(Part II) Lub Luag Haujlwm Ntawm Arachidonic Acid Thiab Nws Cov Metabolites hauv Cov Khoom Noj thiab Tshuaj Kho Mob Ntawm Idiopathic Nephrotic Syndrome
Mar 26, 2022
5. Lub raum Glomerular thiab Tubular FunctionEpoxyeicosatrienoic acids (EETs) yog tsim nyob rau hauv ntau cov ntaub so ntswg, xws li lub plawv, cov leeg,lub raum, pancreas, lub ntsws, thiab lub hlwb [41], tab sis feem ntau nyob rau hauv vascular endothelium, nyob rau hauv teb rau ntau yam PLA2- activating stimuli, EETs kev ua yuav txo tau los ntawm metabolization ua los ntawm soluble epoxide hydrolase (sHE)[ 42] ib. EETs modulatelub raum ua haujlwmua ncaj qha rau tubular ionic thauj, vascular tone, thiab cellular proliferation, thiab muaj lub luag hauj lwm nephroprotective [43] vim lawv cov khoom tiv thaiv. EETs nyob rau hauv qhov tseeb induce vasodilatation nyob rau hauv ib tug autocrine yam [44] thiab muaj anti-apoptotic kev ua si; nws kuj tau qhia tias lawv tiam raug txo nyob rau hauv cov ntaub ntawv ntawmmob raum|42] Txawm hais tias tsis muaj lus piav qhia txog lub tshuab no tau muab.
Ntsiab lus: raum; arachidonic acid; nephrotic syndrome; kab mob raum; raum fibrosis
CISTANCHE yuav txhim kho lub raum / raum ua haujlwm
Glomerular o yog mitigated los ntawm EETs, uas txo cov influx ntawm neutrophils thiab macrophages thiab txo zus tau tej cov cytokines, monocyte chemotactic protein-1, TNF-, macrophage inflammatory protein 2, thiab ICAM-1 45]. Cov nyhuv tiv thaiv yog vim EETslub raumvasodilator thiab antipressor teb rau ntsev loading los ntawm inhibition ntawmlub raumtubular Na * reabsorption thiab nce ntawm Na *lub raumexcretion, uas ua rau muaj kev tiv thaiv-hypertensive nyhuv [46] uas tej zaum kho los ntawm A2A receptors [47]. 20-HETE, lwm eicosanoid muab los ntawm AA metabolism, qhia tib yam kev tiv thaiv zoo li EETs [48].Nws ua lub luag haujlwm tseem ceeb hauv kev tswj hwm ntawmlub raumtubular thiab vascular muaj nuj nqi, thiab txawv nyob rau hauv cov noob encoding rau cov enzymes uas tsim 20-HETE yog txuam nrog kub siab [49]. Nws tau raug pom tias kev tsim khoom ruaj khov ntawm 20-HETE hauv glomerulus yuav tsum tau ua kom lub glomerular permeability barrier rau albumin [48]. Nws tseem tsis tau paub meej tias hom cell twg hauv glomerulus qhia txog CYPenzymes uas ua ke 20-HETE, thiab cov txheej txheem tseeb uas cov molecule no cuam tshuam rau glomerular permeability barrier yog vet yuav tsum tau txhais ib yam nkaus [48l, txawm hais tias nws yuav zoo li ntawd. Nws cov teebmeem yog kho los ntawm kev hloov kho ntawm Na plus -K ntxiv -ATPase, Na ntxiv -K ntxiv rau -2Cl-cotransporter, thiab K ntxiv cov dej num hauv nephrons [49] los ntawm kev ua kom muaj PKC txoj hauv kev [50] . 20-HETE tseem koom nrog hauv podocyte apoptosis, los ntawm kev tswj cov canonical transient receptor peev xwm-6 (TRPC6) channels thiab nce Ca2 ntxiv flux [51]. Hauv cov neeg mob uas cuam tshuam los ntawm nephrotic syndrome uas ua rau mob ntshav siab thaum ntxov [52], qhov txo qis ntawm 20-HETE hauv cov tubule ze ze tau pom [53] nrog rau kev nce albumin permeability hauv glomeruli, uas ua rau cov proteinuria thiab glomerular raug mob. [54]; Qhov kev tshawb pom no txhawb nqa lub luag haujlwm ntawm 20-HETE hauv kev khaws cia glomerular permeability barrier rau albumin. Txawm li cas los xij, nws tsis paub yog tias qhov txo qis ntawm 20-HETE ua rau lossis tshwm sim los ntawm kev kub siab. Hauv kev xaus, 20-HETE tuaj yeem ua ntau txoj hauv kev (tiv thaiv lossis pro-apoptotic) hauv ntau hom cell thiabraumcheeb tsam.
6. Podocyte Physiopathology thiab Kab MobNws yog paub zoo tias, nyob rau hauv cov chav kawm ntawm nephrotic syndrome, kab mob ua rau ib tug exacerbation ntawm proteinuria [55] thiab yog ib qho tseem ceeb txaus ntshai rau relapses [156,57J. Cov kab mob activates lub cev tiv thaiv kab mob, ua rau lub inflammatory cascade. Tsis ntev los no tau tshaj tawm tias thaum lub sijhawm mob ob lub enzymes raug ntxias: 15-lipoxygenase (15-LO) thiab secreted phospholipase A,(sPLA,)[58]. Qhov tseem ceeb, 15-LO tau qhia hauv tib neeg podocytes [59], thaum SPLA, qhia hauv platelets, neutrophils, eosinophils, thiab macrophages [60].sPLA2 tso tawm AA los ntawm daim nyias nyias phospholipids [51,61] ua yeeb yam hauv paracrine. txoj kev. Hauv glomerular podocytes, intracellular free AA yog metabolized rau PGE, uas, los ntawm kev cuam tshuam nrog EP4 receptor (prostaglandin E, receptor 4) qhia los ntawm podocytes, txo AA tso tawm [52]. Lub voj no tswj kev ua haujlwm ntawm podocyte nyob rau hauv ob qho tib si physiological thiab pathological mob thiab muaj peev xwm hloov PGE2 synthesis [62].
CISTANCHE yuav txhim kho lub raum / raum kab mob
Raws li tau piav qhia saum toj no, thaum lub sijhawm kis tus kabmob, AA qib intracellular nce vim qhov kev ua ntawm sPLA, Nws tau tshaj tawm tias hauv podocytes, ntau tshaj ntawm AA activates protein kinase A, uas nyob rau hauv lem txhawb c-Abl activation thiab nephrin phosphorylation, yog li ua rau actin cytoskeleton remodeling thiab podocyte raug mob [63]. Cov txheej txheem no tuaj yeem piav qhia qee qhov kev rov ua dua ntawm cov proteinuria thaum lub sijhawm kis kab mob hauv cov menyuam yaus. Ntxiv mus, qhov nce hauv sPLA2 1B qib thiab PLA2R qhia tau pom tias muaj txiaj ntsig zoo rau podocyte apoptosis hauvlub raumntawm cov neeg mob uas muaj idiopathic membranous nephropathy [64]. Podocyte ko taw txheej txheem raug mob thiab podocyte apoptosis vim cytoskeleton remodeling kuj tau txais txiaj ntsig los ntawm kev hloov pauv ntawm Ca2 ntxiv rau efflux [51], tsav los ntawm 20-HETE, lub ntsiab AA metabolite. Nws kuj tau pom tias 20-HETE nce Ca2 ntxiv rau tam sim no ntws los ntawm TRPC6 raws hauv cov podocyte [51], uas nyob rau ntawm lub diaphragm slit, tejzaum nws ua rau mob cellular. Cov kev tshawb fawb txog kev sib raug zoo ntawm AA thiab podocyte yog qhov tsis txaus tab sis muaj kev cia siab heev rau kev ua kom peb paub txog cov kab mob ntawm cov kab mob.lub raum puashauv INS.
7. Lub raum Fibrosisyog ib tug txheej txheem uas nce nws tus kheej ntawm lub hauv pausmob raum[65] thiab sawv cev rau qhov ua tsis tiav qhov mob-kho cov txheej txheem ntawmcov ntaub so ntswg. Lub raumbiopsies ntawm cov neeg mob uas muaj steroid-resistant nephrotic syndrome feem ntau qhia glomerulosclerosis thiab interstitial fibrosis, uas cuam tshuam nrog kev loj hlob mus rau theem kawg.mob raumnyob rau hauv ntau tshaj 50 feem pua ntawm cov neeg mob [65], ib tug tsis zoo prognosis uas ua rau kom qhov tsim nyog ntawm kev nce peb kev paub txog mechanisms hauv qab fibrosis.Lub raumfibrosis yog tshwm sim los ntawm kev sib txuas cov ntaub so ntswg deposition nyob rau hauv lubraumparenchyma, tshwj xeeb tshaj yog nyob rau hauv lub interstitial qhov chaw thiab nyob rau hauv cov phab ntsa ntawm glomerular capillaries, thiab los ntawm qhov tshwm sim ntawm cellular txheej txheem. Fibrosis kuj cuam tshuam nrog kev ua haujlwm ntawm tubular, ua rau lub cev tsis ua haujlwm [65,66]. Cov ntaub so ntswg muaj cov fibrillar collagen I thiab kuv nrog rau qee cov khoom ntawm lub cev capillary hauv qab daim nyias nyias, xws li collagen IV thiab V, fibronectin, laminin, perlecan, thiab heparin [66]. Fibrosis yog txuam nrog leukocyte recruitment, angiogenesis, vascular leak, thiab cov tsos ntawm myofibroblasts. Hauv particular, ob qho tib si glomerulus thiab interstitium nyiam cov leukocytes ntau, feem ntau ntawm cov kab mob myeloid, thiab feem ntau neutrophils nyob rau hauv mob hnyav, thaum macrophages thiab dendritic hlwb predominate nyob rau hauv tej chaw. Nyob rau hauv rooj plaub ntawm cov kab mob tiv thaiv kab mob ntev, T lymphocytes yog qhov tseem ceeb [66]. Activated macrophages tuaj yeem ua rau cov ntaub so ntswg ncaj qha los yog tsim cov cytokines profibrotic, suav nrog TGF- thiab lwm yam kev loj hlob, thiab muaj peev xwm tsim tau qee qhov sib xyaw matrix. Yog li nws pom tseeb tias fibrosis thiablub raumo, feem ntau yog tsav los ntawm lub cev tiv thaiv kab mob ua kom muaj kev sib raug zoo.
Tshaj nws lub luag haujlwm hauv kev tswj hwm kev tiv thaiv kab mob, AA kuj tseem cuam tshuam ncaj qha rau fibrosis. Hauv vitro kev sim ntawm cov kab lis kev cai ntawm tes incubated nrog PUFAs pom tias AA muaj peev xwm ua kom muaj zog ntawm kev qhia ntawm TGF- , fibronectin 1 (FN1), connective tisue growth factor (CTGF), thiab collagen IV, tag nrho cov tebchaw muaj feem rau fibrosis [67] . AA kuj tseem txhim kho hauv vitro angiotensin Ⅱ (Angel-induced gene expression J67L activating mechanisms that mediate)lub raum puas.Interestingly, omega -3 EPA thiab DHA, yog siv nrog AA. suppress cov teebmeem ntawm AA thiab AngII [67]. Ntawm qhov tod tes, angiotensin Iis degraded los tsim angiotensin-(1-7), uas inhibits angiotensin II-stimulated phosphorylation ntawm mitogen-activated protein kinases (MAPKs) p38. , extracellular signal-related kinase (ERK1/ERK2), thiab C-JUN N-terminal kinase (JNK) nyob rau hauv proximal tubular cells, yog li ua lub luag haujlwm tiv thaiv fibrosis. Raws li qhov tseeb, p38 MAPK phosphorylation ua rau kev tso tawm ntawm AA thiab tsim cov TGF- 1 thiab extracellular matrix proteins [68]. 20-HETE, AA metabolite, kuj ua lub luag haujlwm sib txawv hauv fibrogenesis, los ntawm kev ua kom lub renin-angiotensin-aldosterone system (RAAS), los ntawm inducing vascular qhia ntawm ACE downstream ntawm NF-kB ua kom [69,70]. Nws paub zoo tias RAAS koom nroglub raumfibrosis [71], vim hais tias nws nce TGF- qhia, uas pib ib tug biomolecular cascade tsav mus raulub raumfibrosis.
Ntawm qhov tsis sib xws, PGE,, lwm yam AA metabolite, tau pom tias inhibit collagen hom 1 ntau lawm thiab ua kom cov matrix metalloproteinase 1 (MMP1) qhia hauv dermal fibroblasts |72] los ntawm kev khi rau EP-1 receptor ntawm fibroblasts, pib txoj hauv kev tswj hwm ERK1/2 thiab IP3 teeb liab uas ua rau txo qis hauv collagen qhia thiab nce hauv MMP1 qhia [72]. Hauv cov ntsiab lus, AA thiab nws cov metabolites ua lub luag haujlwm tseem ceeb hauv cov txheej txheem tseem ceeb hauv lub luag haujlwm rau kev hloov tsis tau.lub raum puas, nyob rau hauv ib tug complex network uas qhov kawg tshwm sim tej zaum yuav sib txawv, raws li genetic-thiab ib puag ncig-sociated yam, cov metabolic tshuav nyiaj li cas ntawm cov neeg nruab nrab ntawm cov metabolism hauv nruab nrab, ntau tshaj li ib tug neeg tebchaw, yuav dictate qhov kawg tshwm sim. Tsis tas li ntawd, nws tseem tsis tau paub meej yog qhov kawg, cuam tshuam txog cov txiaj ntsig pathologic, uas yog,lub raumfibrosis, tuaj yeem tswj hwm los ntawm kev noj zaub mov lossis kev ntsuas tshuaj kho mob ncaj qha los hloov kho cov ntshav AA qib lossis hloov pauv tsis ncaj rau cov haujlwm ntawm AA metabolites.
CISTANCHE yuav txhim kho lub raum / raum tsis ua haujlwm
8. Kev sib cuam tshuam ntawm cov tshuaj thiab noob Idiopathic nephrotic syndrome feem ntau yog kho nrog glucocorticoids lossis nrog cov tshuaj tiv thaiv kab mob, tshwj xeeb tshaj yog calcineurin inhibitors (CNI, xws li cyclosporine A(CsA) thiab tacrolimus(Fk). , CYP gene kuj koom nrog hauv AA metabolism, tab sis hauv cov ntaub ntawv, tsis muaj cov ntaub ntawv qhia txog kev sib tw enzymatic ntawm cov tshuaj no thiab AA. Txog rau kev sib raug zoo ntawm CNI thiab AA cov ntshav, ib qho kev tshawb fawb hauv vitro qhia tias CsA txo qis. Kev ua haujlwm ntawm Delta 9 desaturase thiab nce cov haujlwm ntawm Delta6 thiab Delta 5 desaturases [73] los ntawm cov txheej txheem tsis paub. Txawm li cas los xij, raws li Delta 5 desaturase tau koom nrog hauv cov kauj ruam kawg ntawm AA biosynthesis [73], CsA therapy tuaj yeem nce AA cov ntshav ntawm cov neeg mob. nrog INS.
Ntawm tib kab, nws tau pom tias CsA feem ntau nce qhov muaj AA dawb es tsis txhob txo cov ntshav AA los ntawm kev nrawm ntawm AA hloov pauv los ntawm txoj kev cyclooxygenase [74], tab sis kev tshawb fawb ntxiv hauv vitro tau xaus tias CsA tsis muaj txiaj ntsig. ntawm AA tso tawm thiab cov metabolism [75]. Qhov txiaj ntsig no tau lees paub tsis ntev los no hauv kev tshawb fawb ntawm CsA thiab glucocorticosteroids hauv tib neeg peripheral ntshav mononuclear hlwb [76]. Hais txog lub luag haujlwm ntawm AA metabolism hauv kev txiav txim siab CNI cov kev mob tshwm sim, nws paub zoo tias kev kho CsA tuaj yeem ua rau gingival overgrowth, uas nyob ntawm PGE2 ntau lawm hauv gingival fibroblasts. Qhov tseeb, CsA potentiates TNF- los txhawb kev tso tawm ntawm AA los ntawm fibroblasts, nrog rau qhov kev tsim kho ntawm PGE, thiab gingival overgrowth [77]. Tsis muaj kev tshawb fawb qhia txog qhov tshwm sim tib yam hauv lwm cov ntaub so ntswg. Lub nephrotoxicity ntawm CsA tau tsim tau zoo, thiab kev tswj hwm Fk cuam tshuam nrog tib cov kev mob tshwm sim, uas tau txuas nrog CYPC8 * 3 thiab CYP2C8 * 4 polymorphisms thiab qhov ua rau txo qis ntawm EETs: nws tau pom tias kev ncig ntawm Fk ntshav concentration ntawm 10. ng / mL muaj peev xwm txo qis kev tsim tawm ntawm eicosanoids los ntawm 35 feem pua .Nws ua raws li CNIs-induced nephrotoxicity tuaj yeem yog vim txo qis kev ua haujlwm ntawm CYP2C8 * 3, uas txo cov EETs, txhim kho cov tshuaj nephrotoxicity [78]. Kev kho ua ntej nrog Fk kuj tseem paub txog kev txhim kho glucocorticoids kom inhibit AA thiab PGE ntau lawm [7] los ntawm inhibiting COX2 qhia, tab sis kev koom tes ntawm Fk thiab glucocorticoids tsis inhibit COX2 qhia, tso cai rau PGE, tsim tawm-tion[79] ].
Yog li, cov tshuaj tseem ceeb uas feem ntau siv hauv INS yuav muaj ntau yam cuam tshuam rau AA metabolism, uas muaj feem cuam tshuam rau kev siv ntau ntxiv. Thaum sib piv cov kev tshawb pom tau raug tshaj tawm, qee qhov ntawm cov no tuaj yeem suav rau qee qhov kev mob tshwm sim, xws li gingival overgrowth thiab nephrotoxicity, thiab txawm tias kev kho mob. Txawm hais tias kev koom ua ke ntawm omega 3 raws li cov roj excipient rau CsA, kom bioavailability thiab txo nephrotoxicity, tau raug tshawb xyuas nrog cov txiaj ntsig zoo [80,81], tsis muaj cov tswv yim kho mob tau tsim los txog tam sim no.
9. Kev Noj Qab Haus Huv Sib npaug ntawm AA thiab LA thiab AA Qhov ChawAA, uas belongs rau omega-6 series, thiab docosahexaenoic acid (DHA), uas belongs rau omega-3 series, yog cov tseem ceeb tshaj byproducts ntawm tseem ceeb fatty acids linoleic thiab -linolenic acid, thiab lawv. Kev tsis sib haum xeeb tau cuam tshuam nrog inflammatory thiab mob ntev [82]. Thaum LA thiab AA feem ntau hu ua inflammatory molecules, kev khiav hauj lwm nyob rau hauv ib tug interdependent network los ntawm lawv cov metabolites [82], AA metabolites kuj muaj anti-inflammatory thiab tiv thaiv lub luag hauj lwm, thaum LA metabolites cuam tshuam rau lub cev tsis muaj zog los ntawm kev khi cellular receptors thiab hloov pauv cov cim qhia molecules [83 ]. Qib AA thiab DHA nyob ntawm ob qho tib si rau cov caj ces predisposition thiab kev noj haus. Cov ntshav AA qib, raws li qhia hauv daim duab 1, tuaj yeem hloov kho los ntawm kev noj zaub mov noj, suav nrog tias muaj qhov sib txawv ntawm qhov sib txawv ntawm cov khoom noj AA thiab cov nyiaj sib txuas los ntawm tib neeg cov txheej txheem metabolic. Nyob rau hauv rooj plaub tom kawg, lub ntsiab tus nqi-txheej enzymes yog A5-thiab A6-desaturases, uas yog encoded los ntawm cov noob FADS1 thiab FADS2, thiab sib txawv polymorphisms nyob rau hauv fatty acid desaturases noob yuav txawm nce. los yog txo qhov tsim ntawm LC-PUFAs[84]. Raws li qhov tseeb, saib cov zaus ntawm 28 SNPs hauv FADS haplotypes, lawv qhov kev faib tawm hauv 3 lub ntsiab haplotypes tau tshwm sim thoob ntiaj teb [85].
Tsis zoo li lwm cov fatty acids, omega-3 thiab omega{1}} precursors (LA thiab linolenic acid, feem) tsis tuaj yeem raug tsim los ntawm cov tsiaj nyeg (lawv yog cov khoom noj khoom haus tseem ceeb tiag tiag), yog li cov txheeb ze ntau ntawm cov PUFAs. nyob rau hauv kev noj haus muaj ib tug loj cuam tshuam rau tib neeg. LA yog qhov sawv cev tshaj plaws ntawm omega-6 PUFA nyob rau hauv feem ntau cov zaub mov sab hnub poob, thiab tau nthuav dav hauv cov khoom noj: nws sawv cev ntau dua 50 feem pua ntawm cov ntsiab lus lipid hauv ntau cov roj zaub, suav nrog safflower, sunflower, pob kws, thiab taum roj; nws muaj nyob rau hauv cov txiv ntseej thiab noob, thaum qis dua muaj nyob rau hauv cov nplej, legumes, qee cov nqaij, qe, thiab cov khoom noj siv mis [86]. Qhov tseem ceeb, nws tsis ntev los no tau tshaj tawm tias qhov txo qis hauv kev noj zaub mov noj ntawm LA tsis cuam tshuam nrog kev txo qis hauv kev nthuav dav AA qib [87]. Lub xeev AA nyob ntawm qhov endogenous synthesis los ntawm qhov tseem ceeb precursor LA, tab tom desaturation thiab elongation, thiab kev noj zaub mov ncaj qha [88]. Txij li thaum LA mus rau AA kev hloov pauv kev ua tau zoo ntawm tib neeg tsawg, AA tau txais los ntawm kev noj zaub mov zoo li ua tau zoo dua hauv kev nce nws cov qib. Hauv kev sib piv rau LA, AA yog qhov tsawg heev hauv kev noj haus thiab pom muaj nyob hauv cov nqaij (ob leeg liab thiab dawb, nrog rau cov ntses), cov nqaij hauv nruab nrog cev (piv txwv li, daim siab,raum, hlwb), thiab qe, nrog tsawg kawg nkaus ntawm nyuj cov mis nyuj rog thiab cov khoom muab tau los ntawm nws [89]. Qhov yuav tsum tau muaj los ntawm cov tsiaj txhu yog txuas ncaj qha mus rau lub peev xwm ntawm cov tsiaj kom muab tau nws los ntawm kev ua enzyme, ua rau cov zaub tseem ceeb precursor, LA. Tshwj xeeb, cov tsiaj txhu yog cov neeg sawv cev tshaj plaws. Cov khoom noj uas nplua nuj nyob rau hauv nqaij nyuj, yaj, nqaij npuas, thiab nqaij qaib tau thov kom pab txhawb rau cov ntaub so ntswg AA siab [90]. Cov nyiaj no yog cuam tshuam los ntawm kev noj zaub mov muaj pes tsawg leeg, lub plab zom mov, thiab cov txheej txheem biosynthetic hauv tus tsiaj [91]. Macroalgae, fungi, kab mob, thiab cov poov xab tuaj yeem yog qhov tseem ceeb ntawm PUFAs, uas tuaj yeem muab cov roj fatty acids rau tib neeg thaum suav nrog hauv kev noj zaub mov lossis siv ua zaub mov rau ntses thiab tsiaj txhu.
Ntau cov fungi, poov xab, thiab qee cov kab mob tuaj yeem tsim cov LC-PUFAs, feem ntau AA. Qhov ua tau zoo tshaj plaws AA-tsim cov kab mob yog cov tsis muaj kab mob Mortiella spp. nyob rau hauv uas AA ntau lawm suav txog li 70 feem pua ntawm tag nrho cov lipids [92]. Ntawm cov algae, AA tau raug txheeb xyuas hauv ntau pawg uas loj hlob photoautotrophically lossis heterotrophically. Qee hom algal tau tshaj tawm tias muaj cov ntsiab lus AA ntau dua, uas tuaj yeem ncav cuag 77 feem pua ntawm tag nrho cov fatty acids, xws li hauv dej ntsuab ntsuab microalga Parietochloris incisa, 40 feem pua ntawm tag nrho cov fatty acids nyob rau hauv liab alga Porpuridium purpureum, thiab 20-30 feem pua hauv diatoms xws li Phaeodactylum tricornutum thiab Thalassiosira pseudomonas. AA tau raug kuaj pom tsawg dua hauv qee hom lichen (symbiosis kev koom tes ntawm fungi thiab algae). Cov nroj tsuag qis dua, xws li mosses thiab ferns, muaj ntau dua AA dua li seagrasses thiab terrestrial siab dua nroj tsuag [92].
Ntau xyoo dhau los, kev noj zaub mov noj n-3 LC-PUFA tau txo qis, thaum cov khoom noj khoom haus ntawm LA tau nce, uas tau tsav los ntawm kev siv cov khoom noj zaub uas nplua nuj nyob hauv LA, thiab cov khoom noj khoom haus uas muaj LA-nplua nuj. zaub mov [83,93]. Los ntawm kev saib xyuas kev kho mob, qhov ua tiav ntawm qhov sib npaug ntawm tus kheej polymorphisms hauv FADS genes modulation thiab PUFAs kev noj zaub mov tuaj yeem txhim kho lossis tiv thaiv kev mob, tshwj xeeb tshaj yog nyob rau hauv cov kev kawm uas tuaj yeem ua kom zoo dua ntawm kev noj zaub mov exogenous PUFAsupply, vim qhov tsis zoo endogenous synthesis tus nqi. [93]. Kev noj zaub mov Mediterranean, uas yog sib npaug hauv omega-3 fatty acids los ntawm cov nqaij rog thiab ntses, tau txais ob peb AA los ntawm cov khoom siv tsiaj tsawg, thiab tsis zoo hauv LA, tshwm sim hnub no raws li kev pom zoo rau cov qauv kev noj haus raws li nws txhawj txog kev tiv thaiv cov xeev inflammatory. Qhov tseeb, qhov kev xav ua haujlwm yuav tsum tau kuaj pom tias qhov txo qis ntawm LA cov nyiaj hauv kev noj zaub mov, suav nrog kev noj AA sib npaug los ntawm cov peev txheej ntuj, tuaj yeem yog ib txoj hauv kev ntxiv los txo cov peev txheej ntawm kev noj zaub mov, thiab ua ke kom nce cov khoom noj. n-3 fatty acids.
10. Cov lus xausAA thiab nws cov metabolites ua si ntau lub luag haujlwm, cuam tshuam cov qauv thiab kev ua haujlwm ntawm cov hlwb xws li platelets, lymphocytes, thiab podocytes (Daim duab 3), thiab yog li koom nrog cov txheej txheem xws li coagulation, o, thiab fibrosis, nrog rau kev tswj xyuas kev ncaj ncees. ntawm glomerular hauv qab daim nyias nyias. Txawm li cas los xij, kev tshawb fawb txog lub luag haujlwm ntawm AA hauvmob raum, suav nrog INS, tsis tshua muaj. Pharmacological thiab kev noj zaub mov muaj peev xwm hloov kho AA thiab nws cov metabolites tab tom kawm, tab sis tsis muaj kev sim tshuaj ntsuam xyuas txog lub luag haujlwm ntawm kev noj zaub mov nplua nuj hauv PUFAs hauv cov neeg mob INS tau tshaj tawm txog tam sim no. Ntxiv mus, kev noj zaub mov kom raug ntawm AA thiab LA tuaj yeem sawv cev rau kev tiv thaiv kev tiv thaiv ntxiv uas yuav tsum tau sim hauv cov ntsiab lus tswj. Raws li, kev tshawb fawb ntawm AA thiab nws cov metabolites zoo li yog ib qho tseem ceeb ntawm kev tshawb nrhiav, tshwj xeeb tshaj yog nyob rau hauv idiopathic nephrotic syndrome, nrog rau cov txiaj ntsig cuam tshuam ntawm cov qib roj ntsha, kev noj haus, thiab cov tshuaj pharmacological, nrog rau qhov kawg kev xav ntawm kev tau txais kev hloov pauv zoo ntawm AA endogenous metabolism, thaum kawg. counteracting ib co pathogenetic mechanisms ntawmraum puas.
