Los ntawm Lub Tsev Haujlwm Saib Xyuas Kev Noj Qab Haus Huv mus rau Lub Tsev Kho Mob, Lub Pathological Mechanism ntawm IgAN tau siv los ua kev tawg

Immunoglobulin A nephropathy (IgAN) yog ib hom kab mob glomerular. Txawm hais tias feem ntau lees txais cov txheej txheem pathological tam sim no yog ntau txoj kev xav lossis 4-ntau txoj kev xav, muaj qee qhov xwm txheej kho mob uas tsis tuaj yeem piav qhia, xws li kev ua kom tsis zoo ntawm kev sib ntxiv, ua ke nrog cov kab mob autoinflammatory, thiab caj ces. kev cuam tshuam, thiab lwm yam Tsis tas li ntawd, tam sim no muaj ob peb cov tshuaj rau kev kho mob ntawm IgAN, uas tej zaum yuav cuam tshuam nrog qhov tseeb tias peb tsis nkag siab tag nrho cov txheej txheem pathological ntawm qhov tshwm sim thiab kev loj hlob ntawm IgAN.

Nyem rau ntawm Cistanche rau mob raum

Los ntawm lub Plaub Hlis 13 txog 16, 2024, 2024 World Congress on Nephrology (WCN) tau qhib hauv Argentina, lub tebchaws nyob deb tshaj ntawm peb lub tebchaws. Hauv lub rooj sib tham no, tag nrho ntau dua 1,000 cov lus piav qhia tau nthuav tawm, ntawm 5 Qhov kev paub daws teeb meem no qhia meej txog kev nce qib tshiab hauv cov txheej txheem pathological ntawm qhov tshwm sim thiab kev loj hlob ntawm IgAN. Ntawm 5 qhov kev paub daws teeb meem no, 4 yog qhov chaw kho mob lossis kev tshawb fawb soj ntsuam, thiab 1 yog kev tshawb fawb tsiaj / kuaj qauv. Lawv tau tshaj tawm tias qee qhov biomarkers thiab lub raum biopsy tej yam kev mob yuav cuam tshuam rau qhov tshwm sim thiab kev loj hlob ntawm IgAN, thiab kuj tau npaj qee lub hom phiaj kho mob tshiab.

Cov ntaub ntawv tseem ceeb

① Cov ntaub ntawv ceeb toom qhia tias tej zaum yuav muaj kev sib raug zoo ntawm IgAN, lub raum cortical necrosis, thiab kab mob autoinflammatory (SAID).

② Lub xub ntiag ntawm podocyte pathology / kev raug mob hauv cov neeg mob IgAN muaj feem cuam tshuam rau qhov mob hnyav.

③ Lub raum mob raum mob hnyav thiab circulating GDF-15 qib tuaj yeem cuam tshuam rau kev mob plawv ntawm IgAN cov neeg mob.

④ JAK/STAT signaling yog qhib rau hauv cov neeg mob IgAN thiab yog lub hom phiaj kho mob rau IgAN.

⑤ T cell infiltration tej zaum yuav yog lub luag haujlwm tseem ceeb rau IgA tso rau hauv lub raum.

Case Report: Kev sib tsoo los yog Kev Ua Phem, IgAN thiab SAID1

Cov ntaub ntawv keeb kwm yav dhau: Cov kab mob autoinflammatory (SAID) yog ib yam kab mob caj ces tshwm sim los ntawm ntau yam kab mob thoob plaws hauv lub cev, tab sis kev cuam tshuam rau lub raum tsis tshua muaj qhia.

Cov ntaub ntawv qhia: Tus neeg mob, txiv neej, 38 xyoo, kub taub hau ib hlis ib zaug rau 3 mus rau 7 hnub, nrog rau qaug zog, maculopapular pob, aphthous ulcer / stomatitis, cervical lymphadenopathy, splenomegaly, episodic raws plab, thiab mob plab. , mob pob qij txha. Hauv 2011, nws tau mus rau hauv tsev kho mob vim tias tag nrho hematuria nrog rau cov proteinuria me me thaum ua npaws. Hauv kev tshuaj xyuas biochemical, ntshav creatinine yog 0.6 mg / dl, hemoglobin++ muaj nyob hauv cov zis, thiab cov zis protein / creatinine piv (UPCR) yog 0.5 g / g. Qib IgA yog 397 mg / dl (ib txwm siv tus nqi<350). Renal biopsy (RBx) showed IgAN without inflammatory activity and no histological chronicity, so a low-sodium diet and ramipril treatment were given. As systemic symptoms persisted, the patient was treated with prednisone, azathioprine, and tocilizumab. During the follow-up period, the patient developed persistent hematuria, 3 times of RBx monitoring confirmed IgAN, and the level of chronic inflammation increased significantly. During this period, methylprednisolone (MP), cyclophosphamide, rituximab, and mycophenolate mofetil were given. In 2018, he started taking canakinumab 150 mg once a month, and his systemic symptoms completely disappeared.

Xyoo 2022, tus neeg mob tau mus pw hauv tsev kho mob vim muaj cov leeg nqaij paravertebral abscess. Theem III mob raum raug mob (AKI) yuav tsum tau kho lub raum luv luv hloov kho tau tshwm sim ib txhij, tab sis tsis muaj sepsis lossis hypotension. Immunological, serological, thiab prothrombotic nta yog qhov qub. Phase III plab CT pom ob sab diffuse raum cortical hypoperfusion (Daim duab 1-A). Peb tau ua ib qho thib tsib RBx, uas pom tias muaj kev cuam tshuam nrog ischemic necrosis thiab hemorrhage interstitial, IgA-GN nrog fibrocytic crescents, nrog fibrosis, thiab mob nruab nrab mob interstitial o. MP tau muab kho dua, thiab tus neeg mob lub raum ua haujlwm tau pib zoo.

Hauv xyoo 2023, kev tshawb nrhiav caj ces tau txheeb xyuas ob qhov kev hloov pauv caj ces (p.Val377IIe thiab p.Pro11Leu) cuam tshuam nrog mevalonate kinase deficiency (MKD). Vim qhov rov tshwm sim ntawm cov tsos mob tshwm sim, nws tau rov pib dua ntawm canakinumab nrog cov lus teb zoo. Tus neeg mob tam sim no asymptomatic, nrog creatinine ntawm 1.46 mg / dl thiab tsis tu ncua microscopic hematuria thiab proteinuria ntawm kwv yees li 1 g / d.

Cov Kev Sib Tham thiab Cov Ntsiab Lus: Hauv tus neeg mob no, ob yam kab mob sib koom ua ke, uas yog cov kab mob rov ua dua tshiab thiab cov kab mob inflammatory uas ua rau muaj qhov nce ntxiv thiab qhov tsis zoo hauv IgA (uas tuaj yeem piav qhia txog kev sib raug zoo ntawm MDR thiab IgAN), thiab cim kev puas tsuaj histological Progression (tsis teb. rau txawv immunosuppressive regimens).

Ntawm qhov tod tes, SAID cov neeg mob muaj feem xyuam rau cov xwm txheej thrombotic. Qhov tshwm sim Schwartzman tuaj yeem ua lub luag haujlwm hauv kev txhim kho lub raum cortical necrosis (RCN) hauv cov ntsiab lus ntawm kev mob tsis tu ncua thiab kis kab mob. Hauv MKD, tsis muaj ntawv ceeb toom ntawm glomerular kev koom tes hauv canakinumab-kho RCN. Cov txheej txheem pathogenic tau piav qhia tso cai rau peb los xav tias MKD yog qhov thib ob etiology hauv kev loj hlob ntawm lub raum tshwm sim.

Cytopathy cuam tshuam nrog kev mob hnyav 2

Kev tshawb fawb keeb kwm yav dhau los: Txij li xyoo 2017, tib neeg tau pib kawm txog qhov txiaj ntsig ntawm kev puas tsuaj podocyte hauv IgAN. Qhov tshwm sim ntawm podocyte hypertrophy thiab cov kab mob taub hau yog ib qho cim ntawm kev puas tsuaj ntawm podocyte. Nws tau raug pom tias cov kev tshwm sim histological zoo li yuav muaj lub raum zoo dua nrog kev siv tshuaj tiv thaiv kab mob, tab sis cov neeg mob uas tsis tau txais kev tiv thaiv kab mob muaj qhov tsis zoo. Tsis muaj ib pawg neeg soj ntsuam kev kho mob ntawm cov kab mob no hauv Latin America.

Kev Tshawb Fawb Txog Kev Tshawb Fawb: Case thiab Tswj Kev Tshawb Fawb

Cov txiaj ntsig tshawb fawb: Tag nrho ntawm 37 IgAN cov neeg mob tau suav nrog qhov nruab nrab ntawm kev soj ntsuam ntawm (41 ± 32) lub hlis. Ntawm lawv, 27% pom cov kab mob podocyte (IgAN-p) thiab 72.9% pom IgAN tsis muaj histological manifestations ntawm podocyte lesions (IgAN-np). ). Clinically, proteinuria hauv cov neeg mob IgAN-P tau siab dua li ntawm pawg IgAN-np, tshwj xeeb yog 3.9 ± 3.0g / g vs 1.6 ± 1.5g / g, tsis muaj qhov tseem ceeb (p{{19}) }.54). Lub raum ua haujlwm ntawm IgAN-p pawg tau qis dua me ntsis, nrog qhov nruab nrab eGFR ntawm 65.9 ± 45ml / min / 1.73㎡ vs 80.2 ± 36.4 ml / min / 1.73㎡ (p=0.23). Cov pab pawg IgAN-p muaj ntau dua granular cam khwb cia nephropathy. (92% vs 80% p=0.02), qhia tau hais tias nws tuaj yeem raug mob los ntawm tubular raug mob. Histologically, 80% ntawm cov neeg mob IgAN-p qhia podocyte hypertrophy thiab 2% qhia txog hom focal segmental glomerulosclerosis (FSGS). MST-C cov qhab nia tsis txawv ntawm ob pawg, tshwj tsis yog tias mesangial hyperplasia tshwm sim hauv 96.3% ntawm cov neeg mob podocytosis piv nrog 70% ntawm cov neeg mob uas tsis muaj podocytosis (p=0.02). Qhov kev kwv yees raws li cov qhab nia thoob ntiaj teb SCORE tsis yog qhov tseem ceeb ntawm cov pab pawg (p=0.59). Cov neeg mob uas muaj cov kab mob podocytosis nyiam tau txais kev tiv thaiv kab mob ua ntej biopsy (50% vs 37%, p=0.01), thiab thaum kuaj histological tau txais, kev txiav txim siab txuas ntxiv tiv thaiv kab mob ntau dua ntawm cov neeg mob uas muaj tus kab mob podocytosis (90% vs 63%, p=0.11). Thaum kawg, cov txiaj ntsig ntev tau pom tias tsis muaj qhov sib txawv ntawm qhov xav tau kev kho lub raum hloov. Tsis muaj qhov sib txawv ntawm ob pawg hauv cov ntsiab lus ntawm ESKD, 40% txo qis hauv eGFR, thiab xav tau kev kho lub raum hloov.

Kev tshawb fawb xaus: Hauv cov ntawv tshaj tawm dhau los, 16% ntawm cov neeg mob IgAN muaj cov kab mob podocyte hypertrophy thiab cov kab mob taub hau. Hauv txoj kev tshawb no, qhov tshwm sim no tshwm sim ntau dua (27%). Piv nrog rau cov neeg mob IgAN-np, peb tau pom tias cov neeg mob IgAN-p muaj proteinuria ntau dua thiab lub raum tsis ua haujlwm, yog li xav tau kev kho mob ntau dua, tab sis cuam tshuam rau lub raum cov txiaj ntsig zoo ib yam li cov neeg mob uas tsis muaj podocytosis. ib yam. Cov txiaj ntsig tau zoo ib yam li cov uas tau pom hauv pawg pab pawg yav dhau los.

Nruab nrab-rau-mob raum arteriosclerosis thiab circulating GDF-15 ntau ntau yuav cuam tshuam rau cardiorenal prognosis nyob rau hauv cov neeg mob nrog IgAN3

Kev tshawb fawb keeb kwm yav dhau: Kev pheej hmoo ntawm cov hlab plawv ntawm IgAN cov neeg mob tau maj mam tau txais kev saib xyuas. KDIGO cov txheej txheem qhia meej meej txog qhov tseem ceeb ntawm kev ntsuas kev pheej hmoo ntawm lub plawv thiab siv cov kev cuam tshuam tsim nyog thaum tsim nyog hauv kev tswj cov neeg mob nrog IgAN. Txoj kev tshawb no tsom los tshawb txog cov xwm txheej muaj feem cuam tshuam rau kev kuaj mob cardiorenal hauv cov neeg mob nrog IgAN.

Kev Tsim Kho Kev Tshawb Fawb: Qhov kev tshawb fawb no yog kev tshawb nrhiav rov qab. Tag nrho ntawm 353 tus neeg mob IgAN uas tau soj ntsuam tas li tsawg kawg 1 xyoos hauv Tsev Kho Mob Beijing Anzhen tau raug xaiv. Raws li seb qhov kev tshwm sim cardiorenal composite endpoint tshwm sim, cov neeg mob tau muab faib ua pawg A (n=85, yog) thiab pawg B (n=268, tsis). Cov yam ntxwv clincopathological ntawm ob pawg neeg mob tau muab piv thiab tshuaj xyuas. Cov qauv ib leeg thiab ntau tus qauv Cox tau siv los txheeb xyuas cov kev pheej hmoo cuam tshuam rau kev mob plawv thiab lub raum rau cov neeg mob IgAN. Cov ntshav qab zib GDF-15 qib ntawm IgAN cov neeg mob kuj tau kuaj pom.

Cov txiaj ntsig kev tshawb fawb: 14.7% (52/353) ntawm cov neeg mob IgAN muaj kab mob plawv thaum lub raum biopsy. 55.8% (197/353) ntawm cov neeg mob muaj ntshav siab. Kev soj ntsuam kuaj pom pom tias ntshav siab (HR=1.810; 95% CI, 1.073 ~ 3.053; P=0.026), 24h tso zis protein ntau ( 24hUTP) (HR=1.081; 95% CI, 1.006 ~ 1.162; P=0.033), eGFR (HR=0.980; 95% CI, 0.973 ~ 0.987; P<0.001), presence of intracapillary proliferation (E1) (HR=1.697; 95% CI, 1.079~2.669; P=0.022), tubular atrophy/interstitium Fibrosis (T2) (HR=3.757; 95% CI, 1.959~7.203; P<0.001) and moderate to severe intrarenal arteriosclerosis (HR=3.320; 95% CI, 1.289~8.548; P=0.013) are the most important factors affecting the heart disease of IgAN. independent risk factor for renal prognosis. In IgAN patients with moderate to severe intrarenal arteriosclerosis, 24h urine protein quantification (24hUTP) (HR=1.131; 95% CI, 1.014 ~ 1.261; P=0.028), eGFR (HR=0.982; 95% CI, 0.971 ~ 0.993; P=0.001) and E1 (HR=2.583; 95% CI, 1.379 ~ 4.841; P=0.003) are independent risk factors affecting the cardiorenal prognosis of IgAN patients. Serum GDF-15 levels were positively correlated with 24hUTP (r=0.405, P<0.001) and negatively correlated with eGFR (r= -0.606, P<0.001). The serum GDF-15 level in the group with poor cardio-renal composite outcome was significantly higher than that in the group with benign cardio-renal composite outcome [1591.69 (1001.65~2546.36) pg/ml vs 775.85 (546.82~1310.29) pg/ml, P<0.001].

Kev tshawb fawb xaus: IgAN cov neeg mob muaj qhov tshwm sim ntau dua ntawm cov kab mob plawv. Ntxiv nrog rau cov xwm txheej muaj feem cuam tshuam nrog IgAN xws li kub siab, thawj zaug proteinuria, eGFR, E1 thiab T2 qhov txhab, qhov nruab nrab mus rau qhov mob hnyav rau hauv cov hlab ntsha tseem cuam tshuam rau cov kab mob cardiorenal ntawm cov neeg mob IgAN. Ntawm cov neeg mob IgAN uas muaj nruab nrab mus rau qhov mob hnyav intrarenal arteriosclerosis, Oxford-E lesions yog ib qho kev pheej hmoo ntawm kev ywj pheej cuam tshuam rau cov neeg mob cardiorenal prognosis ntawm IgAN cov neeg mob. Txoj kev tshawb no qhia tias kev puas tsuaj rau cov hlwb endothelial tuaj yeem yog qhov sib txuas ntawm cov kab mob plawv thiab lub raum. Circulating GDF-15 theem tej zaum yuav muaj feem xyuam rau cardiorenal prognosis ntawm IgAN.

JAK/STAT signaling pathway, lub peev xwm kho lub hom phiaj rau IgAN4

Kev tshawb fawb keeb kwm yav dhau los: Janus kinase (JAK)-cim transducer thiab activator ntawm transcription (STAT) txoj kev yog ib txoj hauv kev ntawm cov teeb liab intracellular transduction txoj kev uas tau nthuav dav thiab koom nrog ntau yam txheej txheem lom neeg, suav nrog kev loj hlob ntawm tes, sib txawv, apoptosis, thiab kev tiv thaiv kab mob. Kev kho qhov system. Kev tshawb fawb nyob rau hauv xyoo tas los no tau tshawb nrhiav lub luag haujlwm ntawm kev ua kom txawv txav ntawm receptor tyrosine kinases nyob rau hauv lub pathogenesis ntawm IgAN.

Kev tsim qauv: Qhov no yog ib qho kev soj ntsuam rov qab uas suav nrog cov ntaub ntawv kho mob ntawm 63 IgAN cov neeg mob kuaj tau txij lub Ib Hlis 2002 txog Lub Kaum Ob Hlis 2016. Cov ntaub ntawv kho mob thiab chaw kuaj mob tau sau rau ntawm qhov pib thiab thaum kawg ntawm kev soj ntsuam. Lub raum cov ntaub so ntswg tau stained nrog cov tshuaj tiv thaiv tshwj xeeb rau JAK-STAT txoj hauv kev. Cov ntaub so ntswg marginal ntawm lwm 6 kis ntawm lub raum qog tau siv los tswj.

Cov txiaj ntsig ntawm kev tshawb fawb: Cov pej xeem kawm tau ua raws li qhov nruab nrab ntawm 102 lub hlis. Ntau tshaj li ib nrab ntawm cov neeg mob tau txais kev tso cai, thiab 31.1% tau ua tiav cov txiaj ntsig tseem ceeb, txhais tau tias yog kab mob raum kawg (ESRD) lossis ob npaug ntawm cov hauv paus creatinine. JAK3 feem ntau yog qhia nyob rau hauv lub raum tubules thiab glomeruli. Piv nrog rau kev tswj hwm, IgAN cov neeg mob tau txhim kho JAK3 staining.

Cov ntsiab lus tshawb fawb: JAK / STAT txoj kev taw qhia yog qhib rau hauv cov neeg mob IgAN thiab tej zaum yuav yog lub hom phiaj kho rau IgAN.

Muaj ntau qhov CD4+ T cell infiltration hauv ob lub raum ntawm IgAN nas5

Kev tshawb fawb keeb kwm yav dhau los: Cov qauv pathological tam sim no tsis paub meej tias vim li cas IgA cov tshuaj tiv thaiv kab mob (Abs) raug xaiv tso rau hauv thaj chaw glomerular mesangial. Tsis ntev los no, tus qauv tsiaj pom tias IgA autoantibodies tawm tsam mesangial antigen IIspectrin yuav cuam tshuam nrog cov txheej txheem saum toj no. Peb kuj pom tau hais tias muaj coob tus IgA + plasmablasts (PBs) nyob rau hauv lub raum ntawm spontaneous IgAN qauv nas (gddY) nas, thiab cov IgA autoantibodies tsim los ntawm cov PBs khi rau II-membrane contractile proteins thiab mesangial cell nto. ua raws cov cheeb tsam sib txawv ntawm IgA hnyav thiab lub teeb chains ntawm IgA + PBs cais los ntawm gddY nas ob lub raum thiab pom tias feem ntau ntawm lawv muaj ntau tus somatic hloov pauv, qhia tias lawv tau tsim los ntawm cov chaw tua kab mob hauv T-cell-dependent yam. . Txawm li cas los xij, cov txheej txheem ntxaws ntxaws ntawm IgA autoantibody ntau lawm, xws li hom T hlwb twg yog lub luag haujlwm rau inducing autoantibodies, tseem tsis tau meej. Nyob rau hauv txoj kev tshawb no, peb tau soj ntsuam infiltrating CD4+ T hlwb nyob rau hauv lub raum ntawm gddY nas.

Kev tshawb fawb tsim: Txoj kev tshawb no siv tus qauv IgAN tus qauv nas raws li kev tshawb fawb. Tag nrho cov nas gddY pom cov proteinuria thiab glomerular IgA deposition ntawm 8 lub lis piam ntawm lub hnub nyoog thiab tom qab ntawd tsim kom pom tseeb lub raum tsis ua hauj lwm, nrog pathology zoo ib yam li tib neeg IgAN. Leukocytes raug cais tawm ntawm ob lub raum ntawm 8-lub lim tiam gddY lossis BALB/c nas, txhawb nqa nrog monensin, ionolysin, thiab phorbol ester (PMA), stained rau CD4 ntawm qhov chaw, thiab IFN- thiab IL{{5 }} intracellularly. Los yog FoxP3. Flow cytometry tsom xam. Cov qauv raug txheeb xyuas siv FACS Canto II (BD Biosciences).

Cov txiaj ntsig tshawb fawb: Peb pom tias piv nrog cov nas BALB/c, gddY nas muaj ntau cov CD4+ T hlwb hauv ob lub raum. Piv nrog BALB/c, Th1 (CD4+ IFN- +), Th17 (CD4+ IL-17+), regulatory T (Treg, CD4+ Foxp 3+) ​​thiab tus pab follicular T (Tfh, CD4+ CXCR5+ PD-1+) cov hlwb tau nce ntau heev. Ntawm qhov tod tes, tsis muaj qhov sib txawv tseem ceeb ntawm tus lej Th2 (CD4+ IL-4+) cov hlwb hauv lub raum ntawm gddY thiab BALB/c nas.

Kev tshawb fawb xaus: Peb pom tias muaj ntau tus CD4+ T hlwb, suav nrog Th1, Th17, Treg, thiab Tfh, nyob rau hauv ob lub raum ntawm gddY nas, thaum Th2 hlwb tsis sib sau. Tam sim no, qhov ncaj qha kev sib txuas ntawm cov infiltrating CD4+ T hlwb thiab tsim cov IgA-hom autoantibodies yog tsis paub meej. Peb yuav txuas ntxiv qhia lub luag haujlwm ntawm cov hlwb no hauv kev ua rau IgA autoantibodies hauv IgAN. Tom qab nws lub luag haujlwm tau qhia meej, nws yuav yog ib qho ntawm cov peev txheej kho mob rau IgAN.

Cistanche kho mob raum li cas?

Cistancheyog ib hom tshuaj suav tshuaj ntsuab siv rau ntau pua xyoo los kho ntau yam mob, suav nrog kab mob raum. Nws yog muab los ntawm qhuav stems ntawmCistanchedeserticola, ib tsob nroj nyob rau hauv cov suab puam ntawm Tuam Tshoj thiab Mongolia. Lub ntsiab active Cheebtsam ntawm cistanche yogphenylethanoidglycosides, echinacoside cov tshuaj, thiabacteoside, uas tau pom tias muaj txiaj ntsig zoo rau kidneynoj qab haus huv.

Kab mob raum, tseem hu ua kab mob raum, hais txog ib yam mob uas lub raum ua haujlwm tsis zoo. Qhov no tuaj yeem ua rau muaj cov khoom pov tseg thiab cov co toxins hauv lub cev, ua rau muaj ntau yam tsos mob thiab teeb meem. Cistanche tuaj yeem pab kho mob raum ase los ntawm ntau lub tshuab.

Ua ntej, cistanche tau pom tias muaj cov nyhuv diuretic, txhais tau tias nws tuaj yeem ua rau cov zis ntau ntxiv thiab pab tshem tawm cov khoom pov tseg ntawm lub cev. Qhov no tuaj yeem pab txo lub nra ntawm lub raum thiab tiv thaiv kev tsim cov co toxins. Los ntawm kev txhawb nqa diuresis, cistanche kuj tseem tuaj yeem pab txo qis ntshav siab, ib qho teeb meem ntawm cov kab mob raum.

Ntxiv mus, cistanche tau pom tias muaj cov teebmeem antioxidant. Kev ntxhov siab oxidative, tshwm sim los ntawm qhov tsis sib xws ntawm kev tsim cov dawb radicals thiab lub cev tiv thaiv antioxidant, ua lub luag haujlwm tseem ceeb hauv kev mob raum. ies pab neutralize dawb radicals thiab txo Oxidative kev nyuaj siab, yog li tiv thaiv lub raum los ntawm kev puas tsuaj. Cov phenylethanoid glycosides pom hauv cistanche tau tshwj xeeb hauv kev tshem tawm cov dawb radicals thiab inhibiting lipid peroxidation.

Tsis tas li ntawd, cistanche tau pom tias muaj cov nyhuv anti-inflammatory. Kev mob yog lwm yam tseem ceeb hauv kev loj hlob thiab kev loj hlob ntawm cov kab mob raum. Cistanche's anti-inflammatory zog pab txo cov zus tau tej cov pro-inflammatory cytokines thiab inhibit qhov ua kom o yuav tsum tau txoj kev, yog li alleviating o nyob rau hauv lub raum.

Tsis tas li ntawd, cistanche tau pom tias muaj cov teebmeem immunomodulatory. Hauv kab mob raum, lub cev tiv thaiv kab mob tuaj yeem ua rau tsis zoo, ua rau muaj kev mob ntau dhau thiab cov ntaub so ntswg puas. Cistanche pab tswj lub cev tiv thaiv kab mob los ntawm kev hloov kho kev tsim khoom thiab kev ua haujlwm ntawm lub cev tiv thaiv kab mob, xws li T hlwb thiab macrophages. Txoj cai tiv thaiv kab mob no pab txo qhov mob thiab tiv thaiv kev puas tsuaj ntxiv rau lub raum.

Ntxiv mus, cistanche tau pom los txhim kho lub raum kev ua haujlwm los ntawm kev txhawb nqa kev tsim kho ntawm lub raum hlab nrog cov hlwb. Lub raum tubular epithelial hlwb ua lub luag haujlwm tseem ceeb hauv kev pom thiab rov nqus cov khoom pov tseg thiab electrolytes. Hauv kab mob raum, cov hlwb no tuaj yeem raug puas tsuaj, ua rau lub raum ua haujlwm puas. Cistanche lub peev xwm los txhawb kev tsim kho ntawm cov hlwb no pab kho lub raum kom zoo thiab txhim kho lub raum tag nrho.

Ntxiv nrog rau cov kev cuam tshuam ncaj qha rau lub raum, cistanche tau pom tias muaj txiaj ntsig zoo rau lwm yam kabmob thiab lub cev hauv lub cev. Txoj hauv kev zoo rau kev noj qab haus huv no tseem ceeb tshwj xeeb hauv cov kab mob raum, vim tias tus mob feem ntau cuam tshuam rau ntau lub cev thiab lub cev. che tau pom tias muaj kev tiv thaiv rau lub siab, lub plawv, thiab cov hlab ntsha, uas feem ntau cuam tshuam los ntawm kab mob raum. Los ntawm kev txhawb nqa kev noj qab haus huv ntawm cov kabmob no, cistanche pab txhim kho lub raum tag nrho thiab tiv thaiv kev mob ntxiv.

Hauv kev xaus, cistanche yog cov tshuaj suav tshuaj ntsuab siv rau ntau pua xyoo los kho mob raum. Nws cov active Cheebtsam muaj diuretic, antioxidant, anti-inflammatory, immunomodulatory, thiab regenerative teebmeem, uas pab txhim kho lub raum ua haujlwm thiab tiv thaiv ob lub raum los ntawm kev puas tsuaj ntxiv. , cistanche muaj txiaj ntsig zoo rau lwm yam kabmob thiab lub cev, ua rau nws txoj hauv kev zoo rau kev kho mob raum.