Ntu Ⅰ Hydrogen: Ib Txoj Kev Kho Mob Tshiab hauv Kab Mob Raum

Abstract

1. keeb kwm

Hydrogen yog ib yam tshuaj uas tseem tsis tau siv dav hauv tshuaj. Txawm li cas los xij, cov pov thawj tsis ntev los no qhia tau hais tias hydrogen muaj ntau yam tshuaj siv tshuaj xws li tshuaj tua kab mob, tshuaj tiv thaiv kab mob, thiab tshuaj tiv thaiv apoptotic. Kev tshawb fawb ntau ntxiv tau raug ua los ntawm kev siv hydrogen hauv ntau yam kab mob, tshwj xeeb tshaj yog cuam tshuam rau lub raum.

2. Cov ntsiab lus

Hydrogen tuaj yeem nqus tau, ua pa los yog kua, thiab tuaj yeem muab tshuaj rau qhov ncauj, tso rau hauv, lossis hauv zos. Hydrogen tuaj yeem nkag mus rau sub-organelles sai sai xws li mitochondria thiab cov nucleus los ntawm qhov yooj yim diffusion, tsim cov pa oxygen reactive (ROS) thiab ua rau DNA puas. Hydrogen tuaj yeem xaiv tshem tawm hydroxyl radical (•OH) thiab peroxynitrite (ONOO-), tab sis tsis yog lwm yam reactive oxygen radicals nrog physiological functions, xws li peroxy anion (O.₂-) thiab hydrogen peroxide (H₂O₂). Txawm hais tias kev tswj hwm cov nyhuv ntawm hydrogen ntawm lub teeb liab txoj kev hloov pauv tau raug lees paub, cov txheej txheem tshwj xeeb ntawm nws cov kev cuam tshuam ntawm cov teeb liab molecules tseem tsis paub. Txawm hais tias muaj ntau txoj kev tshawb fawb tau tshawb xyuas cov kev kho mob thiab kev tiv thaiv ntawm H₂Hauv kev sim ntawm tes thiab tsiaj, kev sim tshuaj muaj tsawg thiab tseem nyob deb. Yog li ntawd, kev sim tshuaj ntau dua yuav tsum tau tshawb xyuas lub luag haujlwm ntawm hydrogen hauv lub raum kab mob, nrog rau cov txiaj ntsig ntawm nws cov koob tshuaj, sijhawm, thiab daim ntawv ntawm kev ua tau zoo tag nrho. Qhov loj-scale randomized tswj kev sim tshuaj yuav tsum tau ua ntej hydrogen yuav siv tau los kho mob raum.

3. Cov lus tseem ceeb

Kab lus no tshuaj xyuas cov txheej txheem ntawm hydrogen hauv kev kho mob raum kab mob thiab tshawb txog qhov muaj peev xwm ntawm nws siv hauv kev kho mob.

Ntsiab lus

Hydrogen; Kab mob raum; Anti-inflammatory; Antioxidant; Cell tuag.

Nyem qhov no kom tau txaiscov txiaj ntsig Cistanche

Taw qhia

Kab mob raum yog ib yam kab mob uas tshwm sim hauv tib neeg. Hom kab mob raum muaj xws li mob raum raug mob (AKI), lub raum fibrosis, kab mob polycystic raum, thiab lub raum cell carcinoma. Muaj ntau txoj kev kho mob rau cov kab mob hauv lub raum, nrog rau kev kho tshuaj, raum lim ntshav, thiab hloov lub raum. Nyob rau hauv xyoo tas los no, tau txais kev saib xyuas ntxiv rau kev tshawb fawb siv hydrogen los kho cov kab mob no. Hydrogen nthuav tawm muaj zog txo cov khoom thiab feem ntau siv los ua tus neeg sawv cev txo qis hauv cov tshuaj tiv thaiv.

Kev siv kho mob ntawm H₂thawj zaug tau tshaj tawm xyoo 1975 thaum cov qog 'loj txo qis heev thaum cov nas tsis muaj albino nrog cov kab mob squamous cell carcinoma raug sib xyaw ntawm 2.5 feem pua ​​​​ oxygen thiab 97.5 feem pua ​​​​ hydrogen ntawm tag nrho cov siab ntawm 8 cua mus txog 2 lub lis piam [1]. Xyoo 2007, Ohsawa et al. [2] npaj rau thawj zaug uas cov roj hydrogen muaj cov tshuaj tua kab mob antioxidant thiab antiapoptotic uas tuaj yeem tiv thaiv lub hlwb tiv thaiv ischemia-reperfusion (I / R) kev raug mob (IRIs) thiab mob stroke los ntawm kev xaiv neutralizing hydroxyl radicals. Hydrogen tau nyiam ntau xim vim nws cov txiaj ntsig kho mob rau cov kab mob raum. Ntau qhov chaw kho mob thiab kev sim ua qauv ntawm cov kab mob raum, nrog rau cov ntaub ntawv pov thawj hauv lwm qhov chaw kho mob biomedical, tau pom tias hydrogen tuaj yeem ua tus neeg saib xyuas kom tshem tawm cov pa oxygen reactive (ROS). Kev nqus cov pa roj hydrogen lossis siv cov tshuaj hydrogen-muaj cov kua dej tuaj yeem ua rau muaj zog tiv thaiv cellular.

Hauv qhov kev tshuaj xyuas no, peb yuav tsom mus rau lub luag haujlwm ntawm lub cev ntawm hydrogen hauv cov kab mob hauv lub raum, nws lub peev xwm los ua cov tswv yim kho mob, thiab cov txheej txheem uas yuav cuam tshuam rau nws txoj kev tiv thaiv. Tsis tas li ntawd, kev tshawb pom ntawm cov kev tshawb fawb tsis ntev los no ntawm hydrogen hauv ntau hom kab mob raum tau tham txog.

Action Mechanisms

Kom piav qhia meej txog kev tiv thaiv thiab kho cov teebmeem ntawm H₂, Daim duab 1 thiab 2 qhia txog kev lom neeg ntawm H2 thiab nws qhov cuam tshuam rau kev tuag ntawm tes.

Biological teebmeem ntawm H₂

1. Anti-Oxidation

H₂, muaj zog oxidant, tuaj yeem hnov ​​​​mob nrog nucleic acids yam tsis muaj kev ntxub ntxaug. Cov txheej txheem ntawm decomposing tshuaj thiab tso tawm lub zog nyob rau hauv los yog sab nraum lub cev yog hu ua oxidation. Qhov hnyav oxidation ntawm intracellular ROS los yog dawb radicals ua rau oxidative kev nyuaj siab (OS), lub xeev ntawm imbalance ntawm oxidation thiab antioxidant teebmeem nyob rau hauv lub cev uas yog xam tau tias yog ib tug loj contributor rau kev laus thiab kab mob pib thiab kev loj hlob. Mob OS tshwm sim los ntawm I / R lossis o ua rau muaj kev puas tsuaj loj rau cov ntaub so ntswg, thiab OS ntev tau lees paub tias yog tus neeg sawv cev ntawm ntau cov kab mob raum. Hydrogen tuaj yeem tshem tawm cov dawb radicals. Hydrogen xaiv txo cov hydroxyl radicals (•OH) thiab peroxynitrite (ONOO-), uas yog cov oxidants muaj zog uas react indiscriminately nrog nucleic acids, lipids, thiab proteins, ua rau DNA fragmentation, lipid peroxidation, thiab protein inactivation [2]. Cov txiaj ntsig kho tau zoo ntawm H₂tau piav qhia thawj zaug hauv xyoo 2007. Ohsawa li al. [2] pom tias H₂xaiv txo qis •OH thiab ONOO- hauv kab lis kev cai thiab tshuaj xyuas seb H₂ txo cov oxidized cov ntaub ntawv ntawm biomolecules koom nrog hauv metabolic oxidation-txo cov tshuaj tiv thaiv hauv cell-free assay. Nyob rau hauv chav tsev kub thiab nruab nrab pH, cov kev daws teeb meem saturated H2 tsis txo cov oxidized cov ntaub ntawv ntawm nicotinamide adenine dinucleotide, oxidized daim ntawv ntawm flavin adenine dinucleotide, los yog oxidized daim ntawv ntawm cytochrome C. Yog li, H.₂tsis cuam tshuam oxidation-txo metabolism lossis qib O₂ −, H₂O₂, thiab TSIS TAU, tag nrho cov uas ua lub luag haujlwm tseem ceeb ntawm lub cev ntawm qhov tsis tshua muaj siab. Raws li kev tswj hwm kev taw qhia cov molecules, lawv koom nrog ntau lub teeb liab hloov pauv thiab tswj cov txheej txheem lom neeg xws li apoptosis, cell proliferation, thiab sib txawv. Yog li, H2 muaj cov tshuaj tiv thaiv antioxidant uas tiv thaiv lub hlwb tiv thaiv I / R raug mob los ntawm kev ua kom tsis zoo •OH thiab ONOO- tab sis tsis yog O₂ −, H₂O₂, thiab NO [2]. Tsis zoo li ntau lub zog txo cov antioxidants, nws tsis cuam tshuam cov txheej txheem tseem ceeb ntawm lub cev [3]. Ntxiv rau qhov ncaj qha cuam tshuam cov dawb radicals, hydrogen tuaj yeem ua rau Nrf2/ARE txoj hauv kev hauv vivo thiab hauv vitro, nce kev hloov pauv ntawm cov kab mob antioxidant hauv qab, xws li heme oxygenase 1 (HO-1), thiab pab txhawb rau cov antioxidant. kev ua si [4]. Hydrogen tseem tuaj yeem ua rau muaj kev nthuav tawm ntawm endogenous superoxide dismutase, catalase [5], thiab txo glutathione (GSH) [6], tag nrho cov uas pab txo qis oxidative puas tsuaj. Hydrogen plays ntau lub luag haujlwm hauv kev xaiv scavenging ntawm ROS, downstream cascade teeb liab transduction, thiab kev tswj ntawm antioxidant enzyme kev ua. Yog li ntawd, kev tshawb fawb txog cov tshuaj tiv thaiv antioxidant ntawm hydrogen thiab nws lub zog hauv kev txo qis kev puas tsuaj vim OS hauv lub raum muab cov kev taw qhia tshiab rau kev kho mob raum rau yav tom ntej.

2. Kev tiv thaiv kab mob

Cov kev tshawb fawb tseem ceeb thiab kev kho mob tau pom tias H₂yog ib qho tseem ceeb regulator nrog antioxidant, anti-inflammatory, thiab antiapoptotic teebmeem [7]. H₂pom tias muaj kev tiv thaiv kab mob hauv LPS-activated macrophages, raws li Hong li al. [8], los ntawm inhibiting qhov kev tso tawm ntawm proinflammatory cytokines thiab nce qhov tso tawm ntawm anti-inflammatory cytokine, uas tuaj yeem kho los ntawm HO-1. Tom qab ntawd, qee cov kws tshawb fawb pom tias kev rov ua kom rov zoo nrog hydrogen-enriched saline tuaj yeem txhim kho cov ntaub so ntswg thiab lub cev puas tsuaj, ua rau txo qis cov lus teb thiab OS los ntawm inhibiting kev qhia thiab ua kom NF-κB [9]. H₂kuj tseem tuaj yeem cuam tshuam qhov kev qhia ntawm pro-inflammatory cytokines thaum lub sij hawm o thiab txo qhov kev nthuav tawm ntxov ntawm pro-inflammatory cytokines, xws li interleukin (IL)- 1, IL-6, IL-8 , IL-10, thiab qog necrosis factor-alpha (TNF- ) hauv ntau hom tsiaj [10]. Lub network ntawm inflammatory mediators thiab inflammatory effector cells thiab qhov tsis sib xws ntawm pro-inflammatory cytokines thiab anti-inflammatory cytokines ua lub luag haujlwm tseem ceeb hauv kev tshwm sim thiab kev loj hlob ntawm cov kab mob raum. Yog li, kev kho mob ntawm lub raum kab mob los ntawm kev xav ntawm pro-inflammatory cytokines thiab anti-inflammatory cytokines tej zaum yuav yog ib txoj kev nthuav rau kev tshawb nrhiav ntxiv ntawm lub luag hauj lwm ntawm hydrogen hauv kev tswj thiab tswj homeostasis nyob rau hauv inflammatory raum kab mob.

Mob ntshav qab zib nephropathy (DN) yog ib qho teeb meem loj ntawm ntshav qab zib mellitus. Cov kab mob metabolic tuaj yeem tshwm sim hauv DN thiab tshwm sim raws li kev mob hauv lub raum hauv zos uas tuaj yeem ua rau fibrosis thiab kev hloov kho ntawm lub cev. Yog li ntawd, tackling lub cev tiv thaiv kab mob yog qhov tseem ceeb heev rau kev kho mob ntawm DN [11]. Hauv AKIs, xws li lub raum hlab ntsha infarction lossis toxin-mediated raum raug mob, cov tshuaj tiv thaiv kab mob hauv lub raum tau qhib. Kev puas tsuaj rau lub raum epithelial hlwb ua rau txoj kev ntxhov siab, ua rau lub zais ntawm cytokines thiab vasoactive yam, ua rau muaj kev puas tsuaj rau immunopathological [12]. Hydrogen, ntawm qhov tod tes, tuaj yeem cuam tshuam kev tsim cov tshuaj tiv thaiv kab mob [13]. Peb kwv yees tias hydrogen muaj lub neej yav tom ntej hauv kev tiv thaiv kab mob raum vim nws muaj kev sib raug zoo rau cov teebmeem antioxidant tseem ceeb. Txawm li cas los xij, tam sim no tsis muaj cov ntaub ntawv kho mob los lees paub qhov no. Cov kev tshawb fawb ntxiv yuav tsum tau ua kom paub tseeb tias qhov kev xav no.

Cistanche extract thiab Cistanche hmoov

3. Txoj Cai ntawm ER Kev Nyuaj Siab

Endoplasmic reticulum (ER) kev ntxhov siab tshwm sim thaum kev ntxhov siab pathological induces ib qho tsub zuj zuj ntawm unfolded proteins nyob rau hauv lub ER. Zhao et al. [14] pom tias qhov nqus tau hydrogen txo qis ER cov protein cuam tshuam txog kev ntxhov siab thiab txo cov ntaub so ntswg puas hauv myocardial IRI. Tom qab ntawd, nws tau pom tias qhov sib xyaw ntawm H₂thiab O₂tuaj yeem cuam tshuam ER kev ntxhov siab ntawm PKR-zoo li ER-localized eIF2 kinase-eukaryotic pib qhov tseem ceeb 2 alpha-activating transcription factor 4 (PERK-eIF2 -ATF 4), inositol-xav tau enzyme 1-X-box khi protein 1 (IRE 1-XBP1), thiab ATF 6 txoj hauv kev. Kev tshawb fawb txog kev sib raug zoo ntawm H₂thiab ER kev nyuaj siab hauv nas nrog IRI pom tias H₂txo qhov kev qhia ntawm GRP78 thiab TNF receptor-associated factor 2 [15], qhia tias qhov kev tiv thaiv ntawm H₂ntawm myocardial IRI muaj feem xyuam rau qhov txo qis hauv ER kev ntxhov siab. Hais txog kab mob raum, kev tshawb fawb tsom rau kev cuam tshuam ntawm hydrogen raws li kev tswj hwm ntawm ER kev ntxhov siab tsis tshua muaj; Txawm li cas los xij, peb xav tias qhov no yog ib qho kev nthuav qhia yav tom ntej ntawm kev tshawb fawb.

4. Mitochondria Kev Tswj Xyuas Zoo

Txoj kev urate-induced inflammasome txoj hauv kev hauv urate nephropathy cuam tshuam nrog kev nkag ntawm urate crystals rau hauv intracellular lysosomes, uas yog decomposed los tsim mitochondrial ROS, activating NLRP3 inflammasomes [16]. Ntau ROS ntau lawm yog vim kev tso tawm calcium hauv ER, ua rau mitochondrial depolarization, thiab mitochondrial membrane yuav poob. Mitochondrial depolarization ua rau kev tso tawm ntau ROS hauv mitochondria. Kev tswj tsis zoo ntawm ROS los ntawm hydrogen tuaj yeem pab tswj kev ua haujlwm mitochondrial [13, 17]. Tam sim no, txoj cai ntawm mitochondrial muaj nuj nqi siv hydrogen tseem tsis tau tshaj tawm txog kev kho mob raum kab mob, tab sis qhov no tuaj yeem yog thaj chaw tshawb fawb muaj txiaj ntsig.

Herba Cistanche

Cov teebmeem ntawm H₂ntawm Cell Tuag

1. Anti-apoptosis

Apoptosis yog ib hom kab mob ntawm cov cell tuag uas tshwm sim los ntawm cov cell shrinkage, apoptotic lub cev tsim, karyorrhexis, thiab chromatin condensation. Apoptosis tuaj yeem tshwm sim los ntawm ob txoj hauv kev endogenous thiab exogenous. H₂plays lub luag hauj lwm antiapoptotic los ntawm upregulating los yog downregulating apoptotic-txog yam. H₂kuj inhibits qhov kev qhia ntawm proapoptotic yam tseem ceeb B-cell lymphoma- 2- koom nrog X-protein (Bax), caspase-3, -8, thiab -12, thiab upregulates antiapoptotic yam. B-cell lymphoma-2 (Bcl-2) ​​thiab B-cell lymphoma-extra-large (Bcl-xl) [18]. Nws tau pom tias kev txhaj tshuaj intraperitoneal ntawm cov tshuaj hydrogen-nplua nuj 10 min ua ntej cov leeg pob txha hauv I / R tuaj yeem txo qhov kev qhia ntawm apoptotic protein Bax thiab cytochrome C (uas tuaj yeem qhib qhov kev qhia ntawm caspase-induced caspase cascade cov tshuaj tiv thaiv), thiab nce. kev qhia ntawm antiapoptotic protein Bcl -2, yog li alleviating skeletal leeg raug mob tom qab reperfusion [19]. Lwm cov kws tshawb fawb tau pom tias kev txhaj tshuaj intraperitoneal ntawm cov tshuaj hydrogen-nplua nuj tuaj yeem ua rau kom muaj sia nyob ntawm daim tawv nqaij flaps, uas cuam tshuam nrog kev tswj hwm ntawm ASK-1/JNK txoj kev thiab Bax/Bcl{21}} piv. [20]. Txawm li cas los xij, qhov tseeb mechanism ntawm antiapoptotic nyhuv ntawm hydrogen nyob rau hauv lub raum kab mob yog tsis meej kiag li.

2. Autophagy

Autophagy yog ib qho tseem ceeb rau kev tswj hwm cell homeostasis thiab txhawb kev siv zog [21]. Autophagy muaj feem cuam tshuam rau lub raum ua haujlwm thiab homeostasis. Hauv kev tshawb fawb lub raum siv cov tsiaj laus, autophagy tau pom tias cuam tshuam rau ntau hom ntawm lub raum hlwb los pab tswj lub raum pathology thiab homeostasis [22]. Ntau dhau autophagy lossis autophagy-txog kev ntxhov siab tuaj yeem ua rau muaj kev puas tsuaj ntawm cov ntaub so ntswg thiab kabmob. Thaum cov protein aggregates dhau los ua tshuaj lom, autophagy yog qhib, thiab ib zaug autophagy ntau dhau ua rau cov ntaub so ntswg puas, autophagy raug thaiv. H2 zoo li ua lub luag haujlwm tswj hwm [7]. Guan et al. [23] qhia tias H2 muaj peev xwm ameliorate chronic intermittent hypoxia (CIH)-vim lub raum raug mob los ntawm kev txo qis ER kev nyuaj siab thiab ua kom autophagy los ntawm inhibiting OS-dependent p38 thiab JNK MAPK activation. Txawm li cas los xij, yuav tsum muaj kev sim tshuaj ntxiv rau tsiaj thiab kho mob, txhawm rau tshawb nrhiav cov txheej txheem hauv qab.

cov teebmeem ntawm Cistanche

3. Pyroptosis

Lub ntsiab lus ntawm pyroptosis yog thawj zaug tau npaj rau xyoo 2012. Nws yog nrog los ntawm cov tsub zuj zuj ntawm reactive lipid oxygen catalyzed los ntawm hlau, cell apoptosis, necrosis, thiab autophagy [24]. Nyob rau hauv xyoo tas los no, muaj pov thawj tias pyroptosis plays lub luag haujlwm tseem ceeb hauv qhov tshwm sim thiab kev loj hlob ntawm AKI [25, 26], raum fibrosis [27], polycystic raum kab mob [28], thiab lub raum cell carcinoma [24, 29]. Txij li thaum muaj kev sib tshooj ntau ntawm kev tswj hwm hydrogen thiab txoj hauv kev pyroptosis, peb xav tias hydrogen tuaj yeem ua lub luag haujlwm hauv kev kho mob raum los ntawm kev tswj cov kab mob pyroptosis. Muaj kev tshawb fawb me me ntawm qhov teeb meem no, yog li kev tshawb fawb ntxiv yuav xav tau los lees paub qhov kev xav no.

4. Ferroptosis

Ferroptosis yog morphologically, biochemically, thiab caj ces txawv ntawm apoptosis, autophagy, thiab ntau hom necrosis. Nws yog tus cwj pwm los ntawm cov hlau-raws li kev sib sau ntawm ROS thiab lipid peroxidation, thiab nws tuaj yeem cuam tshuam los ntawm cov hlau chelators, lipophilic antioxidants, thiab inhibitors ntawm lipid peroxidation [24]. Ib txoj kev tshawb fawb tsis ntev los no [30] tau pom tias HMGB1 yog ib qho tshiab ferroptosis regulator ntawm RAS-JNK/p38 txoj hauv kev. Yus et al. [31] qhia tias kev kho mob nrog H₂nyob rau hauv daim ntawv ntawm cov roj txo cov theem ntawm HMGB1. Yog li ntawd, peb xav tias H₂tej zaum yuav yog ib qho tshuaj muaj peev xwm rau cov kab mob raum. Ferroptosis yog ib hom hlau-raws li kev tswj hwm ntawm nonapoptotic cell tuag, uas ua rau muaj kev puas tsuaj hauv cov qauv ntawm AKI. HO-1, qhov muaj peev xwm ntawm cov hlau intracellular, yog cytoprotective enzyme induced los ntawm cellular stress.

Vim nws cov antiapoptotic thiab anti-inflammatory zog [32], nws muaj kev tiv thaiv zoo ntawm AKI. HO-1 kev ua haujlwm tuaj yeem nce los ntawm hydrogen. Ib txoj kev tshawb fawb tsis ntev los no [32] tau pom tias HO-1- lub raum tsis muaj lub raum epithelial hlwb tau nkag siab ntau dua rau ferroptosis, qhia tias cov hlau dawb uas tsim los ntawm HO-1 tsis txhawb ferroptosis nws tus kheej, thiab HO-1 muaj cov nyhuv anti-ferroptosis. Txawm hais tias cov txheej txheem tom qab hydrogen cov txiaj ntsig ntawm ferroptosis tseem tsis tau qhia meej, nws tuaj yeem ntxiv cov lus qhia tshiab rau kev tshawb nrhiav kev kho mob raum.

Cov ntaub ntawv

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Bo Wang^aZhuoshu Li^{b, c}Longfei Mao^dMingyi Zhao^bBingchang Yang^eXiaowu Tau^aYuxiang Li^a Guangming Yin^a

ib lub Department of Urology, Lub Tsev Kho Mob Thib Xiangya, Central South University, Changsha, Suav;

bDepartment of Pediatrics, Lub Tsev Kho Mob Thib Peb Xiangya, Central South University, Changsha, Suav;

c Xiangya Tsev Kawm Ntawv Tshuaj, Central South University, Changsha, Suav teb;

d Bioinformatics Center, College of Biology, Hunan University, Changsha, Suav;

e Department of Critical Care Medicine, Central South University, Changsha, Suav