Redox Effects Ntawm Molecular Hydrogen Thiab Nws Txoj Kev Kho Mob Hauv Kev Kho Mob Ntawm Cov Kab Mob Neurodegenerative Part 1

Abstract:

Oxidative stress (OS) thiab neuroinflammatory stress muaj feem xyuam rau ntau yam neurological disorders.Txawm hais tias qhov chaw kho mob tseem ceeb ntawm oxidative puas nyob rau hauv neurological ntshawv siab, tseem, tsis muaj zoo thiab kev nyab xeeb txoj kev kho mob rau cov neurodisease muaj. Nrog rau qhov no, molecular hydrogen (H2) tsis ntev los no tau tshaj tawm tias yog cov tshuaj tua kab mob antioxidant thiab tiv thaiv kab mob los kho ntau yam kab mob oxidative kev nyuaj siab.

Oxidative stress yog ib lub ntsiab lus uas tau nyiam ntau xyoo tsis ntev los no thiab tau kawm dav dav hauv kev kawm txog biology thiab tshuaj. Kev ntxhov siab oxidative yog hais txog cov txheej txheem ntawm kev hloov pauv txawv txav hauv ib puag ncig sab hauv thiab sab nraud ntawm cov hlwb vim muaj ntau cov dawb radicals lossis peroxides. Nrog rau kev hloov pauv hauv tib neeg txoj kev ua neej thiab kev ua qias tuaj ib puag ncig, qhov cuam tshuam ntawm oxidative kev nyuaj siab yog nce.

Hmoov zoo, txawm li cas los xij, kev tshawb fawb pom tau tias oxidative kev nyuaj siab tsis yog qhov tsis zoo tag nrho. Nruab nrab oxidative kev nyuaj siab txhawb nqa lub cev thiab lub cev ua haujlwm thiab cuam tshuam nrog kev nco zoo. Ntau cov kev tshawb fawb tau pom tias cov tib neeg uas raug oxidative kev nyuaj siab rau lub sij hawm ntev, xws li cov neeg laus thiab cov neeg mob uas muaj tej yam kab mob, yeej muaj kev pheej hmoo rau nco poob. Txawm li cas los xij, rau cov neeg noj qab haus huv, kev ntxhov siab oxidative nruab nrab yog qhov zoo rau kev txhim kho kev nco thiab kev kawm muaj peev xwm.

Kev ntxhov siab oxidative tuaj yeem cuam tshuam rau kev ua haujlwm ntawm neurons hauv lub hlwb hauv ntau txoj hauv kev. Ua ntej, oxidative kev nyuaj siab txhawb kev sib txuas ntawm cov neurons, txhawb kev xa xov xwm thiab kev txawj ntse. Thib ob, kev ntxhov siab oxidative nruab nrab tuaj yeem ua rau muaj cov kab mob neural qia hlwb hauv lub hlwb, yog li txhawb kev ua siab ntev ntawm kev nco thiab kev kawm. Tsis tas li ntawd, oxidative kev nyuaj siab kuj tuaj yeem nce qib ntawm qee cov neurotransmitters hauv lub hlwb, xws li dopamine thiab norepinephrine, uas cuam tshuam nrog kev kawm thiab kev nco.

Hauv cov ntsiab lus, kev ntxhov siab oxidative nruab nrab yog qhov zoo rau kev nco thiab kev kawm muaj peev xwm. Txawm hais tias oxidative kev nyuaj siab tuaj yeem ua rau qee qhov tsis zoo, peb yuav tsum ua tib zoo saib thiab tuav cov txiaj ntsig zoo ntawm kev ntxhov siab oxidative. Hauv lub neej, peb tuaj yeem tswj hwm qib ntawm oxidative kev nyuaj siab los ntawm kev noj qab haus huv ntawm kev noj qab haus huv, kev noj haus, thiab kev tawm dag zog, yog li kev tiv thaiv zoo dua thiab txhim kho peb lub cim xeeb thiab kev kawm. Nws tuaj yeem pom tias peb yuav tsum txhim kho kev nco, thiab Cistanche deserticola tuaj yeem txhim kho kev nco, vim Cistanche deserticola muaj antioxidant, tiv thaiv kev mob, thiab tiv thaiv kev laus, uas tuaj yeem pab txo qis oxidation thiab inflammatory tshwm sim hauv lub hlwb, yog li tiv thaiv cov kab mob. kev noj qab haus huv ntawm lub paj hlwb. Tsis tas li ntawd, Cistanche deserticola kuj tseem tuaj yeem txhawb kev loj hlob thiab kho cov paj hlwb, yog li txhim kho kev sib txuas thiab kev ua haujlwm ntawm neural networks. Cov teebmeem no tuaj yeem pab txhim kho kev nco, kev kawm, thiab kev xav nrawm, thiab tseem tuaj yeem tiv thaiv kev loj hlob ntawm kev paub tsis meej thiab kab mob neurodegenerative.

Nyem paub ntxiv los txhim kho kev nco

Hauv kev sim tshuaj tsiaj thiab tib neeg, txoj hauv kev rau kev tswj hwm H2 feem ntau yog faib ua peb hom: H2 pa nqus pa, H2 dej dissolving, thiab H2-H2-solved saline txhaj.Qhov kev tshuaj xyuas no tshawb txog qee qhov kev nce qib tseem ceeb hauv Kev tshawb fawb ntawm H2 siv hauv cov kab mob neurodegenerative (NDs), suav nrog Alzheimer's kab mob, Parkinson's disease, neonatal disorders ntawm lub hlwb, thiab lwm yam NDs (retinal ischemia thiab traumatic hlwb raug mob).

Txawm hais tias feem ntau cov teeb meem neurological tsis tuaj yeem kho tau tam sim no, cov kev tshawb fawb no tau pom tias muaj peev xwm kho tau rau kev tiv thaiv, kho, thiab txo qis ntawm H2 kev tswj hwm. Muaj ntau qhov ua tau H2--cov txiaj ntsig, suav nrog cov xov tooj ntawm tes taw qhia cov tshuaj molecules thiab cov tshuaj hormones, uas tiv thaiv OS thiab mob, kuj yuav raug hais. Txawm li cas los xij, ntau qhov chaw kho mob thiab lwm cov kev tshawb fawb ntsig txog yuav tsum tau ntsuas qhov ncaj qha H2target molecule.

Ntsiab lus: molecular hydrogen; mob; neuroprotection; neurological teeb meem; oxidative kev nyuaj siab; antioxidant.

1. Taw qhia

Cov kab mob Neurodegenerative (NDs) yog cov pab pawg ntawm ntau yam kev laus uas feem ntau ua rau kev tuag zuj zus thiab nce hauv cov hlwb hlwb, ua rau cov neeg cuam tshuam rau lub cev muaj zog thiab kev nco [1].

Lub caij nyoog mechanism rau pathogenesis ntawm NDs tseem undefined; Txawm li cas los xij, cov pov thawj tshwm sim qhia tias oxidative stress (OS) plays lub luag haujlwm tseem ceeb hauv cov kab mob ntawm ntau lub paj hlwb, suav nrog Alzheimer's disease (AD), Parkinson's disease (PD), cerebral ischemia, thiab lwm yam mob hlwb [2–4].

Peb cov hlwb yuav tsum tau tswj cov theem nrab ntawm cov kab mob reactiveoxygen (ROS) kom ua tiav cov haujlwm lom neeg. Txawm li cas los xij, kev tsim khoom hnyav ROS yog lub luag haujlwm rau qhov ua rau oxidative puas tsuaj uas yuav ua rau apoptosis [5]. Qhov kev tsim tawm ntau dhau ntawm ROS zoo li yog qhov ua tau ntawm cov qauv thiab kev ua haujlwm ntawm cov cellular biomolecules, suav nrog cov proteins, deoxyribonucleic acid (DNA), thiab lipids, thiab yog li nws thiaj li kaw cov kev ua haujlwm ntawm neuronal thiab ciaj sia thiab feem ntau pom nyob rau hauv lub hlwb ntawm cov neeg mob uas muaj cov kab mob neurodegenerative [ 3, 4] ib.

Lub hauv paus ntawm lub paj hlwb (CNS) siv ntau cov pa oxygen los ua cov txheej txheem physiological, ua rau muaj ntau theem ntawm cov dawb radicals [5]. Endogenous antioxidant systems, xws li cov suav nrog superoxide dismutase (SOD), catalase (CAT), glutathioneperoxidase (GPx), thiab glutathione, ua lub luag haujlwm tseem ceeb hauv kev cawm lub hlwb hlwb los ntawm OS thiab khaws cov redox tshuav nyiaj li cas hauv lub hlwb, los ntawm stimulating antioxidativedefense mechanisms rau counterbalance ROS.

Cov enzymatic antioxidants yog saw-tawg antioxidants uas tuaj yeem tshem tawm cov kab mob radical [6]. Manganese-muaj SOD txo qis cov superoxide radical anion uas tsim thaum lub sij hawm xa hluav taws xob thauj khoom hauv mitochondrial matrix, thaum CAT thiab / lossis GPx ua lub luag haujlwm tseem ceeb hauv decomposing hydrogen peroxide rau dej thiab oxygen [6,7].

Ntau qhov kev tshawb fawb tau tshaj tawm txog kev txo qis ntawm cov tshuaj tiv thaiv oxidative enzyme xws li CAT thiab SOD, hauv cov kab mob neurological suav nrog PD [8,9]. Interestingly, ib txoj kev tshawb fawb tau pom tias kev ua tsis zoo ntawm SOD ua rau muaj kev cuam tshuam txog OS hauv PD thiab AD [10]. Tsis tas li ntawd, kev tshawb fawb tau pom tias kev ua haujlwm ntawm CAT ua rau muaj kev nce siab ntawm cytotoxicity thiab nce ROS, uas sawv cev rau lub luag haujlwm tseem ceeb ntawm CAT hauv kev tswj oxidative tshuav [11].

Cov ntaub ntawv pov thawj tshwm sim tseem ceeb thiab lees paub lub luag haujlwm ntawm OS hauv cov kab mob ntawm NDs [2–4]. Yog li ntawd, nyob rau hauv xyoo tas los no, cov kws tshawb fawb tau xav txog kev ntsuas lub luag haujlwm ntawm cov tshuaj antioxidants hauv kev tiv thaiv thiab txo cov kab mob no. Nws yog qhov lees paub qhov tseeb tias ntuj antioxidants thiab antioxidative enzymes muaj lub luag haujlwm tseem ceeb hauv kev txo cov cellular ROS [12].

Tsis ntev los no, molecular hydrogen (H2) tau nyiam kev saib xyuas zoo hauv kev kho mob raws li cov pa roj tsis ua haujlwm uas muaj kev nyab xeeb thiab ua haujlwm zoo thiab ua kom OS los ntawm kev ua raws li cov khoom siv hluav taws xob rau hydroxyl radical (•OH) thiab peroxynitrite (ONOO-) [13].

Ntau yam kev tshawb fawb tau qhia txog cov txiaj ntsig zoo ntawm H2 hauv kev txo qis pathophysiology ntawm ntau yam kab mob los ntawm kev txo OS [13,14]. Muaj ntau txoj hauv kev yooj yim thiab siv tau zoo rau kev tswj hwm H2, xws li nqus pa, nqus dej hauv qhov ncauj (HRW), txhaj tshuaj hydrogen-nplua nuj saline (HS), thiab kev koom ua ke ncaj qha (da dej, qhov muag tee, thiab lwm yam) [14,15 ].

H2 tau raug tshaj tawm tias yog cov roj siv kho mob hauv cov qauv ratmodel ntawm ischemia-reperfusion (IR) lub hlwb raug mob thiab tau tshaj tawm tias muaj kev tiv thaiv IR raug mob hauv cov hlab ntsha hauv cov hlab ntsha hauv cov qauv ntawm lub hlwb dawb teeb meem [16]. Ntxiv mus, kev tiv thaiv ntawm H2 hauv dej haus los ntawm cov tshuaj tiv thaiv oxidative ntawm dopaminergic neuronsin substantia nigra pars compacta (SNpc) tau kawm hauv tus qauv tsiaj [17].

Ntxiv mus, nthuav, lwm txoj kev tshawb fawb pom tau hais tias haus H2- dej yaj (HW) thiab sib cuam tshuam H2 tiv thaiv PD neurotoxicity [18]. Kev sim tshuaj ntsuam xyuas ua los ntawm Nagatani thiab cov npoj yaig tau pom tias kev tswj hwm cov hlab ntsha ntawm HRW tau pom tias muaj kev nyab xeeb rau cov neeg mob uas mob cerebral infarction, suav nrog cov neeg kho nrog atissue plasminogen activator [19].

Tsis tas li ntawd, ib txoj kev tshawb fawb pom tau hais tias qhov nqus tau ntawm H2 gasconcealed hlwb puas-induced nruab nrab-cerebral occlusion nyob rau hauv nas txhim khu kev txawj ntse, thiab txo lub hlwb raug mob nyob rau hauv cov neeg mob uas mob cerebral infarction [20].

H2 tau pom tias muaj kev kho thiab ergogenic cuam tshuam hauv kev soj ntsuam sib txawv thiab kev tshawb fawb ua ntej kho mob me me rau kev paub tsis meej [21,22]. Feem ntau ntawm lub hlwb raug mob nyob rau hauv peb lub paj hlwb teb rau neuroinflammation, uas yog txawv los ntawm phenotypical hloov nyob rau hauv microglia thiab astrocytes, thiab ntau ntau lawm ntawm dawb radicals, cytokines, thiab neurotrophins.

Cov ntaub ntawv pov thawj qhia tias kev tswj hwm ntawm microglial redox xwm txheej ua lub luag haujlwm tseem ceeb hauv kev hloov kho cov lus teb neuroinflammatory [23]. Cov kev tshawb fawb tau pom tias kev noj HW tsis tu ncua txo qhov kev siv ntawm kev coj tus cwj pwm hnyav thiab txhawb kev rov qab los ntawm neuroinflamation [24]. H2 tuaj yeem txo qhov kev ua kom muaj zog ntawm cov cytokines, microglia, thiab 8-hydroxy-2-deoxyguanosine (8-OHdG) kom txo tau oxidative puas thiab neuroinflammation hauv lub hlwb fetal hauv tsiaj qauv [24,25] .

Tsis tas li ntawd, ib txoj kev tshawb fawb tau pom tias HW muaj kev tiv thaiv zoo tiv thaiv neonatal hypoxic-ischemia encephalopathy los ntawm kev txo qis ntawm cov ntshav hauv cov hlab ntsha tshwj xeeb enolase, interleukin-6 (IL-6), thiab qog necrosis factor- (TNF- Ib.) [26]. Yog li, tsab xov xwm tshuaj xyuas no qhia txog kev koom tes ntawm OS hauv NDs thiab cov txiaj ntsig ntawm H2 hauv kev kho cov kab mob no.

2. Cov yam ntxwv ntawm Molecular Hydrogen

H2 ua haujlwm raws li qhov nruab nrab tab sis muaj txiaj ntsig antioxidant [13,27]. Hydrogen yog lub ntiaj teb cov khoom siv ntau tshaj plaws, suav txog li 75% ntawm lub ntiaj teb huab hwm coj. Hydrogen muaj nyob rau hauv dej thiab cov organic thiab inorganic tebchaw. H2 roj yog cov tsis muaj xim, tsis muaj ntxhiab, roj-intensive diatomic gas. Muaj tsawg dua 1 ppm ntawm hydrogen gas hauv ntiaj teb huab cua [28].

H2 tsis hnov ​​​​mob nrog ntau lub tebchaw, suav nrog cov pa oxygen, ntawm chav tsev kub. H2 roj tsuas yog kub hnyiab tau ntawm qhov kub siab tshaj 537 ◦C. H2 (4–75%, v / v) yog tawg vim yog cov tshuaj tiv thaiv oxidation sai. H2 tuaj yeem yaj nyob rau hauv dej hauv huab cua siab mus rau 0.8 mM (1.6 ppm, w/v) [28].Nyob rau xyoo tas los no, ntau yam kev tshawb fawb txog H2 tau nyiam cov kws tshawb fawb thoob ntiaj teb, vim nws tiv thaiv thiab kho. cov teebmeem [14,15]. Tsis tas li ntawd, hydrogen muaj qhov zoo dua qub dua lwm cov roj siv rau kev kho mob, hais txog nws cov tshuaj lom; hydrogen tseem tsis muaj tshuaj lom mus txog qhov siab siab thiab txawm tias siv hauv kev dhia dej [29,30].

Cov kev tshawb fawb tau pom tias cov teebmeem ntawm hydrogen inhalation tsis pom meej thiab tsis cuam tshuam rau ntshav siab lossis lwm yam tsis zoo, xws li pH thiab kub. Yog li, hauv kev sib piv, hydrogen muaj kev phiv tsawg dua li lwm cov tshuaj antioxidants, vim nws tsuas yog txo qis •OH [13,31].

3. Txoj Kev Tswj Xyuas Hydrogen

H2 yuav raug muab los yog coj mus rau hauv lub cev ntawm ntau txoj hauv kev. Cov kev no yuav muab faib ua peb hom: H2 pa nqus pa, haus HW, thiab HS txhaj. H2gas inhalation yog qhov yooj yim tshaj plaws thiab feem ntau siv txoj kev txij li thawj zaug qhia txog kev siv H2 [13]. Inhaled H2 diffuses rau hauv lub ntsws alveoli thiab thauj mus rau tag nrho lub cev.

Cov txheej txheem no tuaj yeem, txawm li cas los xij, tsis xis nyob thiab txaus ntshai, txij li H2 roj yog tawg ntawm qhov siab tshaj 4% hauv huab cua [27]. Yog li, qhov sib xyaw gasconcentration ntawm H2 feem ntau yog khaws cia ntawm 1% thiab 4%. Kev nqus cov pa H2 txhim kho cov mob xws li mob ischemia-reperfusion raug mob (IRI) thiab ntau qhov kev raug mob hauv nruab nrog cev.HRW muaj kev nyab xeeb thiab xis dua li H2 pa nqus pa.

Nws tau raug tshaj tawm tias HW ad libitum tiv thaiv arteriosclerosis ntawm nas nrog knockout apolipoprotein E, amodel rau atherosclerosis uas loj hlob spontaneously [32]. Kev noj H2 tiv thaiv kev ntxhov siab vim kev puas tsuaj hauv hippocampus-dependent kev kawm ua haujlwm thaum lub sijhawm ua haujlwm ntev hauv cov nas [33].

Tsis ntev los no, qhov nqus ntawm H2 thiab haus HW pom qhov txawv ntawm kev hloov pauv rau cov teeb liab thiab cov noob qhia hauv nas [34]. Txawm hais tias tus txheej txheem yog invasive, neuroprotective efficiency nyob rau hauv lub hlwb tom qab IRI intraperitoneal txhaj ntawm HS tau zoo ib yam li cov H2 gas inhalation [35]. Hauv tib neeg lub plab zom mov, H2 yog tsim los ntawm cov kab mob hauv plab hnyuv thiab ua lub luag haujlwm tseem ceeb hauv cov txheej txheem metabolic.

Nws ua haujlwm raws li qhov tshwj xeeb antioxidant thiab tiv thaiv kab mob plawv [15]. Ib qho ntawm cov kev tshawb fawb pom tau tias cov kab mob plab ua lub luag haujlwm hauv kev loj hlob ntawm cov kab mob neurological. Hauv qhov no, cov neeg mob uas muaj ntau yam kab mob CNS tau pom tias muaj cov plab hnyuv permeability ntxiv uas ua rau muaj kev cuam tshuam rau cov metabolites los ntawm txoj hnyuv mus rau cov ntshav uas cuam tshuam rau CNS [36].

Ib txoj kev tshawb nrhiav pom tias oraladministration ntawm HW ua rau muaj kev tiv thaiv hauv nas thiab nas qauv ntawm PD [17]. Cov kev tshawb pom no qhia tau hais tias muaj peev xwm siv HRW rau kev tiv thaiv NDs, nrog rau kev siv HRW los kho cov mob hlwb, raws li pom hauv daim duab 1.The nuclear factor erythroid 2-txog yam 2 (Nrf2) txoj hauv kev plays ib qho tseem ceeb heev. Lub luag haujlwm tiv thaiv cov hlwb tiv thaiv kev ntxhov siab sib txawv thiab nws txoj haujlwm tsis zoo cuam tshuam nrog kev txo qis rau OS [37]. Nrf2 yog ib qho tseem ceeb tiv thaiv mechanism ntawm lub hlwb tiv thaiv co toxins nyob rau hauv ob qho tib si, glial thiab neuronal hlwb [38,39].

Txoj hauv kev Nrf2 tsom rau ntau yam genes piv txwv li heme oxygenase-1 (HO-1), glutathione S-transferase, SOD, CAT, NAD(P)Hdehydrogenase (quinone)1, thiab lwm yam, yog li, tiv thaiv cov neurons. of the CNS againstOS [40,41]. Nrf2 thiab ntau yam tshuaj antioxidant enzymes kuj tseem tuaj yeem ua rau muaj kev cuam tshuam ntawm cov tshuaj tiv thaiv kab mob, theem I thiab II tshuaj-metabolizing enzymes, thiab mitochondrial txoj kev [42,43].

Cov kev tshawb fawb tshawb fawb tsis ntev los no tau pom tias Nrf2 ua si tiv thaiv cov neurotoxins xws li 6-hydroxydopamine thiab 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine ( MPTP), hauv ob qho tib si, hauv vitro thiab hauv vivo qauv ntawm PD [44,45]. Hauv qhov no, kev tswj hwm qhov ncauj ntawm HRW tau pom tias muaj kev tiv thaiv neuroprotective tiv thaiv kev raug mob traumaticbrain (TBI) los ntawm kev ua kom lub Nrf2 signaling pathway.

Tsis tas li ntawd, cov kev tshawb pom zoo sib xws tau tshaj tawm nyob rau hauv ntau yam NDs xws li PD, AD, IR, thiab hemorrhagic stroke, thiab cov txiaj ntsig tau raug ntaus nqi rau cov khoom antioxidant ntawm HRW [46-48].

4. H2 Ua raws li cov tshuaj tiv thaiv antioxidant

Hz yog reactive heev, protein denaturing, thiab txhawb DNA kev puas tsuaj. Nws tuaj yeem xaiv txo OH thiab ONOO-, ua rau muaj kev cuam tshuam dav dav nrog cov proteins, lipids, thiab nucleic acids [49]. Raws li cov qauv tsiaj thiab kev soj ntsuam soj ntsuam, cov ntaub ntawv pov thawj ntawm lub cev tau pom tias H tuaj yeem siv tau zoo los tiv thaiv cov kab mob oxidative puas-txuas nrog [50].

Nws txo tus nqi ntawm cytotoxic ROS (®OH), ua tiav kev tiv thaiv hlwb [50]. Lwm cov kev tshawb fawb pom tau hais tias muaj kev tiv thaiv zoo li lRl hauv cov kabmob, xws li lub siab, lub plawv, thiab cov hnyuv [51]. Hauv nas mob stroke qauv 1% mus rau 4% H, inhalation alleviates infarction qhov ntev [52]. H, inhalation tiv thaiv kev puas tsuaj oxidative tseem ceeb hauv 1% mus rau 3% ntawm cov neeg mob [53].

HRW tau txais txiaj ntsig txo qis kev kawm thiab kev nco tsis zoo hauv cov nas los ntawm kev txo qis oxidative puas tsuaj. Tsawg-theem (l, 3 v / 100 v) pa roj ua pa tshaj tawm txo OS, tshwj xeeb hypoxia-induced dyslipidemia, cardiomyocyte hypertrophy, thiab perivascular fibrosis nyob rau hauv sab laug ventricular hauv C57BL/6] nas [54 Tsis tas li ntawd, kev noj ntawm HRW ua rau Nrf2/ Kev tiv thaiv antioxidant txoj hauv kev thiab cov tshuaj tiv thaiv kab mob antioxidant kom ua kom qhov txo qis hauv qhov ncauj mucosal tsis zoo hauv nas [55].

Ib yam li ntawd, qhov kev tshawb pom ntawm lwm txoj kev tshawb fawb pom tias HRW muaj txiaj ntsig zoo rau cov tawv nqaij mob hauv cov nas uas tshwm sim los ntawm hluav taws xob [56]. Ob peb txoj hauv kev hloov pauv tam sim no tau kawm raws li cov khoom tseem ceeb ntawm lub zog hloov pauv cov yam ntxwv ntawm Hz, suav nrog (1) ghrelin-txuas upregulation ntawm ghrelin receptor (GHS-R1 ); (2) ghrelin-txuas kev txhawb nqa ntawm glucose transporter 1; (3) non-ghrelin txuas stimulation ntawm glucose transporter 4; thiab (4) uas tsis yog-ghrelin txuas txhim kho kev nthuav qhia ntawm fibroblast kev loj hlob zoo tshaj 21 (FGF21), tus tswj hwm ntawm cov nqi hluav taws xob [57,58].

HRW tau pom cov khoom tiv thaiv neuroprotective hauv murine MTTP-induced PD qauv [45,59,60]. Lin thiab cov npoj yaig tau tshaj tawm tias HRW txo OS hauv cov neeg mob uas muaj kab mob siab B thiab metabolic syndrome [61].Studies tau pom tias H2 yuav tau txais txiaj ntsig los ntawm kev ua kom Nrf2 signalingpathway, yog li txhim kho kev ua haujlwm antioxidant thiab txo OS, apoptosis, thiab o [46,62 ].

H2 nce cov kev ua haujlwm antioxidant ntawm enzymes hauv hluav taws xob thiab TBI los ntawm kev tswj hwm ntawm Nrf2 [63]. Lub hauv paus kev tiv thaiv kev tiv thaiv ntawm H2 tuaj yeem txawm siv los ntawm macrophages ntawm Nrf2 signaling pathway [64]. Nrf2 yog ib qho kev hloov pauv uas sib txuas cov ntsiab lus ntawm cov tshuaj tiv thaiv antioxidant los tswj cov kev qhia ntawm cov tshuaj antioxidants, tiv thaiv lub cev los ntawm kev raug mob thiab o ntawm oxidative puas tsuaj [65].

5. Los tiv thaiv kab mob ntawm H2 nyob rau hauv txawv Neurodegenerative kab mob qauv

Ntau cov kev tshawb fawb tau tshaj tawm cov tshuaj tiv thaiv kab mob ntawm H2 [63,64,66]. Therapid kis tau, siab penetrability, thiab tsis muaj tseeb kev phiv yog ib co ntawm nws zoo. H2 scavenges ROS radicals thiab muaj txiaj ntsig zoo hauv kev txo qis kev mob ntau ntawm cov ntaub so ntswg thiab kabmob, nrog rau lub plawv, hlwb, thiab ntsws, thiab tau lees paub tias yog tus tiv thaiv tiv thaiv oxidative puas tsuaj [67,68].

HRW tau kawm dav dav rau nws lub peev xwm los tiv thaiv kev mob tshwm sim thiab txo qis neuronal apoptosis [18,69]. Microglia zoo li ua rau neuroinflamation hauv lub hlwb. Activated microglia thiab ROS tsim cov cytokines pro-inflammatory. Ib qho ntawm cov kev tshawb fawb pom tau hais tias H2 muaj kev cog lus muaj txiaj ntsig zoo tiv thaiv thiab mob ntsig txog perinatal hlwb raug mob hauv vitro thiab hauv vivomodels [70].

Tsis tas li ntawd, tib txoj kev tshawb fawb tau tshaj tawm tias HW tiv thaiv lipopolysaccharide (LPS)-vim kev tsim tawm ntawm ROS los ntawm microglia thiab txo qis LPS-induced microglial neurotoxicity [70]. Ntau qhov kev tshawb fawb tau pom tias HS tuaj yeem txo cov kab mob hauv plab hnyuv xws li plab hnyuv IR puas, mob plab ulcerative, thiab mob plab [71,72].

Tsis tas li ntawd, HRW tau qhia txog kev tiv thaiv kev tiv thaiv ntawm cov superoxide ions tsim nyob rau hauv vitamin C-depletedSMP30/GNL-knockout nas thaum lub sij hawm hypoxia-rexygenation mob [73]. Tsis tas li ntawd, ib qho ntawm cov kev tshawb fawb tau tshaj tawm tias qhov sib ntxiv ntawm H2 rau cov kev daws teeb meem hemodialysis muaj cov tshuaj tiv thaiv kab mob thiab cov tshuaj tiv thaiv kab mob siab rau cov neeg mob hemodialysis, qhia tias nws yog qhov kev xaiv kho mob rau cov neeg mob uremia [74]. Hauv lwm txoj kev tshawb fawb, lub luag haujlwm ntawm kev txo qis hauv cov leeg nqaij tau txhim kho los ntawm kev siv H2 nyob rau hauv rooj plaub ntawm kev siv lub cev hnyav [21].

Domoki thiab cov npoj yaig tau tshaj tawm tias 2.1% huab cua ua pa augmented los ntawm hydrogen tau tswj hwm cerebrovascular reactivity rau hypercapnia thiab txo qis neuronaldamage los ntawm asphyxia-re-ventilation nyob rau hauv perinatal asphyxia yug me nyuam npua qauv [75] . Tsis tas li ntawd, HRW tiv thaiv endoplasmic stress thiab upregulated {5}} qhia [64].HRW kuj ua rau kev puas siab puas ntsws hauv nas nrog nrawm nrawm [53].

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