Ntu Ib Lub Luag Haujlwm Ntawm Hydrogen Sulfide hauv Lub Raum Physiology Thiab Kab Mob Xeev

Abstract

Hydrogen sulfide (H2S), uas yog endogenous gaseous signaling transmitter, tau txais kev lees paub rau nws cov teebmeem physiological. Hauv qhov kev tshuaj xyuas no, peb tsom mus sau thiab sib tham txog cov kev tshawb fawb uas twb muaj lawm txog lub luag haujlwm ntawm H2S hauv lub raum kev ua haujlwm thiab lub raum kab mob nrog rau cov txheej txheem hauv qab. H2S feem ntau yog tsim los ntawm plaub txoj hauv kev, thiab ob lub raum yog H2S loj-ua lub cev. Cov kev tshawb fawb yav dhau los tau pom tias H2S tuaj yeem cuam tshuam ntau txoj hauv kev ntawm kev siv sulfhydration. Nyob rau hauv lub raum physiology, H2S txhawb lub raum excretion, tswj renin tso tawm, thiab nce ATP ntau lawm raws li ib tug sensor rau oxygen. H2S kuj muaj feem cuam tshuam rau kev tsim cov kab mob raum. H2S tau cuam tshuam rau hauv lub raum ischemia / reperfusion thiab cisplatin-thiab sepsis-induced raum kab mob. Hauv cov kab mob hauv lub raum, tshwj xeeb tshaj yog mob ntshav qab zib nephropathy, hypertensive nephropathy, thiab obstructive raum kab mob, H2S txo cov kab mob kev loj hlob los ntawm kev tswj oxidative kev nyuaj siab, o, thiab renin-angiotensin-aldosterone system. Txawm hais tias khaws cov pov thawj los ntawm cov kev tshawb fawb sim qhia txog lub luag haujlwm ntawm H2S cov neeg pub dawb hauv kev kho mob raum, cov txiaj ntsig no xav tau kev txhais lus kho mob ntxiv. Yog li ntawd, kev nthuav dav kev nkag siab ntawm H2S tuaj yeem tsis tsuas yog txhawb nqa peb txoj kev nkag siab ntxiv ntawm lub raum physiology tab sis kuj tsim lub hauv paus rau kev hloov H2S rau hauv lub hom phiaj rau cov kab mob hauv lub raum.

Ntsiab lus

Hydrogen sulfide; sulfhydration; lub raum physiology; mob raum mob; mob raum mob.

Nyem qhov no kom tau txaiscov txiaj ntsig Cistanche

Taw qhia

Hydrogen sulfide (H₂S) yog ib qho tshuaj lom, tsis muaj xim, nrog cov ntxhiab tsw ntawm cov qe lwj. Nws muaj nyob rau hauv cov xwm txheej thiab tuaj yeem pom hauv cov pa roj carbon monoxide, volcanic emissions, thiab roj av [1]. Xyoo 1989, Warenycia thiab Goodwin [2] thawj zaug pom tias tib neeg lub cev muaj H.₂S, uas feem ntau muaj nyob rau hauv lub hlwb, thiab qhia tau hais tias lub hlwb yog ntau rhiab heev rau exogenous H₂S dua lwm qhov ntawm lub hlwb. Kev ua haujlwm physiological ntawm H₂S tsuas yog nyuam qhuav tau maj mam lees paub. High concentration ntawm H₂S yuav ua kom tiav inhibition ntawm tes ua pa, mitochondrial membrane muaj peev xwm depolarization, thiab superoxide tiam [3]. Qib qis ntawm H₂S tuaj yeem tswj hwm homeostatic mechanisms xws li ntshav siab (BP) tswj thiab apoptosis thiab koom nrog cov txheej txheem pathological suav nrog oxidative stress (OS) thiab mob [4,5]. Hauv lub cev, H₂S muaj kev koom tes hauv kev tswj lub raum, thiab H₂S ntau lawm kab mob muaj feem xyuam rau qhov pib thiab kev loj hlob ntawm ntau lub raum kab mob [6]. Txawm hais tias exogenous H₂S tau pom tias ua lub luag haujlwm tseem ceeb hauv kev txo qis ntau yam tsiaj qauv ntawm lub raum kev puas tsuaj, nws cov txheej txheem molecular tshwj xeeb tsis paub.

Hauv kev tshuaj xyuas no, peb xub piav txog H₂S tiam thiab muaj nuj nqi. Tom ntej no, peb qhia lub luag haujlwm ntawm H₂S nyob rau hauv lub raum physiology. Tsis tas li ntawd, peb tham txog H₂S raws li qhov muaj feem cuam tshuam rau qhov tshwm sim thiab kev loj hlob ntawm lub raum kab mob thiab nthuav tawm qee cov txheej txheem. Thaum kawg, peb xaus qhov kev thov ntawm H₂S pub dawb thiab inhibitors hauv kev ua haujlwm preclinical thiab ntsuas qhov ntsuas qhov peev xwm ntawm H₂S nyob rau hauv cov kab mob raum.

Cistanche tubulosa

H₂S tiam thiab muaj nuj nqi

Txawm hais tias Ameslikas pom tsuas yog cov pa roj toxic, H₂S tam sim no lees paub tias yog cov pa roj carbon monoxide uas muaj qee txoj hauv kev zoo ib yam li nitric oxide (NO) thiab carbon monoxide (CO) [7]. Tsis zoo li NO thiab CO, H₂S yog acidic, uas tso cai rau nws yaj hauv dej. Tsis tas li ntawd, vim H₂S yog lipophilic heev, nws tuaj yeem kis tau dawb rau cov cell membranes ntawm txhua hom cell [8]. Cov enzymes ua lub luag haujlwm rau kev tsim ntawm endogenous H₂S suav nrog cystathionine-b-synthase (CBS), cystathionine-c-lyase (CSE), thiab mitochondrial 3-mercaptopyruvate sulfurtransferase (3-MST) [9]. CBS thiab CSE ob leeg tsim endogenous H2S hauv cytosol, thaum 3-MST tsim endogenous H2S hauv mitochondria [4,10]. Endogenous H2S yog tsim nyob rau hauv plaub txoj kev loj. Hauv thawj cov txheej txheem, L-homocysteine ​​thiab serine tsim L-cystathionine raws li kev ua ntawm CBS; L-cystathionine tom qab ntawd hloov mus rau L-cysteine ​​los ntawm CSE. Thaum kawg, H2S tau tsim nyob rau hauv cov txheej txheem kho los ntawm CBS thiab CSE hauv cytoplasm [6]. Hauv qhov thib ob mechanism, CSE reacts nrog L-homocysteine ​​​​los tsim H2S, a-ketobutyrate, thiab L-homolanthionine [4]. Hauv qhov thib peb txheej txheem, cysteine ​​aminotransferase hloov L-cysteine ​​​​rau 3-mercapto pyruvate (3-MP), uas yog siv los ntawm 3-MST rau kev tsim H2S hauv mitochondria [11]. Hauv cov txheej txheem kawg, D-amino acid oxidase mediates hloov pauv ntawm D-cysteine ​​​​rau 3-MP, thiab H2S yog tom qab tsim los ntawm kev ua ntawm 3-MST. Nws yog ib qho tsim nyog sau cia tias 3-MP yuav tsum tau xa mus rau mitochondria rau qib tom ntej. Hauv ob lub raum, lub ntsiab substrate rau H2S ntau lawm yog D-cysteine, thiab H2S los ntawm D-cysteine ​​muaj ntau ntau tshaj li ntawm L-cysteine ​​[12] (Daim duab 1).

Daim duab 1. Endogenous synthesis ntawm H2S los ntawm plaub txoj kev. (A) CSE catalyzes cov tshuaj tiv thaiv ntawm L-homocysteine ​​​​kom induce zus tau tej cov H2S. (B) CBS reacts nrog L-homocysteine ​​​​, nce lub cim ntawm L-cystathionine, uas tom qab ntawd hloov mus rau L-cysteine ​​ntawm CSE, uas ntxiv ua H2S. (C) L-cysteine ​​hloov dua siab tshiab rau hauv 3MP los ntawm CAT, thiab 3-MST catalyzes cov tshuaj tiv thaiv ntawm 3MP los ntxias H2S tiam hauv mitochondria. (D) DAO reacts nrog D-cysteine ​​​​los tsim 3MP, uas tom qab ntawd nkag mus rau mitochondria thiab ua haujlwm ua lub substrate rau kev tsim H2S. CBS (cystathionine b-synthase); CSE (cystathionine c-lyase); CAT (cysteine ​​aminotransferase); 3MP (3-mercapto pyruvate); DAO (D-amino acid oxidase); 3-MST (3-mercapto pyruvate sulfurtransferase).

H2S ua haujlwm lom neeg li cas? Cov kev tshawb fawb tsis ntev los no tau muab cov lus teb. H2S tuaj yeem tswj cov kev taw qhia sib txawv uas cuam tshuam rau cell metabolism. H2S koom nrog hauv cov teeb liab kis tau los ntawm kev taw qhia txoj hauv kev los ntawm sulfhydration, thaum lub sij hawm nws reacts nrog cysteine ​​residues ntawm ntau lub hom phiaj proteins los tsim persulfide bonds. Lub reactivity ntawm sulfhydration yog txiav txim los ntawm cov kua qaub dissociation tas li ntawm cysteine ​​residues [13]. Mustafa et al. [14] pom tias kwv yees li 10-25 feem pua ​​​​ntawm lub siab cov protein tuaj yeem ua haujlwm los ntawm S-sulfhydration, xws li actin, tubulin, thiab glyceraldehyde-3-phosphate dehydrogenase. S-sulfhydration yog qhov tseem ceeb rau kev ua haujlwm ntawm daim siab cov protein; Piv txwv li, nws txhim kho glyceraldehyde-3-phosphate dehydrogenase kev ua haujlwm thiab actin polymerization. H2S yog endothelium-derived hyperpolarizing yam uas tuaj yeem ua rau hyperpolarization thiab vasodilation ntawm vascular endothelial thiab cov leeg nqaij du. Qhov vasodilation no yog ua tiav los ntawm kev ua kom lub ATP-sensitive, nruab nrab, thiab me me conductance potassium raws, thiab cov kauj ruam tseem ceeb tshaj plaws rau kev ua kom channel yog S-sulfhydration [15]. H2S koom nrog cov tshuaj tiv thaiv kab mob raws li tus neeg xa xov molecule, thiab cov teebmeem hauv qab ntawm sulfhydration cuam tshuam rau nuclear factor jB (NF-jB). NF-jB ua lub luag haujlwm tseem ceeb hauv cov lus teb inflammatory hauv hlwb. Nil Kantha et al. [5] pom tias qog nqaij hlav necrosis factor-a (TNF-a) tuaj yeem txhawb nqa cov ntawv sau ntawm CSE los tsim H2S. H2S sulfhydrates Cys38 ntawm p65, txhim kho nws txoj kev khi rau cov coactivator ribosomal protein S3, yog li tswj cov haujlwm ntawm NF-jB. Hauv CSE-tsis muaj nas, p65 tsis tuaj yeem ua rau nws tus kheej-hydrated, ua rau txo qis NF-jB hom phiaj kev ua haujlwm ntawm noob. Cov protein tyrosine phosphatase-1B yog nyob rau ntawm lub ntsej muag cytoplasmic ntawm endoplasmic reticulum (ER) thiab tau cuam tshuam rau hauv ER kev nyuaj siab signaling. H2S-induced sulfhydration ntawm cov protein tyrosine phosphatase-1B koom nrog ER kev ntxhov siab [16]. P66Shc yog ib qho dej ntws tawm ntawm mitochondrial redox signaling. Hauv kev teb rau OS, p66Shc yog qhib los ntawm cov protein kinase C-bII-mediated phosphorylation ntawm Ser36. Xie et al. [17] pom tias H2S downregulates phosphorylation ntawm p66Shc los ntawm sulfhydration ntawm Cys59 residue, yog li txo mitochondrial zus tau tej cov reactive oxygen hom (ROS) thiab ua kom tiav cov teebmeem antioxidant. Nuclear factor-erythroid 2-related factor 2 (Nrf2) yog tus thawj tswj hwm ntawm cov lus teb antioxidant. Feem ntau, Nrf2 yog ubiquitinated thiab sai sai degraded los ntawm cov proteasome nyob rau hauv qhov kev txiav txim ntawm Kelch-zoo li ECH-sociated protein 1 (Keap1). Sodium sulfide (NaHS) tau tshaj tawm tias yog S-sulfhydryl Keap1 ntawm Cys151 thiab txhawb nqa Nrf2 nuclear translocation [18].

Cistanche ntxiv

H2S ntau lawm nyob rau hauv lub raum thiab nws lub luag hauj lwm nyob rau hauv lub raum physiology

1. H2S ntau lawm hauv lub raum

Qee qhov kev tshawb fawb tau pom tias peb lub enzymes uas tsim cov endogenous H2S tau nthuav tawm ntau hauv cov ntaub so ntswg, xws li ob lub raum [19]. CBS, CSE, thiab 3-MST tuaj yeem kuaj pom nyob rau hauv lub raum proximal tubules. CSE kuj tseem qhia nyob rau hauv lub raum glomeruli, interstitial, thiab interlobular hlab ntsha [19,20]. Raws li ib txwm muaj, cov protein CSE tau qhia nyob rau theem siab tshaj plaws hauv lub raum, mus txog qib 20 npaug ntawm CBS. Hauv cov ntaub so ntswg ntawm lub raum ntawm Sprague-Dawley nas, tag nrho peb H2S-tsim enzymes tam sim no, thiab CSE mRNA tau nthuav tawm ntau dua 3MST thiab CBS mRNA [4]. Yog li ntawd, CSE ua lub luag haujlwm tseem ceeb hauv kev tsim H2S [21,22]. CBS thiab CSE synergistically tsim H2S, thiab ob lub enzymes no tuaj yeem sib koom ua ke ua kom muaj H2S endogenous hauv ob lub raum [23].

Peb ib txwm H2S-synthesizing txoj hauv kev (suav nrog CSE, CBS, thiab 3-MST ua ke nrog cysteine ​​aminotransferase) tau txheeb xyuas hauv ob lub raum, raws li tau piav qhia hauv "H2S Generation and Functions" section. Yog li ntawd, peb tsom mus rau txoj kev thib plaub H2S tiam, uas yog, txoj kev DAO/3–MST [24]. Hauv txoj kev no, D-cysteine ​​hloov mus rau 3-MP los ntawm peroxisome-nyob DAO. Vim yog cov metabolite pauv ntawm peroxisomes thiab mitochondria, 3-MP raug xa mus rau hauv mitochondria thiab catalyzed rau hauv H2S los ntawm 3-MST [24] (Daim duab 1). Shibuya et al. pom tias lub raum lysate tuaj yeem tsim 60 npaug ntau dua H2S thaum D-cysteine ​​siv los ua substrate dua li thaum siv L-cysteine ​​[12]. Qhov kev tshawb pom ntawm qhov tshwj xeeb DAO/3-MST txoj hauv kev hauv lub raum thiab lub hlwb tuaj yeem cuam tshuam lub luag haujlwm tseem ceeb ntawm 3-MST-mediated H2S tiam hauv cov kabmob no. Qhov muaj peev xwm no tsim nyog tshawb nrhiav ntxiv.

2. H2S hauv lub raum physiology

2.1. Cov nyhuv ntawm H2S ntawm lub raum excretory muaj nuj nqi

H2S plays lub luag haujlwm tseem ceeb hauv lub raum excretion. Xia et al. pom tias ob qho tib si CBS thiab CSE tuaj yeem tsim H2S hauv lub raum thiab tias thaum twg ob qho enzyme inhibited, qhov kev qhia ntawm lwm yam nce ntxiv kom them nyiaj. Lawv kuj pom tau hais tias nyob rau hauv cov tshuaj loog Sprague-Dawley nas, infusion ntawm NaHS nyob rau hauv lub raum cov hlab ntsha tuaj yeem ua rau kom cov ntshav khiav thiab lub glomerular filtration rate (GFR). Vim tias qhov nce hauv qhov pom, cov kws sau ntawv tau kwv yees tias lub luag haujlwm ntawm H2S hauv cov hlab ntsha vasodilating ntau dua hauv cov hlab ntsha preglomerular dua li hauv postglomerular arterioles. H2S tseem tuaj yeem cuam tshuam cov Na-K-2Cl cotransporter nyob rau hauv lub nce toj ceg ntawm lub voj ntawm Henle thiab Na-K ATPase enzyme, uas yuav ua rau kom cov kua qaub thiab poov tshuaj los ntawm cov zis. Yog li, H2S koom nrog ob qho tib si vascular thiab tubular ua hauv ob lub raum [23].

Cistanche ntsiav tshuaj

2.2. H2S raws li oxygen sensor

H2S tuaj yeem ua raws li cov pa oxygen (O2) sensor los kho O2 tshuav, qhov tshwm sim uas tau lees paub hauv ntau yam O2-sensing cov ntaub so ntswg, xws li lub cev carotid, adrenal medulla, thiab lwm yam chemoreceptive cov ntaub so ntswg, nrog rau cov leeg nqaij hauv lub cev. cov hlab ntsha thiab cov hlab ntsha [25] H2S metabolism yog nyob ntawm qhov concentration ntawm O2 [25]. Raws li lub cev muaj zog, pO2 txo qis hauv lub raum medulla, thiab oxidation ntawm H2S tsis zoo cuam tshuam nrog pO2 hauv mitochondria, yog li kev ua haujlwm ntawm H2S hauv medulla yuav siab dua li hauv lub raum cortex [4]. H2S, uas sib sau ntau ntxiv hauv lub raum medulla nyob rau hauv cov xwm txheej hypoxic, tuaj yeem rov qab O2 cov khoom los ntawm kev ua kom cov ntshav medullary nce [26]. Ntxiv mus, cov kev tshawb fawb tau pom tias nyob rau hauv cov xwm txheej ntawm cov pa txaus, cov qib CBS thiab CSE hauv mitochondria tsawg. Thaum hypoxia tshwm sim, cov concentrations ntawm CBS thiab CSE nce, uas ua rau cov H2S ntau lawm [27,28]. H2S tau txais kev pab raws li tus neeg pub khoom siv hluav taws xob thiab nce ATP ntau lawm [27]. Hypoxia yog qhov tseem ceeb tshaj plaws uas muaj feem cuam tshuam rau pathogenesis thiab kev loj hlob ntawm ntau yam kab mob raum. Endogenous H2S deficiency tuaj yeem ua rau muaj kev cuam tshuam medullary oxygenation thiab ua rau muaj qhov tshwm sim thiab kev loj hlob ntawm cov kab mob raum [26]. Txawm li cas los xij, cov txheej txheem tshwj xeeb tseem tsis meej thiab xav tau kev kawm ntxiv.

2.3. H2S modulates renin tso tawm

H2S attenuates pathological signaling ntawm renin-angiotensin-aldosterone system (RAAS) kom khaws lub raum ua haujlwm. RAAS yog ib qho kev tswj hwm kev lom zem uas tsim los ntawm cov tshuaj hormones thiab cov enzymes sib xws uas tswj cov kua dej thiab sodium. Kev tso tawm ntawm renin los ntawm juxtaglomerular hlwb txiav txim qhov pib thiab kev loj hlob ntawm renovascular hypertension, ib txoj kev kho los ntawm intracellular 30 -50 -cyclic adenosine monophosphate (cAMP). H2S tau tshaj tawm kom txo qis cAMP los ntawm inhibiting adenylate cyclase kev ua, yog li tswj renin tso tawm thiab tswj BP [29,30]. Hauv thawj kab lis kev cai ntawm renin-nplua nuj lub raum hlwb, NaHS txo qis cov qib ntawm intracellular cAMP thiab txo cov kev ua renin. Nyob rau hauv tus qauv Dahl nas ntawm high-ntse-induced kub siab, kev kho mob nrog H2S tau pom tias inhibit RAAS system ua rau lub raum thiab tswj BP [31]. H2S kuj tswj BP ntawm angiotensin-hloov enzyme, uas belongs rau RAAS system. Hauv tib neeg cov hlwb endothelial, H2S tuaj yeem cuam tshuam ncaj qha rau zinc hauv qhov chaw nquag ntawm angiotensin-hloov enzyme [32].

Standardized Cistanche

Hauv luv luv, H2S ua lub luag haujlwm tseem ceeb hauv lub raum physiology; Txawm li cas los xij, kev kawm ntxiv yog yuav tsum tau tsim kom muaj cov txheej txheem tshwj xeeb koom nrog.

Cov ntaub ntawv

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Jianan Feng, Xiangxue Lu, Han Li, thiab Shixiang Wang

Department of Nephrology, Beijing Chao-Yang Tsev Kho Mob, Capital Medical University, Beijing, Suav