Dab tsi bilirubin ua rau koj?

Bilirubin yog ib qho tseem ceeb ntawm cov khoom lag luam bile thiab yog ib qho ntawm cov khoom kawg ntawm Henne Metabolism, feem ntau yog muab los ntawm Bile Bile (SentCes liab cov qe ntshav). Muaj ob hom bilirubin,Ib qho yog pub dawb (unbound lub xeev) thiab lwm lub xeev khi. Muaj qhov tseem ceeb sib txawv hauv cov solubility nruab nrab ntawm lawv. Unbound bilirubin yog cov rog - Soluble, thiab yooj yim solvle hauv cov kuab tshuaj yeeb yaj kiab xws li chloroform thiab methanol. Bilirubin yog dej - soluble thiab soluble hauv dej.

Nws cov qauv tseem ceeb yog linear tetrapyrrrotrole. Lub hom tsis muaj zog yog cov rog - soluble thiab dej - insolule vim yog incetamolecular hydrogen bonds. Nws yog neurotoxic thiab xav tau yooj yim excreted tom qab daim siab hloov mus rau hauv dej {}} soluble khi hom.

Nws cov tsos yog txiv kab ntxwv - daj lossis liab qab {{1} xim av crystalline hmoov uas feem ntau decomposes ncig 192 degree.

1.STRong Antioxidant nyhuv

Methylene choj nyob rau hauv bilirubin molecules yog qhov chaw txo qis, uas tuaj yeem tawm tsam ncaj qha nrog radicals dawb thiab oxidized rau hauv biliverin. Bilivin tuaj yeem raug txo sai raubilirubinLos ntawm cov choleverin reductase nyob rau hauv lub hlwb, sib sau ua rau antioxidant ncig.

Yog li ntawd, bilirubin tuaj yeem zoo neutraling reactive oxygen xws li peroxides, thiab tiv thaiv cell cov ntaub txaij, protein thiab DNA los ntawm oxidative kev puas tsuaj. Qhov no tiv thaiv lipids, thiab lawv liipid solubility tso cai rau lawv kom tau embedded hauv cell weepranes thiab lipoproteins, tiv thaiv lipid peroxidation thiab txo kev pheej hmoo ntawm atherosclerosis.

Hauv neonates, bilirubin ua raws li antioxidant los tawm tsam oxidative kev ntxhov siab tshwm sim los ntawm cov hyperoxygenic ib puag ncig tom qab yug. Txawm li cas los xij, rau cov kev sib dhos daj ntseg, ntaub ntawv xov tooj lossis ntshav pauv yuav tsum zam kom tsis txhob keratinous jaundice (neurotoxicity). Nyob rau lub sijhawm no, nws yog qhov tsim nyog los ua kom muaj qhov muaj txiaj ntsig zoo nws cov txiaj ntsig tau zoo thiab kev pheej hmoo loj.

Hauv cov neeg mob uas muaj hom ntshav qab zib hom 2, bilirubin tuaj yeem ne}}}}}} Nws tuaj yeem txo cov ntshav qab zib.

2.anti - inflammatory teebmeem

BilirubinKev Ua Kom Zoo Inhibition Inhibition ntawm kev kos npe rau kev kos npe yuav pab txo qhov mob.

Txog kev tiv thaiv kab mob siab, tshwj xeeb yog tsis -}}}}}} los ntawm hepatocytes, yog li txo hepatocyte kev puas tsuaj.

Yog tias koj muaj rheumatoid mob caj dab, nws haum rau cov neeg mob uas muaj mob caj dab koj tuaj yeem nqa bilirubin{-} Cov khoom lag luam uas muaj feem cuam tshuam li tus kws kho mob cov lus qhia, muaj kev phom sij.

3.Cardiovascular kev tiv thaiv

Los ntawm inhibing oxidative kev puas tsuaj rau vascular endothelial hlwb, tswj hwm nitric oxide bioavailability thiab txhim kho vasodility.

Nws tuaj yeem txo qis qis qis - cov lipoprotein (LDL) Oxidation thiab ncua AtheClerotic plaqueent quav. Qhov siab me me ntawm cov ntshav dej hiav txwv bilirubin qib tsis dhau ntawm cov kab mob plawv (CVD), yog li nws tuaj yeem txo qhov mob plawv hiav txwv thiab mob atherosclerosis.

Lub ntsab:

Bilirubin Ua lub luag haujlwm tseem ceeb yog "tus saib xyuas" hauv kev ua kom muaj peev xwm muab kev tiv thaiv rau cov hlab ntsha, thiab lwm yam.

1. Cov txiaj ntsig ntawm bilirubin tsuas yog xav txog ib txwm muaj los yog mob siab rau lub cev muaj zog. Txhua qib bilirubin tau nce siab dua li qhov qub yog pathological thiab xav tau kev pabcuam kho mob.

2. BilirubinTsis yog tsuas yog ib qho tseem ceeb antioxidant, tab sis kuj yog ib tug neurotoxic metosolic pov tseg. Nws cov nyhuv yog heev nyob ntawm kev xav thiab lub xaib ntawm muaj.

3. Bilirubinyog kiag li tsis pom zoo kom tau txais nws txoj "txiaj ntsig" los ntawm kev noj mov lossis txhaj rau bilirubin. Exogenous supplementation yog tsis muaj txiaj ntsig thiab yuav muaj kev phom sij. Nws tus nqi lus dag nyob rau hauv kev nkag siab nws lub siab lub luag haujlwm thiab tej zaum yuav siv los ntawm kev tswj hwm endogenous pathways enduction endogenous enduction oo-1.

1. The most serious one is keratinous jaundice, which mostly occurs in the neonatal population. The neonatal serum is not combined with bilirubin >20 mg / dl, thiab ntshav -} lub hlwb lub hlwb tsis txaus. DawbbilirubinDhau los ntawm cov ntshav -}} bioriding thiab yog tso rau hauv basal hlab ntsha Nucleus thiab Hippirecampus, uas tuaj yeem ua rau kev txawj ntse thiab tsis muaj kev puas tsuaj rau kev xav.

2

Thaum kev pub mis ntawm cov menyuam mos, plab hnyuv siab thiab ntuav yuav tshwm sim, thiab hyperbilirubinemia suppresses lub zog.

3. Kev phom sij rau cov pab pawg tshwj xeeb

Cov menyuam yug tshiab (tshwj xeeb yog menyuam ntxov) thiab mob siab thiab lub txim tsis muaj peev xwm

Kiag kiag li zam exogenous bilirubin ntxiv (seb qhov ncauj lossis txhaj), uas ua rau muaj kev tsis tshua muaj txiaj ntsig thiab tswj tsis tau muaj txiaj ntsig. Nruj zog hluav taws xob ntau ntau (0.2-1.2 mg / dl), yog tias nws tshaj nws, nws yog qhov tsis zoo. Nyob rau tib lub sijhawm, nruj me ntsis ua raws li cov lus qhia kho mob.

Nco tseg:

"Cov ntsiab lus no tau muab tso ua ke raws li cov kev tshawb fawb uas twb muaj lawm, thiab cov txiaj ntsig sib txawv ntawm ib tus neeg mus rau lwm tus. Thov sab laj nrog kws kho mob txiav txim siab tom qab ua tiav

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