis muaj rog thiab muaj ob pawg MedDiet, ib qho ntxiv nrog EVOO thiab lwm qhov nrog cov txiv ntoo sib xyaw. Hauv kev txheeb xyuas ntu ntu ntawm lub hauv paus, kev ua raws li MedDiet zoo dua yog cuam tshuam nrog ntev telomeres tsuas yog hauv cov poj niam. Txawm li cas los xij, kev xa mus rau pawg MedDiet-ntxiv tau cuam tshuam nrog kev pheej hmoo siab ntawm telomere luv luv 5 xyoo tom qab kev cuam tshuam, tsis muaj qhov sib txawv rau pab pawg ntxiv nrog EVOO [88]. Tsis muaj kev piav qhia zoo ib yam rau cov kev tshawb pom no, txawm hais tias muaj kev sib txawv xws li haiv neeg, caj ces, lossis poj niam txiv neej tuaj yeem cuam tshuam. Hauv kev ua haujlwm ntawm Gu et al., muaj kev koom tes zoo tau pom ntawm MedDiet adherence thiab telomere ntev hauv cov neeg tsis yog neeg Mev dawb [90]. Lub koom haum no tsis pom nyob rau hauv African Americans lossis Hispanics [90]. Txawm li cas los xij, hauv lwm qhov kev tshawb fawb ntawm PREDIMED-Navarra txoj kev tshawb fawb, nws tau pom tias Pro12Ala polymorphism hauv peroxisome proliferator-activated receptor 2 (PPAR 2) gene cuam tshuam nrog MedDiet los tiv thaiv telomere shortening [91].

Hais txog PUFAs, omega -3 tau zoo dua li omega-6 txij li thaum cov telomere luv luv tau pom nyob rau hauv pawg neeg ntawm cov neeg muaj hnub nyoog tshaj 65 xyoo uas muaj kev puas siab puas ntsws me me ntxiv nrog cov fatty acids no [92]. Ib yam li ntawd, qhov kev sim tshuaj Breitas-Simoes tau pom qhov txo qis hauv telomere attrition hauv cov neeg laus uas tsis muaj kev paub tsis meej uas tau ntxiv lawv cov khoom noj ib txwm nrog walnuts (qhov chaw ntawm omega-3 PUFAs) rau 2 xyoos [36]. Txawm li cas los xij, LA supplementation nyob rau hauv cov pej xeem ntawm 299 cov neeg laus uas tsis ntev los no myocardial infarction yog txuam nrog nce leukocyte telomere ntev, thiab tsis muaj kev sib raug zoo nrog lwm cov PUFAs [93]. Feem ntau, nws tuaj yeem txiav txim siab tias nws muaj txiaj ntsig zoo los ua raws li kev noj qab haus huv uas muaj PUFAs.

Telomere ntev tau txuas nrog ntau hom mob qog noj ntshav. Qhov kev tshawb pom ntawm luv telomeres hauv CRC qhia tias telomere shortening ua rau cov qog nqaij hlav thiab cov caj ces tsis ruaj khov ntawm cov hlwb premalignant. Cov telomeres luv luv tau pom tias ua rau muaj qhov tsis zoo hauv cov hlwb noj qab haus huv lossis genomic instability hauv cov hlwb premalignant [83,94,95]. Tseeb tiag, hloov telomere ntev homeostasis thiab tsis kho DNA puas tau suav hais tias yog qhov tseem ceeb hauv qhov pib, kev loj hlob, thiab kev kwv yees ntawm CRC [95]. Hauv qhov no, MedDiet tuaj yeem muaj txiaj ntsig zoo raws li kev tiv thaiv kev kho mob vim ntau qhov kev tshawb fawb qhia txog kev sib raug zoo ntawm kev ua raws li MedDiet thiab telomere preservation [84,91].

Tsis tas li ntawd, telomere shortening tau cuam tshuam rau cov kab mob neurodegenerative [96,97]. Guo et al. qhia tias telomere ntev muaj qhov ua rau muaj kev pheej hmoo ntawm AD vim oxidative kev nyuaj siab thiab mob [97]. Tsis tas li ntawd, telomere shortening tau cuam tshuam nrog kev paub tsis meej, amyloid pathology, thiab tau protein hyperphosphorylation hauv AD [96]. Hauv qhov no, oleuropein aglycone los ntawm OO inhibits protein aggregation hauv AD [98]. Tsis tas li ntawd, kev noj zaub mov Mediterranean tuaj yeem tiv thaiv telomere luv luv tom qab oxidative puas tsuaj ua tsaug rau cov zaub mov nplua nuj antioxidant xws li txiv ntoo thiab noob [99]. Resveratrol (ib qho tshuaj tiv thaiv antioxidant tam sim no hauv cov txiv hmab txiv ntoo) tsim cov teebmeem neuroprotective hauv kev tshawb fawb ntawm tus qauv nas ntawm AD [100].

Hauv cov ntsiab lus, nce kev ua raws li MedDiet tuaj yeem txo qis telomere attrition. Txawm li cas los xij, cov txiaj ntsig zoo no tuaj yeem txwv rau cov pab pawg tshwj xeeb ntawm cov pej xeem. Cov kev tshawb fawb ntxiv yog xav tau los daws cov kev sib cav sib ceg.

4.1.3. Cov teebmeem Epigenetic

Epigenetics suav nrog kev hloov pauv genomic uas tshwm sim thaum tsis muaj kev puas tsuaj DNA ncaj qha. Cov tub ntxhais hluas, noj qab haus huv cov neeg muaj kev cog lus chromatin thiab kev pom zoo ntawm kev tswj hwm ntawm cov txheej txheem lom neeg. Txawm li cas los xij, kev laus nyiam qhov sib xyaw ntawm chromatin kev puas tsuaj, uas cuam tshuam genome kev ncaj ncees thiab hloov pauv cellular function [101]. DNA methylation (mDNA) yog suav tias yog ib qho ntawm qhov zoo tshaj plaws-paub cov cim epigenetic. mDNA yog siv los ua lub moos rau kev suav cov hnub nyoog lom neeg [102]. Qhov ntev interspersed nuclear lub caij (LINE-1) tau siv los ua tus cim ntawm mDNA thoob ntiaj teb vim nws yog qhov feem ntau rov ua ntu zus hauv tib neeg genome, thiab 1/3 ntawm mDNA tshwm sim hauv LINE-1 [103,104 ]. Tshwj xeeb, qhov hypomethylation ntawm LINE-1 tshwm sim thaum laus thiab muaj feem cuam tshuam nrog ntau yam qog noj ntshav thiab CVD [105]. Tsis tas li ntawd, oxidative kev nyuaj siab plays lub luag hauj lwm nyob rau hauv mDNA ntawm cov pa roj carbon voj voog [42], yog li ntau ROS muaj, qhov ntau dua DNA puas; Thaum kawg, DNA ua rau hypomethylation los tiv thaiv nws tus kheej [106]. Hauv cov ntsiab lus no, kev noj zaub mov nplua nuj nyob rau hauv antioxidants, xws li Mediterranean noj zaub mov, tau npaj ua ib qho kev noj haus epigenetic.

Txog hnub tim, ntau qhov kev tshawb fawb tau txuas MedDiet ua raws li LINE-1 hypomethylation. Tshwj xeeb, ob qhov kev sim tshuaj ntsuam xyuas tsim kev sib raug zoo ntawm ob yam no [107,108]. Hauv kev ua haujlwm ntawm Agodi li al., cov poj niam uas muaj hnub nyoog me nyuam yaus uas tsis ua raws li MedDiet, tshwj xeeb tshaj yog cov neeg uas muaj cov txiv hmab txiv ntoo qis dua, muaj kev pheej hmoo siab dua ntawm LINE-1 hypomethylation [109]. Qhov kev tshawb pom no yuav cuam tshuam nrog qhov tseeb tias txiv hmab txiv ntoo yog cov khoom noj uas muaj folate, thiab folate yog ib qho tseem ceeb ntawm cov pab pawg methyl. Lwm cov khoom tshwj xeeb ntawm MedDiet, xws li txiv ntseej thiab EVOO, tuaj yeem ua rau muaj kev hloov pauv methylation hauv ntau lub peripheral cov qe ntshav dawb cov noob muaj feem xyuam rau ntshav qab zib, o, thiab cov teeb liab hloov pauv, uas yuav muaj txiaj ntsig kev noj qab haus huv [110]. Ib yam li ntawd, MedDiet tuaj yeem pab txhawb kom ncua cov txheej txheem carcinogenesis uas cuam tshuam nrog DNA methylation txheej txheem txij li ntau qhov kev tshawb fawb tau pom tias qis dua LINE-1 qib methylation hauv ntau hom qog, xws li CRC lossis mob qog noj ntshav [111,112].

Hais txog CVD, kev tshuaj xyuas luam tawm los ntawm Muka li al. txhawb cov lus pom zoo tias mDNA thoob ntiaj teb, raws li rov qab LINE-1 hypomethylation, yog inversely txuam nrog CVD kev pheej hmoo ntawm nws tus kheej ntawm tsim muaj kab mob plawv [105]. Hauv cov ntsiab lus dav dav, LINE-1 hypomethylation yog txuas rau qhov tsis txaus siab ntawm cov hlab plawv cov kab mob vim nws koom nrog ntshav qab zib, rog rog, txo qis HDL-cholesterol, nce qib roj cholesterol tag nrho, thiab mob [113,114].

Txawm li cas los xij, kev qhia ntawm RNA (ribonucleic acid) pab txhawb rau kev hloov pauv ntawm cov noob caj noob ces uas hloov pauv kev ua haujlwm ntawm tes. Hauv cov ntsiab lus no, qhov overexpression ntawm miR-155-3p tau txuas rau carcinogenesis [115]. Ping Li et al. kuaj pom muaj kev nthuav qhia ntau ntxiv ntawm miR-155-3p hauv CRC qog loj hlob [116]. Tsis tas li ntawd, Let-7b, tus tswj hwm ntawm histone H2B ubiquitination, tau pom qhov tshwm sim ntawm cov nyhuv antitumor [117]. Hauv kev hwm ntawm kab no, Li et al. qhia tau tias cia-7b-3p inhibited qog loj hlob thiab metastasis hauv ntsws cancer, cuam tshuam nrog qhov qis qis ntawm cov molecule no nrog rau cov neeg mob tsis zoo hauv cov neeg mob ntsws adenocarcinoma [118]. Raws li kev tiv thaiv kev kho mob, kev ua raws li MedDiet zoo tuaj yeem txo qhov kev qhia ntawm miR-155-3p thiab nce kev qhia ntawm let{11}}b-3p, txhim kho txoj kev pheej hmoo thiab evolution ntawm mob qog noj ntshav [ 119] ib.

Hais txog cov kab mob neurodegenerative cuam tshuam nrog kev laus, kev hloov kho epigenetic ua lub luag haujlwm tseem ceeb hauv AD [120]. Tshwj xeeb tshaj yog, mDNA yog ib qho kev tswj xyuas zoo heev uas cuam tshuam nrog nicotinamide adenine dinucleotide (NAD)-nyob deacetylase Sirtuin 1 (SIRT1) uas tiv thaiv kev hloov pauv methylation [121]. Hauv qhov no, Luccarini et al. pom tau tias quercetin thiab lwm yam EVOO polyphenols qhib txoj hauv kev SIRT1 nrog kev qhia txog kev kho mob thiab kev tiv thaiv kev pab cuam [122,123].

Yog li, nws zoo li yuav muaj kab mob ntsig txog hnub nyoog - kev sib cuam tshuam ntawm epigenetic uas yuav tau txais txiaj ntsig los ntawm kev noj qab haus huv Mediterranean qauv.

4.1.4. Proteostasis

Proteostasis, los yog protein homeostasis, yog hais txog kev ua haujlwm ntawm kev sib txuas ntawm txoj hauv kev uas yog qhov tseem ceeb rau kev ua haujlwm ntawm tes thiab kev muaj peev xwm, ua kom muaj qhov tsim nyog, folding, thiab kev sib cuam tshuam ntawm cov proteins los ntawm kev sib txuas mus rau degradation [5]. Tshwj xeeb, chaperones thiab ob lub tshuab proteolytic (ubiquitin-proteasome thiab lysosome-autophagy system) yog lub luag haujlwm rau kev saib xyuas ntawm proteostasis [124]. Qhov kev poob qis ntawm cov cellular protein homeostasis raug kuaj pom thaum lub sijhawm laus, thiab cov proteomes uas ruaj khov dua los yog ntau dua rau cov kev hloov pauv tau pom nyob rau hauv cov tsiaj nyob ntev tshaj [125].

Lub hnub nyoog cuam tshuam txog kev puas tsuaj ntawm proteostasis cuam tshuam rau kev ua haujlwm ntawm chaperone vim yog cellular zog tsis txaus uas yog muaj nyob rau hauv senescence [126]. Tsis tas li ntawd, autophagy thiab proteasome hloov nrog lub hnub nyoog, cuam tshuam rau proteostasis [127,128]. Hauv qhov no, kev sim kev cuam tshuam uas txhim kho autophagy-ua kom muaj zog tau cuam tshuam nrog kev noj qab haus huv kev laus [129]. Kev noj zaub mov zoo tuaj yeem muaj txiaj ntsig zoo rau kev ua kom zoo ntawm proteostasis. Tseeb tiag, MedDiet polyphenols xws li resveratrol tuaj yeem ncaj qha qhib autophagy [129]. Ib yam li ntawd, oleuropein tau raug qhia tias yog ib qho autophagy enhancer los ntawm cov protein mammalian lub hom phiaj ntawm rapamycin (mTOR) thiab adenosine monophosphate-activated protein kinase (AMPK)-dependent mechanism [130]. Tsis tas li ntawd, cov khoom antioxidant ntawm MedDiet Cheebtsam no tuaj yeem txo qis cov protein ntau oxidized cuam tshuam nrog kev laus thiab cov kab mob uas muaj hnub nyoog [131].

Cov kab mob muaj hnub nyoog xws li cov kab mob neurodegenerative (tshwj xeeb, AD thiab Parkinson's disease, PD) tau cuam tshuam txog kev puas tsuaj ntawm proteostasis [132]. Nyob rau hauv AD, hyperphosphorylated tau protein tau sib sau ua ke txawv txav thiab tsim insoluble neurofibrillary tangles, uas tau koom nrog hauv neurodegeneration [133,134]. Tsis tas li ntawd, amyloid-beta (A) peptide tau sau thiab tsim cov plaques uas puas hlwb neuronal [135]. Txog PD, aggregates ntawm insoluble -synuclein protein fibrils muaj nyob rau hauv cov neurons ntawm cov neeg nrog PD thiab yog neurotoxic [136]. Zuag qhia tag nrho, qhov kev poob ntawm proteostasis nyob rau hauv cov kab mob neurodegenerative yog ze rau o thiab cellular senescence [13,137]. Shannon et al. thov MedDiet ua ib lub tswv yim los tiv thaiv neurodegeneration vim nws modulating nyhuv ntawm protein homeostasis [30]. Los ntawm kev txhim kho autophagy, OO tuaj yeem txo qhov cuam tshuam ntawm cov kab mob toxic vascular, nyiam kev tiv thaiv kab mob lig AD [29]. Tshwj xeeb, oleocanthal tuaj yeem txo tau protein ntau polymerization [138]. Kev sib cuam tshuam ntawm oleocanthal thiab tau proteins induces ib tug tau rearrangement uas yuav piav qhia txog cov nyhuv antifibrillogenic ntawm oleocanthal [139]. Yog li, kev cuam tshuam oleocanthal hauv cov nas tau pom tias yuav ua rau muaj txiaj ntsig zoo hauv kev ua haujlwm ntawm cov ntshav-hlwb lub hlwb barrier transporter proteins uas tshem tawm A peptides (P-glycoprotein thiab low-density lipoprotein receptor-related protein 1). Yog li, feem pua ​​​​ntawm A peptides degraded tau siab dua hauv pab pawg kho mob [140]. Cov txiaj ntsig zoo ntawm oleocanthal hauv nas tau txuas ntxiv mus rau tib neeg cov kab ntawm tes txij li kev txhim kho hauv A thauj los ntawm A -secreting hlwb tau pom tom qab siv oleocanthal rau 72 h [141]. Tsis tas li ntawd, resveratrol txo qis -secretase kev ua haujlwm thiab A -peptide aggregation hauv AD murine qauv thiab ua raws li cov tshuaj tiv thaiv neuroprotectant hauv AD thiab PD [142].

Txog CVD, kev hloov pauv hauv cov protein homeostasis thiab kev ruaj ntseg hauv cov proteome tuaj yeem cuam tshuam rau kev noj qab haus huv plawv kev laus [143]. Qhov nce ntxiv ntawm misfolded protein aggregates tau kuaj pom hauv CVD los ntawm kev txo qis ntawm HSP70 chaperone hauv cov ntaub so ntswg thaum laus [144,145]. Hauv cov ntsiab lus dav dav, txo qis kev ua haujlwm ntawm proteasome tau kuaj pom hauv cov atherogenic plaques ntawm cov laus nas thiab cov neeg laus [124,146]. Nyob rau hauv cov ntsiab lus no, oleuropein tsa tus nqi ntawm proteosome-mediated degradation nyob rau hauv tib neeg fibroblast kab lis kev cai, lawv lifespan tau nce, thiab senescence tau ncua los ntawm 15 feem pua ​​[147]. Kev noj zaub mov nplua nuj nyob rau hauv EVOO kuj nce tus tub txib RNA qib ntawm autophagy marker LC3 hauv cov nas laus piv rau cov nas uas tau noj siv lwm qhov chaw noj zaub mov [148].

Urra et al. tau txheeb xyuas qhov hloov pauv proteostasis raws li lub cim ntawm kev mob qog noj ntshav. Lub hypermetabolism ntawm cov qog nqaij hlav cancer thiab overexpression ntawm oncogenes muaj feem xyuam rau ER kev nyuaj siab. Hauv kev teb rau qhov kev ntxhov siab no, cov lus teb tsis muaj protein ntau (UPR) tau tsim [149]. Yog li ntawd, UPR ua haujlwm raws li kev hloov kho thaum lub sijhawm mob qog noj ntshav [149]. Txawm li cas los xij, kev ua kom UPR nyob rau theem sib txawv ntawm kev hloov pauv qog noj ntshav tau ntsib kev nyuaj [149]. Lub luag haujlwm ntawm UPR thaum lub sijhawm ntxov ntawm kev txhim kho kabmob kheesxaws tiv thaiv oncogene-induced malignant progression [150]. Cells muaj sia nyob oncogene-induced apoptosis nce qib UPR ua kom muaj zog. Yog li, nyob rau theem tom qab ntawm kev mob qog noj ntshav, UPR tau hloov kho ib feem ntawm nws txoj haujlwm thiab pab txhawb qog nqaij hlav, kev ua phem, microenvironment adaptation, thiab tiv thaiv kev kho mob [149]. Qhov tseeb, nyob rau hauv tib neeg biopsies ntawm mob qog noj ntshav mis, lymphoma, los yog ntau yam myeloma, x-box-binding protein-1 (XBP-1), ib qho protein uas qhia txog kev ua kom UPR complex, tau hais ntau heev. thiab muaj feem cuam tshuam nrog kev ua tsis zoo [151–154]. Tsis tas li ntawd, IRE1 -XBP1 UPR qhia txoj hauv kev tau txuas mus rau kev txhawb nqa ntawm peb tus tib neeg lub mis [155], prostate [156], thiab qog nqaij hlav hepatocellular [157]. Hauv qhov kev nkag siab no, MedDiet tuaj yeem tiv thaiv qhov kev pheej hmoo ntawm cov txheej txheem no. Kev ua haujlwm ntawm Yubero-Serrano li al. pom tias MedDiet txo qis kev qhia ntawm cov noob ntsig txog endoplasmic erythrocyte kev nyuaj siab, xws li XBP1 [158]. Tsis tas li ntawd, OO MUFAs "colonized" cell lipid membranes, uas tau cuam tshuam nrog kev txo qis rau ER kev ntxhov siab thiab apoptosis [159]. Tsis tas li ntawd, secoiridoids xws li oleuropein los ntawm EVOO nyiam qhov kev hloov pauv ntawm misfolded proteins hauv lub cell los ntawm kev txhawb nqa kev them nyiaj UPR. Txawm li cas los xij, cov tshuaj bioactive no muaj peev xwm inhibit qhov kev loj hlob ntawm cov qog mammary malignant heev [160,161].

Zuag qhia tag nrho, kev tiv thaiv ntawm neurodegenerative, CVD, thiab kab mob oncological tej zaum yuav muaj kev txaus siab rau lub luag haujlwm ntawm proteostasis-activates ua si los ntawm qee yam ntawm MedDiet. Txawm li cas los xij, kev tshawb fawb ntxiv yog xav tau los qhia meej txog lub luag haujlwm ntawm MedDiet cov khoom noj tshwj xeeb hauv kev tiv thaiv cov kab mob no.

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