{"id":6568,"date":"2024-08-06T12:34:37","date_gmt":"2024-08-06T12:34:37","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=6568"},"modified":"2024-08-06T12:34:37","modified_gmt":"2024-08-06T12:34:37","slug":"mtor-signaling-pathway","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/mtor-signaling-pathway\/","title":{"rendered":"A SIRT3\/AMPK\/mTOR jel\u00e1tviteli \u00fatvonalat szab\u00e1lyoz\u00f3 magnolol hat\u00e1sa a Th17\/Treg immunegyens\u00falyra fek\u00e9lyes vastagb\u00e9lgyullad\u00e1sos egerekben"},"content":{"rendered":"

A SIRT3\/AMPK\/mTOR jel\u00e1tviteli \u00fatvonalat szab\u00e1lyoz\u00f3 magnolol hat\u00e1sa a Th17\/Treg immunegyens\u00falyra fek\u00e9lyes vastagb\u00e9lgyullad\u00e1sos egerekben
\nA fek\u00e9lyes vastagb\u00e9lgyullad\u00e1s (UC) kr\u00f3nikus gyullad\u00e1sos b\u00e9lbetegs\u00e9g, amely a b\u00e9l mikrobi\u00f3ta diszbi\u00f3zis\u00e1val j\u00e1r. Jelenleg, b\u00e1r a gy\u00f3gyszeres kezel\u00e9s (bele\u00e9rtve az 5-aminosalicilsavat, a kortikoszteroidokat, az immunszuppressz\u00e1nsokat, a biol\u00f3giai szereket \u00e9s a probiotikumokat) enyh\u00edtheti a t\u00fcneteket, ezeket a kezel\u00e9seket korl\u00e1tozza a magas ki\u00fajul\u00e1si ar\u00e1ny \u00e9s az elker\u00fclhetetlen mell\u00e9khat\u00e1sok (p\u00e9ld\u00e1ul h\u00e1nyinger, h\u00e1ny\u00e1s, csontvel\u0151-szuppresszi\u00f3, fert\u0151z\u00e9s \u00e9s r\u00e1kkock\u00e1zat). Ez\u00e9rt s\u00fcrg\u0151s sz\u00fcks\u00e9g van az UC \u00faj \u00e9s hat\u00e9kony ter\u00e1pi\u00e1inak kifejleszt\u00e9s\u00e9re. A genetikai t\u00e9nyez\u0151k, a b\u00e9lk\u00f6rnyezet, az immunv\u00e1lasz, a sejtek apopt\u00f3zisa \u00e9s a fert\u0151z\u00e9s mind kapcsolatban \u00e1llnak az UC-vel. A jelent\u00e9sek szerint az UC-betegekn\u00e9l k\u00e1rosodott a b\u00e9l mikrobi\u00f3ta, ami a b\u00e9lh\u00e1msejtek g\u00e1tj\u00e1nak fokozott \u00e1tereszt\u0151k\u00e9pess\u00e9g\u00e9hez vezet, \u00e9s b\u00e9lgyullad\u00e1sos v\u00e1laszokat v\u00e1lt ki; az UC progresszi\u00f3ja sor\u00e1n pedig a gyullad\u00e1st okoz\u00f3 T helper 17 sejtek (Th17) \u00e1ltal\u00e1ban megn\u0151nek, m\u00edg a gyullad\u00e1st g\u00e1tl\u00f3 szab\u00e1lyoz\u00f3 T-sejtek (Treg) cs\u00f6kkennek. A Th17\/Treg egyens\u00faly szab\u00e1lyoz\u00e1sa a b\u00e9l mikrobi\u00f3ta modul\u00e1l\u00e1s\u00e1val kezelheti az UC-t. Ez\u00e9rt a Th17\/Treg egyens\u00faly szab\u00e1lyoz\u00e1sa az UC kezel\u00e9s\u00e9nek fontos c\u00e9lpontj\u00e1v\u00e1 v\u00e1lt.<\/p>\n

Az ozmanthus kivonat egy term\u00e9szetes term\u00e9k, amely sz\u00e9les k\u00f6rben megtal\u00e1lhat\u00f3 k\u00fcl\u00f6nb\u00f6z\u0151 n\u00f6v\u00e9nyekben, p\u00e9ld\u00e1ul krizant\u00e9mokban, paprik\u00e1ban \u00e9s perill\u00e1ban. Gyullad\u00e1scs\u00f6kkent\u0151, antioxid\u00e1ns, daganatellenes \u00e9s v\u00edrusellenes hat\u00e1ssal rendelkezik. Egyre t\u00f6bb bizony\u00edt\u00e9k utal arra, hogy a magnolol cs\u00f6kkentheti a gyullad\u00e1skelt\u0151 citokinek, p\u00e9ld\u00e1ul a TNF - \u03b1 \u00e9s az IL-6 szekr\u00e9ci\u00f3j\u00e1t, ez\u00e1ltal g\u00e1tolja a gyullad\u00e1sos v\u00e1laszokat. Alkalmazz\u00e1k a gyullad\u00e1ssal \u00f6sszef\u00fcgg\u0151 betegs\u00e9gek, k\u00f6zt\u00fck az UC kezel\u00e9s\u00e9ben. A jelent\u00e9sek szerint a luteolin szab\u00e1lyoz\u00f3 hat\u00e1ssal van a b\u00e9lmikrobi\u00f3t\u00e1ra, \u00e9s a b\u00e9lmikrobi\u00f3ta \u00f6sszet\u00e9tel\u00e9nek \u00e9s szerkezet\u00e9nek be\u00e1ll\u00edt\u00e1s\u00e1val hat\u00e9konyan befoly\u00e1solhatja az UC kezel\u00e9s\u00e9t. Az azonban m\u00e9g mindig nem vil\u00e1gos, hogy a magnolol k\u00e9pes-e szab\u00e1lyozni a Th17\/Treg egyens\u00falyt az UC-ben.<\/p>\n

A Treg \u00e9s a Th17 k\u00f6z\u00f6tti dinamikus egyens\u00falyt t\u00f6bb jel\u00e1tviteli \u00fatvonal szab\u00e1lyozza, amelyek k\u00f6z\u00fcl az AMP aktiv\u00e1lt protein kin\u00e1z (AMPK)\/mammalian target of rapamycin (mTOR) jel\u00e1tviteli \u00fatvonal az egyik fontos szab\u00e1lyoz\u00f3 \u00fatvonal. Kutat\u00e1sok kimutatt\u00e1k, hogy az AMPK foszforil\u00e1ci\u00f3s szintj\u00e9nek fokoz\u00e1s\u00e1val \u00e9s az mTOR foszforil\u00e1ci\u00f3s szintj\u00e9nek cs\u00f6kkent\u00e9s\u00e9vel szab\u00e1lyozhat\u00f3 a hum\u00e1n Th17\/Treg sejtek differenci\u00e1l\u00f3d\u00e1sa, \u00e9s ez a hat\u00e1s blokkolhat\u00f3 az AMPK jel\u00e1tviteli inhibitor C vegy\u00fclettel; A dextr\u00e1n-szulf\u00e1t-n\u00e1trium (DSS) - induk\u00e1lt UC patk\u00e1ny modellben a fokozott AMPK foszforil\u00e1ci\u00f3 cs\u00f6kkentheti az mTOR expresszi\u00f3t \u00e9s a k\u00fcl\u00f6nb\u00f6z\u0151 gyullad\u00e1sos citokinek szintj\u00e9t, ami a Th17 sejtek differenci\u00e1l\u00f3d\u00e1s\u00e1nak cs\u00f6kken\u00e9s\u00e9hez vezet. A Silent information regulator 3 (SIRT3) egy gyullad\u00e1scs\u00f6kkent\u0151 \u00e9s tumorszupresszor g\u00e9n, amely k\u00f6lcs\u00f6nhat\u00e1sba l\u00e9p a b\u00e9l mikrobi\u00f3t\u00e1val a vastagb\u00e9l tumorigenezis sor\u00e1n. Arr\u00f3l sz\u00e1moltak be, hogy a SIRT3-hi\u00e1nyos egerek rendk\u00edv\u00fcl \u00e9rz\u00e9kenyek a vastagb\u00e9lgyullad\u00e1sra \u00e9s a tumor kialakul\u00e1s\u00e1ra. Tipp: A SIRT3 \u00f6sszef\u00fcgg\u00e9sbe hozhat\u00f3 az UC progresszi\u00f3j\u00e1val. Ek\u00f6zben a SIRT3 az AMPK\/mTOR \u00fatvonal upstream szab\u00e1lyoz\u00f3ja is, \u00e9s t\u00falterjed\u00e9se felszab\u00e1lyozhatja az AMPK foszforil\u00e1ci\u00f3t \u00e9s leszab\u00e1lyozhatja az mTOR foszforil\u00e1ci\u00f3t, g\u00e1tolva a gyullad\u00e1st. Egy nemr\u00e9giben v\u00e9gzett vizsg\u00e1lat kimutatta, hogy a magnolol n\u00f6velheti a SIRT3 expresszi\u00f3j\u00e1t \u00e9s megakad\u00e1lyozhatja az agyi iszk\u00e9mi\u00e1s-reperf\u00fazi\u00f3s k\u00e1rosod\u00e1st a SIRT3\/AMPK\/mTOR jel\u00e1tviteli \u00fatvonal szab\u00e1lyoz\u00e1s\u00e1val. Ez\u00e9rt e tanulm\u00e1ny c\u00e9lja annak felt\u00e1r\u00e1sa, hogy a magnolol UC-re gyakorolt v\u00e9d\u0151 hat\u00e1sa \u00f6sszef\u00fcgg-e a Th17 \/ Treg immunegyens\u00faly\u00e1val, \u00e9s elemezze annak mechanizmus\u00e1t, annak \u00e9rdek\u00e9ben, hogy tiszt\u00e1zza a magnolol UC-re gyakorolt v\u00e9d\u0151 hat\u00e1s\u00e1t, \u00e9s referenci\u00e1t ny\u00fajtson az UC kezel\u00e9s\u00e9hez \u00e9s a magnolol alkalmaz\u00e1s\u00e1hoz.<\/p>\n

\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"Az ut\u00f3bbi \u00e9vekben a hagyom\u00e1nyos k\u00ednai orvosl\u00e1st sz\u00e9les k\u00f6rben alkalmazz\u00e1k az UC kezel\u00e9s\u00e9re. Egyre t\u00f6bb tanulm\u00e1ny utal arra, hogy a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s fontos szerepet j\u00e1tszik a b\u00e9l mikrobi\u00f3ta szab\u00e1lyoz\u00e1s\u00e1ban az UC kezel\u00e9se sor\u00e1n. Az Osmanthus fragrans az egyik legalaposabban vizsg\u00e1lt bioflavonoid. A flavonoidok alacsony toxicit\u00e1s\u00fa term\u00e9szetes vegy\u00fcletek, \u00e9s eddig nem regisztr\u00e1ltak komoly mell\u00e9khat\u00e1sokat, \u00edgy haszn\u00e1latuk rendk\u00edv\u00fcl biztons\u00e1gos. Ebben a tanulm\u00e1nyban a magnolol DSS \u00e1ltal kiv\u00e1ltott UC-re gyakorolt hat\u00e1s\u00e1t vizsg\u00e1lt\u00e1k in vivo. Eredm\u00e9nyeink azt mutatj\u00e1k, hogy a magnolol jelent\u0151s hat\u00e1ssal van az UC-re, ami a s\u00falycs\u00f6kken\u00e9ssel, a DAI pontsz\u00e1mmal, a ny\u00e1lkah\u00e1rtya-nekr\u00f3zis \u00e9s a gyullad\u00e1sos sejtek besziv\u00e1rg\u00e1s\u00e1nak cs\u00f6kken\u00e9s\u00e9vel mutathat\u00f3 ki. Ez \u00f6sszhangban van a kor\u00e1bbi kutat\u00e1sokkal, ism\u00e9t meger\u0151s\u00edtve a magnolol UC-re gyakorolt v\u00e9d\u0151 hat\u00e1s\u00e1t.
\nKor\u00e1bbi tanulm\u00e1nyok kimutatt\u00e1k, hogy a luteolin g\u00e1tolhatja a Th17 v\u00e1laszt a T-sejt-medi\u00e1lt autoimmun betegs\u00e9gekben; \u00e9s gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejthet ki az\u00e1ltal, hogy a CD4+CD25-\u00f6t Treg-sejtekk\u00e9 alak\u00edtja. Arr\u00f3l is besz\u00e1moltak, hogy a luteolin k\u00e9pes g\u00e1tolni a pro-inflammatorikus citokinek, mint a TNF - \u03b1, IL-1 \u03b2, IL-6 \u00e9s IL-17 termel\u00e9s\u00e9t UC modell egerekben; Az Osmanthus sz\u00e1rmaz\u00e9kok in vivo v\u00e9d\u0151hat\u00e1st fejthetnek ki DSS induk\u00e1lt UC modellekben a Th1, Th2 \u00e9s Th17 sejtek szintj\u00e9nek cs\u00f6kkent\u00e9s\u00e9vel. Megvizsg\u00e1ltuk tov\u00e1bb\u00e1 a magnolol hat\u00e1s\u00e1t a Th17\/Treg egyens\u00falyra, amely az UC progresszi\u00f3j\u00e1nak egyik fontos mechanizmusa. Ebben a vizsg\u00e1latban a Treg-sejtek sz\u00e1zal\u00e9kos ar\u00e1ny\u00e1nak szignifik\u00e1ns cs\u00f6kken\u00e9s\u00e9t \u00e9s a Th17-sejtek sz\u00e1zal\u00e9kos ar\u00e1ny\u00e1nak szignifik\u00e1ns n\u00f6veked\u00e9s\u00e9t tal\u00e1ltuk az UC egerek l\u00e9pi limfocit\u00e1iban. A Th17\/Treg ar\u00e1ny az UC egerekben s\u00falyosan kiegyens\u00falyozatlan. A l\u00e9p fontos immunszerv, \u00e9s a DSS immunrendszeri diszfunkci\u00f3t induk\u00e1lhat UC egerekben, ami kompenz\u00e1ci\u00f3s l\u00e9pm\u00e9rgess\u00e9ghez vezet; A luteolin pedig cs\u00f6kkentheti a l\u00e9pindexet \u00e9s enyh\u00edtheti a DSS \u00e1ltal kiv\u00e1ltott vastagb\u00e9lgyullad\u00e1st egerekben. Ez a vizsg\u00e1lat tov\u00e1bb er\u0151s\u00edti a jelent\u0151s Th17\/Treg egyens\u00falyhi\u00e1nyt az UC egerek l\u00e9pi limfocit\u00e1iban, ami \u00f6sszhangban van a hum\u00e1n UC-vel.
\nA Th17 sejtek differenci\u00e1l\u00f3d\u00e1si folyamat\u00e1t a ROR \u03b3 t transzkripci\u00f3s szab\u00e1lyoz\u00e1sa k\u00f6zvet\u00edti. A Th17 sejtek pro-inflammatorikus citokineket termelnek, bele\u00e9rtve az IL-17, IL-21, IL-22, IL-23 \u00e9s IL-25 sejteket, amelyek hozz\u00e1j\u00e1rulnak az UC progresszi\u00f3j\u00e1hoz. A Tregek differenci\u00e1l\u00f3d\u00e1s\u00e1t a Foxp3 szab\u00e1lyozza, \u00e9s az \u00e9rett Tregek magas Foxp3-szintet expressz\u00e1lnak. Ezenk\u00edv\u00fcl a Tregek g\u00e1tl\u00f3 citokineket, k\u00f6zt\u00fck IL-10-et, IL-35-\u00f6t \u00e9s TGF - \u03b2-t szekret\u00e1lnak, amelyek elnyomhatj\u00e1k az adapt\u00e1lt \u00e9s velesz\u00fcletett immunv\u00e1laszokat. Kutat\u00e1sok kimutatt\u00e1k, hogy a megn\u00f6vekedett Th17 sejtek magas IL-17 \u00e9s IL-23 szintet termelnek, ez\u00e1ltal el\u0151seg\u00edtve a gyullad\u00e1st. A Treg sejtek differenci\u00e1l\u00f3d\u00e1sa azonban g\u00e1tolt, ami az immunszuppressz\u00edv citokinek, k\u00f6zt\u00fck az IL-10 cs\u00f6kken\u00e9s\u00e9hez vezet. A Th17\/Treg egyens\u00falyhi\u00e1ny jav\u00edt\u00e1sa seg\u00edthet a b\u00e9lrendszeri immunhomeoszt\u00e1zis helyre\u00e1ll\u00edt\u00e1s\u00e1ban \u00e9s az UC cs\u00f6kkent\u00e9s\u00e9ben. Ez a vizsg\u00e1lat kimutatta, hogy a luteolin csoportban az IL-10 gyullad\u00e1scs\u00f6kkent\u0151 citokin megn\u00f6vekedett, az IL-6, IL-17 \u00e9s IL-23 pro-inflammatorikus citokinek pedig cs\u00f6kkentek; Tipp: A magnolol beavatkoz\u00e1sa jav\u00edtotta a Th17\/Treg egyens\u00falyhi\u00e1nyt a DSS induk\u00e1lt UC modellben, \u00f6sszhangban a kor\u00e1bbi vizsg\u00e1latokkal; Ezen t\u00falmen\u0151en, tov\u00e1bbi elemz\u00e9sek kimutatt\u00e1k, hogy a magnolol jelent\u0151sen lefel\u00e9 szab\u00e1lyozta a ROR \u03b3 t \u00e9s felfel\u00e9 szab\u00e1lyozta a Foxp3-t UC egerekben. A ROR \u03b3 t \u00e9s a Th17 sejtek differenci\u00e1l\u00f3d\u00e1sa k\u00f6z\u00f6tti pozit\u00edv korrel\u00e1ci\u00f3, valamint a Foxp3 \u00e9s a Treg sejtek differenci\u00e1l\u00f3d\u00e1sa k\u00f6z\u00f6tti pozit\u00edv korrel\u00e1ci\u00f3 miatt kutat\u00e1si eredm\u00e9nyeink tov\u00e1bb bizony\u00edtj\u00e1k, hogy a magnolol hozz\u00e1j\u00e1rul a Th17\/Treg sejtek differenci\u00e1l\u00f3d\u00e1s\u00e1nak egyens\u00faly\u00e1hoz.
\nA Th17\/Treg sejtek differenci\u00e1l\u00f3d\u00e1s\u00e1t k\u00e9t f\u0151 t\u00e1panyag\u00e9rz\u00e9kel\u0151 \u00fatvonal, az AMPK \u00e9s az mTOR szab\u00e1lyozza. A SIRT3 egy hat\u00e9kony deacetil\u00e1z, amely bizony\u00edtottan aktiv\u00e1lja az AMPK\/mTOR \u00fatvonalat az autof\u00e1gia el\u0151seg\u00edt\u00e9se \u00e9rdek\u00e9ben, m\u00edg a SIRT3 hi\u00e1nya g\u00e1tolhatja az AMPK\/mTOR \u00fatvonalat. Ebben a vizsg\u00e1latban megfigyelt\u00fck, hogy a SIRT3 feh\u00e9rje szintje \u00e9s a p-AMPK\/AMPK ar\u00e1ny az UC egerek vastagb\u00e9lsz\u00f6vet\u00e9ben szignifik\u00e1nsan alacsonyabb volt, mint a norm\u00e1l egerek\u00e9, m\u00edg a p-mTOR\/mTOR ar\u00e1ny szignifik\u00e1nsan magasabb volt, mint a norm\u00e1l egerek\u00e9, ami a SIRT3 hi\u00e1ny\u00e1ra utal az UC egerekben \u00e9s az AMPK aktiv\u00e1ci\u00f3 g\u00e1tl\u00e1s\u00e1ra. Az Osmanthus fragrans szab\u00e1lyozhatja az AMPK aktivit\u00e1st a csendes\u00edt\u0151 szab\u00e1lyoz\u00f3 feh\u00e9rj\u00e9k expresszi\u00f3j\u00e1nak modul\u00e1l\u00e1s\u00e1val. Liu \u00e9s munkat\u00e1rsai tanulm\u00e1nya kimutatta, hogy a magnolol n\u00f6velheti a SIRT3 transzdukci\u00f3j\u00e1t, aktiv\u00e1lhatja a SIRT3\/AMPK\/mTOR \u00fatvonalat, \u00e9s enyh\u00edtheti az agyi iszk\u00e9mi\u00e1s s\u00e9r\u00fcl\u00e9st. Ez\u00e9rt felt\u00e9telezz\u00fck, hogy a magnolol hat\u00e1sa a Th17\/Treg egyens\u00falyra UC egerekben a SIRT3\/AMPK\/mTOR \u00fatvonalhoz kapcsol\u00f3dhat. A Western blot eredm\u00e9nyek azt mutatt\u00e1k, hogy a magnolol k\u00e9pes n\u00f6velni a SIRT3 feh\u00e9rje szintj\u00e9t az UC egerek vastagb\u00e9lsz\u00f6vet\u00e9ben, fokozza az AMPK foszforil\u00e1ci\u00f3s szintj\u00e9t, \u00e9s lefel\u00e9 szab\u00e1lyozza az mTOR foszforil\u00e1ci\u00f3s szintj\u00e9t, ami meger\u0151s\u00edti hipot\u00e9zis\u00fcnket. A 3-TYP a SIRT3 szelekt\u00edv inhibitora, \u00e9s a jelent\u00e9sek szerint g\u00e1tolja a SIRT3 expresszi\u00f3j\u00e1t. Ebben a vizsg\u00e1latban a magnolol UC egereken kifejtett v\u00e9d\u0151mechanizmus\u00e1nak tov\u00e1bbi tiszt\u00e1z\u00e1sa \u00e9rdek\u00e9ben a magnolol beavatkoz\u00e1s\u00e1t 3-TYP-pel kombin\u00e1ltuk. Az eredm\u00e9nyek azt mutatt\u00e1k, hogy a 3-TYP jelent\u0151sen g\u00e1tolni tudta az AMPK aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s jelent\u0151sen gyeng\u00edtette a magnolol hat\u00e1s\u00e1t a Th17\/Treg sejtek differenci\u00e1l\u00f3d\u00e1si egyens\u00faly\u00e1ra UC egerekben. Tipp: Az osmanthus kivonat el\u0151seg\u00edtheti a Th17\/Treg egyens\u00falyt UC egerekben a SIRT3\/AMPK\/mTOR \u00fatvonal aktiv\u00e1l\u00e1s\u00e1val.
\n\u00d6sszefoglalva, a magnolol jav\u00edthatja a Th17\/Treg egyens\u00falyhi\u00e1nyt a DSS \u00e1ltal induk\u00e1lt UC eg\u00e9rmodellekben, \u00e9s hat\u00e1smechanizmusa a SIRT3\/AMPK\/mTOR \u00fatvonal aktiv\u00e1l\u00e1s\u00e1hoz kapcsol\u00f3dhat. Ez a tanulm\u00e1ny el\u0151zetesen felt\u00e1rta a magnolol v\u00e9d\u0151 mechanizmus\u00e1t UC egereken a Th17\/Treg egyens\u00faly szempontj\u00e1b\u00f3l, jelezve, hogy a magnolol hat\u00e9kony jel\u00f6lt \u00f6sszetev\u0151 lehet a b\u00e9lgyullad\u00e1s kezel\u00e9s\u00e9re, \u00edg\u00e9retes kezel\u00e9si m\u00f3dszert biztos\u00edtva az UC sz\u00e1m\u00e1ra, \u00e9s ir\u00e1nyt adva az UC-t jav\u00edt\u00f3 magnolol mechanizmus\u00e1nak tov\u00e1bbi kutat\u00e1s\u00e1hoz. P\u00e9ld\u00e1ul a SIRT3\/AMPK\/mTOR \u00fatvonal szab\u00e1lyozza az autof\u00e1gi\u00e1t, \u00e9s hogy a magnolol UC-ben bet\u00f6lt\u00f6tt szerepe \u00f6sszef\u00fcgg-e az autof\u00e1gi\u00e1val, azt a j\u00f6v\u0151beni kutat\u00e1sok sor\u00e1n tov\u00e1bb vizsg\u00e1ljuk. Ezenk\u00edv\u00fcl az \u00e1llatk\u00eds\u00e9rletek a preklinikai kutat\u00e1s kulcsfontoss\u00e1g\u00fa l\u00e1ncszemei, \u00e9s a j\u00f6v\u0151beli tanulm\u00e1nyokban a magnolol toxicit\u00e1s\u00e1nak \u00e9s biztons\u00e1goss\u00e1g\u00e1nak m\u00e9lyrehat\u00f3 elemz\u00e9s\u00e9t fogj\u00e1k elv\u00e9gezni, megalapozva ezzel a preklinikai kutat\u00e1s el\u0151mozd\u00edt\u00e1s\u00e1t \u00e9s a gy\u00f3gyszerek klinikai ford\u00edt\u00e1s\u00e1nak el\u00e9r\u00e9s\u00e9t.<\/p>","protected":false},"excerpt":{"rendered":"

The effect of magnolol regulating the SIRT3\/AMPK\/mTOR signaling pathway on the Th17\/Treg immune balance in ulcerative colitis mice Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with dysbiosis of the gut microbiota. At present, although drug therapy (including 5-aminosalicylic acid, corticosteroids, immunosuppressants, biologics, and probiotics) can alleviate symptoms, these treatments are limited by […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[20],"tags":[],"yoast_head":"\nThe effect of magnolol regulating the SIRT3\/AMPK\/mTOR signaling pathway on the Th17\/Treg immune balance in ulcerative colitis mice - China Chemical Manufacturer<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/longchangextracts.com\/hu\/mtor-signaling-pathway\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The effect of magnolol regulating the SIRT3\/AMPK\/mTOR signaling pathway on the Th17\/Treg immune balance in ulcerative colitis mice - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"The effect of magnolol regulating the SIRT3\/AMPK\/mTOR signaling pathway on the Th17\/Treg immune balance in ulcerative colitis mice Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with dysbiosis of the gut microbiota. 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