Oleoylethanolamide hmoov

Oleoylethanolamide (OEA) yog dab tsi?

Oleoylethanolamide hmoovmuab los ntawm oleoylethanolamide, tseem hu ua OEA, uas yog lub ntuj fatty acid amide uas feem ntau modulates noj thiab lub zog homeostasis los ntawm kev khi rau peroxisome proliferator-activated receptor-alpha (PPAR-), anorexic lipid mediator tswj los ntawm pub. Raws li kev tshawb fawb ua ntej, OEA tswj kev noj zaub mov thiab lub cev hnyav los ntawm kev ua kom lub PPAR- . Thaum cov receptor no qhib rau hauv cov hnyuv ntawm nas, cov tsiaj noj tsawg dua. Txawm hais tias nws qhov kev txiav txim siab ntawm kev noj qab haus huv zoo li yog nyob ntawm qhov ua kom muaj qhov cuam tshuam ntawm vagal sensory afferent neurones, cov txheej txheem koom nrog hauv cov hlwb zoo siab no tseem tsis meej. Tab sis nrog rau txoj kev tshawb no, muaj ob lub zog uas tau nyiam cov neeg tshawb fawb ntau: cov tshuaj tiv thaiv kab mob thiab tshuaj tiv thaiv kab mob.

Yog li, cov kws tshawb fawb feem ntau tau tshawb xyuas seb OEA puas muaj cov tshuaj tiv thaiv kab mob no hauv ob hom tsiaj ntawm visceral thiab inflammatory mob. Thiab tam sim no ob lub zog no kuj dhau los ua lub luag haujlwm tseem ceeb thiab kev siv ntawm OEA hauv kev ua lag luam. Raws li OEA tus neeg muag khoom, Xi'an Sonwu tuaj yeem muab cov hmoov zoo nrog tus nqi sib tw. Yog tias koj txaus siab rau OEA, txais tos hu rau Xi'an Sonwu.

Specification

Lub luag haujlwm ntawm OEA yog dab tsi & Nws Ua Haujlwm li cas hauv lub cev?

Oleoylethanolamide hmoovmuaj anti-inflammatory thiab analgesic zog. OEA belongs rau FAE, lub npe tag nrho yog fatty-acid ethanolamides (FAEs), uas yog ib tsev neeg ntawm lipids tshwm sim uas muaj nyob rau hauv cov nroj tsuag thiab tsiaj cov ntaub so ntswg. Tsiaj hlwb synthesizes thiab tso tawm FAEs nyob rau hauv ib tug stimulus-dependent yam, nyob rau hauv teb rau ntau yam physiological thiab pathological stimuli, tawm tswv yim hais tias cov tebchaw yuav koom nyob rau hauv kev sib txuas lus ntawm cell-to-cell. OEA yog ib qho tsis ntev los no tau piav qhia tias yog cov tshuaj uas tuaj yeem tswj kev noj zaub mov thiab lipid metabolism. Nws yog lub ntuj ligand ntawm peroxisome proliferator-activated receptor-alpha (PPAR-). Ntau cov ntawv ceeb toom hais tias OEA yog lub ntuj tswj hwm kev noj qab haus huv, qhov hnyav thiab cov roj cholesterol thiab tuaj yeem pab txhawb kev poob phaus. Txawm li cas los xij, nws qhov kev txiav txim siab ntawm kev noj qab haus huv zoo li yog nyob ntawm kev ua kom lub vagal hnov ​​​​qab afferent neurones, cov txheej txheem koom nrog hauv cov hlwb zoo siab no tseem tsis meej.

Tab sis txij li FAEs xws li anandamide thiab palmitoylethanolamide ua rau muaj zog analgesic thiab anti-inflammatory teebmeem, xav tias OEA tsis muaj kev zam. Yog li, cov kws tshawb fawb feem ntau tau kawm seb OEA tseem muaj cov tshuaj tiv thaiv kab mob hauv ob hom tsiaj ntawm visceral thiab inflammatory mob.

1. Cov nyhuv tiv thaiv kab mob

Kev mob tshwm sim zoo sib xws rau kev txhim kho cov kab mob vascular, xws li restenosis, kub siab, thiab atherosclerosis. Lipopolysaccharide (LPS) yog qhov tseem ceeb ntawm cov phab ntsa sab nrauv ntawm cov kab mob gram-tsis zoo thiab ua lub luag haujlwm tseem ceeb hauv kev kho mob.

Txoj kev tshawb no tsom los tshuaj xyuas cov tshuaj tiv thaiv kab mob ntawm oleoylethanolamide (OEA) hauv lipopolysaccharide (LPS)-induced THP-1 hlwb. Cov hlwb raug txhawb nrog LPS (1 ug / ml) nyob rau hauv lub xub ntiag lossis tsis muaj OEA (10, 20 thiab 40 μM). Cov pro-inflammatory cytokines tau soj ntsuam los ntawm qRT-PCR thiab ELISA. Lub THP-1 cov hlwb tau hloov pauv mus rau PPAR me me-interfering RNA, thiab TLR4 kev ua haujlwm tau txiav txim siab nrog kev ntsuas thaiv kev siv tshuaj tiv thaiv TLR4 antibody. Tsis tas li ntawd, ib qho tshwj xeeb inhibitor tau siv los txheeb xyuas txoj hauv kev hauv lub cev. OEA tau ua kom muaj zog tiv thaiv kab mob los ntawm kev txo qis kev tsim cov cytokines pro-inflammatory cytokines thiab TLR4 qhia, thiab los ntawm kev txhim kho PPAR qhia. Cov teebmeem modulatory ntawm OEA ntawm LPS-induced o yog nyob ntawm PPAR thiab TLR4. Qhov tseem ceeb, OEA inhibited LPS-induced NF-κB ua kom, IκB degradation, qhia ntawm AP{21}}, thiab phosphorylation ntawm ERK1/2 thiab STAT3. Hauv cov ntsiab lus, cov txiaj ntsig tau pom tias OEA tawm dag zog los tiv thaiv kev mob tshwm sim los ntawm kev txhim kho PPAR signaling, inhibiting TLR4-koom haum NF-κB signaling txoj hauv kev, thiab cuam tshuam nrog ERK1/2-nyob ntawm cov teeb liab cascade (TLR4/ ERK1/2/AP-1/STAT3), uas qhia tias OEA tej zaum yuav yog tus kws kho mob rau cov kab mob inflammatory.

2. Cov nyhuv analgesic

Cov kev tshawb fawb cuam tshuam tau qhia tias OEA tuaj yeem ua rau lwm lub luag haujlwm ntawm lub cev, suav nrog kev nkag siab qhov mob. Lawv tau soj ntsuam cov txiaj ntsig ntawm OEA nyob rau hauv ob hom nociceptive teb evoked los ntawm visceral thiab inflammatory mob nyob rau hauv nas. Cov txiaj ntsig tau qhia tias OEA muaj cov tshuaj tua kab mob txo qis cov lus teb nociceptive tsim los ntawm kev tswj hwm ntawm acetic acid thiab formalin hauv ob qho kev sim tsiaj txhu. Kev tshawb fawb ntxiv tau ua los tshawb xyuas cov txheej txheem hauv qab no cov nyhuv analgesic. Txog qhov kawg no, cov kev tshawb fawb tau soj ntsuam cov kev ua ntawm OEA hauv cov nas null rau PPAR- receptor gene thiab piv nws cov kev ua nrog cov PPAR- receptor tsiaj qus. Lawv kuj tau sib piv cov txiaj ntsig ntawm MK-801 txhawm rau ntsuas lub luag haujlwm ntawm NMDA receptor hauv qhov tshuaj tiv thaiv kab mob no. Cov ntaub ntawv tau qhia tias OEA txo cov visceral thiab inflammatory teb los ntawm PPAR- - ua kom muaj kev ywj pheej mechanism. Kev sib koom ua ke ntawm cov koob tshuaj subanalgesic ntawm MK-801 thiab OEA tau tsim cov nyhuv analgesic, qhia txog kev koom tes ntawm kev sib kis ntawm glutamatergic hauv cov nyhuv antinociceptive ntawm OEA. Txoj kev tshawb no sawv cev rau txoj hauv kev tshiab rau kev tshuaj xyuas qhov ua tau zoo ntawm OEA hauv cov lus teb nociceptive thiab muab lub hauv paus rau kev nkag siab txog nws cov haujlwm lom neeg thiab cov hom phiaj endogenous hauv visceral thiab inflammatory mob. Yog li nws tau pom tias OEA muaj cov tshuaj tua kab mob.

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Cov ntawv pov thawj

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Vim Li Cas Xaiv Peb

1. Xi'an Sonwu tau koom nrog ntshuam-export rau ntau tshaj 10 xyoo nrog kev nplua nuj nyob rau hauv txoj kev loj hlob, kev tshawb fawb thiab zus tau tej cov API, cog extract, khoom noj khoom haus additives, thiab lwm yam raw cov khoom xyaw ntawm cov khoom kho mob;

2. Xi'an Sonwu muaj cov kws tshaj lij nrog kev faib ua haujlwm kom meej;

3. Cov khoom raug kuaj los ntawm cov neeg thib peb;

4. Qauv muaj;

5. Kev pabcuam OEM tau txais kev txhawb nqa.

Yog koj xav pauboleoylethanolamide hmoovnqe, thov hu rau Xi'an Sonwu.

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