{"id":6324,"date":"2024-08-06T11:40:48","date_gmt":"2024-08-06T11:40:48","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=6324"},"modified":"2024-08-06T11:40:48","modified_gmt":"2024-08-06T11:40:48","slug":"emodin","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/emodin\/","title":{"rendered":"Az emodin hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a szepszissel \u00f6sszef\u00fcgg\u0151 akut vesek\u00e1rosod\u00e1s kezel\u00e9s\u00e9ben adatb\u00e1ny\u00e1szat \u00e9s k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n"},"content":{"rendered":"<p>Az emodin hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a szepszissel \u00f6sszef\u00fcgg\u0151 akut vesek\u00e1rosod\u00e1s kezel\u00e9s\u00e9ben adatb\u00e1ny\u00e1szat \u00e9s k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n<br \/>\nA szepszis olyan \u00e9letvesz\u00e9lyes szervi m\u0171k\u00f6d\u00e9si zavar, amelyet a gazdaszervezet fert\u0151z\u00e9sre adott v\u00e1lasz\u00e1nak egyens\u00falyzavara okoz. A szepszisben a ves\u00e9k az egyik leggyakrabban \u00e9rintett szerv, \u00e9s a szepszishez t\u00e1rsul\u00f3 akut vesek\u00e1rosod\u00e1s (SA-AKI) gyakran v\u00e1lik a szepszisben szenved\u0151 betegek hal\u00e1l\u00e1nak k\u00f6zvetlen ok\u00e1v\u00e1, magas hal\u00e1loz\u00e1si ar\u00e1nnyal, ami p\u00e9ld\u00e1tlan kih\u00edv\u00e1sok el\u00e9 \u00e1ll\u00edtja a klinikai orvosokat. Az AKI tart\u00f3san fenn\u00e1ll, \u00e9s n\u00f6veli a kr\u00f3nikus vesebetegs\u00e9g (CKD) potenci\u00e1lis kock\u00e1zat\u00e1t. A t\u00fal\u00e9l\u0151 betegek gyakran elker\u00fclhetetlen\u00fcl v\u00e9gst\u00e1dium\u00fa vesebetegs\u00e9gg\u00e9 (ESRD) fejl\u0151dnek, ami komoly vesz\u00e9lyt jelent \u00e9letmin\u0151s\u00e9g\u00fckre \u00e9s biztons\u00e1gukra.<br \/>\nSajnos a SA-AKI megel\u0151z\u00e9s\u00e9re \u00e9s kezel\u00e9s\u00e9re jelenleg nagyon korl\u00e1tozottak a lehet\u0151s\u00e9gek. Az akt\u00edv folyad\u00e9k alap\u00fa ter\u00e1pia nem felt\u00e9tlen\u00fcl rendelkezik megb\u00edzhat\u00f3, bizony\u00edt\u00e9kokon alapul\u00f3 orvosl\u00e1ssal, \u00e9s ak\u00e1r k\u00e1ros is lehet. A v\u00e9rnyom\u00e1s fenntart\u00e1s\u00e1ra szolg\u00e1l\u00f3 vazoakt\u00edv gy\u00f3gyszerek alkalmaz\u00e1sa egyens\u00falyt ig\u00e9nyel a nagy kering\u00e9s \u00e9s a mikrocirkul\u00e1ci\u00f3 k\u00f6z\u00f6tt, \u00e9s nincs konszenzus arr\u00f3l, hogy mekkora c\u00e9l\u00e9rt\u00e9ket kell fenntartani a v\u00e9rnyom\u00e1snak, hogy seg\u00edtsen megel\u0151zni az AKI kialakul\u00e1s\u00e1t. Ha a veseprevenci\u00f3 nem siker\u00fcl, a kezel\u00e9shez vesep\u00f3tl\u00f3 ter\u00e1pi\u00e1t (RRT) kell alkalmazni, de az RRT-beavatkoz\u00e1s optim\u00e1lis id\u0151z\u00edt\u00e9se \u00e9s m\u00f3dja nem egy\u00e9rtelm\u0171. Ha az SA-AKI betegek t\u00fal\u00e9lik, b\u00e1r a legt\u00f6bb beteg vesefunkci\u00f3ja helyre\u00e1ll, a vese helyre\u00e1ll\u00edt\u00e1s\u00e1nak mechanizmusair\u00f3l vagy a vesefunkci\u00f3 helyre\u00e1ll\u00edt\u00e1s\u00e1nak kudarc\u00e1r\u00f3l keveset tudunk, \u00e9s a CKD \u00e9s az ESRD kialakul\u00e1s\u00e1nak \u00e9lethosszig tart\u00f3 kock\u00e1zata magasabb. Eddig nincs hat\u00e1rozott \u00e9s megb\u00edzhat\u00f3 gy\u00f3gyszer az AKI kezel\u00e9s\u00e9re. A hagyom\u00e1nyos klinikai kezel\u00e9si int\u00e9zked\u00e9sek els\u0151sorban a vesep\u00f3tl\u00e1s \u00e9s a t\u00fcneti \u00e1tfog\u00f3 kezel\u00e9s. A vesefunkci\u00f3 helyre\u00e1ll\u00edt\u00e1sa mag\u00e1nak a ves\u00e9nek a szervezet eg\u00e9sz\u00e9nek megb\u00edzhat\u00f3 t\u00e1mogat\u00e1s\u00e1t\u00f3l f\u00fcgg. Ez\u00e9rt az olyan gy\u00f3gyszerek vagy int\u00e9zked\u00e9sek felt\u00e1r\u00e1sa, amelyek hat\u00e9konyan megel\u0151zhetik vagy kezelhetik az SA-AKI-t korai \u00e9s id\u0151ben, elker\u00fclhetik a kr\u00f3nikus vesebetegs\u00e9g kialakul\u00e1s\u00e1t vagy el\u0151seg\u00edthetik a vese helyre\u00e1ll\u00edt\u00e1s\u00e1t, fontos klinikai \u00e9rt\u00e9kkel b\u00edr a szepszisben szenved\u0151 betegek hal\u00e1loz\u00e1si ar\u00e1ny\u00e1nak cs\u00f6kkent\u00e9se \u00e9s a t\u00fal\u00e9l\u0151 betegek \u00e9letmin\u0151s\u00e9g\u00e9nek jav\u00edt\u00e1sa szempontj\u00e1b\u00f3l.<br \/>\nAz emodin egy term\u00e9szetes vegy\u00fclet, amelyet k\u00ednai gy\u00f3gyn\u00f6v\u00e9nyekb\u0151l, p\u00e9ld\u00e1ul rebarbar\u00e1b\u00f3l \u00e9s Polygonum cuspidatumb\u00f3l vonnak ki, \u00e9s amely k\u00fcl\u00f6nb\u00f6z\u0151 farmakol\u00f3giai hat\u00e1sokkal rendelkezik, p\u00e9ld\u00e1ul gyullad\u00e1scs\u00f6kkent\u0151, v\u00edrusellenes \u00e9s daganatellenes. Kor\u00e1bbi tanulm\u00e1nyok meger\u0151s\u00edtett\u00e9k, hogy az emodin v\u00e9d\u0151 hat\u00e1ssal van a szepszisben szenved\u0151 betegekre; A leg\u00fajabb tanulm\u00e1nyok kimutatt\u00e1k, hogy az emodin v\u00e9d\u0151 hat\u00e1ssal rendelkezik az oxidat\u00edv stressz, a gyullad\u00e1s \u00e9s a sejt apopt\u00f3zis okozta k\u00e1rosod\u00e1ssal szemben. Azonban m\u00e9g mindig nem vil\u00e1gos, hogy az emodin jav\u00edthatja-e a SA-AKI betegek progn\u00f3zis\u00e1t. Ez a tanulm\u00e1ny felt\u00e1rja az SA-AKI patogenezis\u00e9ben szerepet j\u00e1tsz\u00f3 kulcsfontoss\u00e1g\u00fa g\u00e9neket az \u00e9lettudom\u00e1nyokkal kapcsolatos adatb\u00e1zisokon kereszt\u00fcl, \u00e9s elemzi az ezekben a kulcsfontoss\u00e1g\u00fa g\u00e9nekben r\u00e9szt vev\u0151 gyullad\u00e1sos jel\u00e1tviteli utakat; Tov\u00e1bb\u00e1 \u00e1llatk\u00eds\u00e9rleteket v\u00e9geztek annak vizsg\u00e1lat\u00e1ra, hogy az emodin befoly\u00e1solja-e az SA-AKI gyullad\u00e1sos \u00fatj\u00e1t, valamint v\u00e9d\u0151hat\u00e1s\u00e1t \u00e9s mechanizmus\u00e1t SA-AKI patk\u00e1nyokon, \u00faj \u00f6tleteket ny\u00fajtva a megel\u0151z\u00e9shez \u00e9s kezel\u00e9shez.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6325\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/1-221.png\" alt=\"\" width=\"723\" height=\"254\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6326\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/2-183.png\" alt=\"\" width=\"737\" height=\"338\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6327\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/3-169.png\" alt=\"\" width=\"732\" height=\"341\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6328\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/4-149.png\" alt=\"\" width=\"748\" height=\"341\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6329\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/5-134.png\" alt=\"\" width=\"673\" height=\"238\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6330\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/6-119.png\" alt=\"\" width=\"729\" height=\"161\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6331\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/7-109.png\" alt=\"\" width=\"725\" height=\"291\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6332\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/8-98.png\" alt=\"\" width=\"732\" height=\"183\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6333\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/9-91.png\" alt=\"\" width=\"715\" height=\"180\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6334\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/10-73.png\" alt=\"\" width=\"695\" height=\"281\" \/><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-6335\" src=\"https:\/\/longchangextracts.com\/wp-content\/uploads\/2024\/08\/11-67.png\" alt=\"\" width=\"715\" height=\"351\" \/><br \/>\nA kutat\u00e1sok kimutatt\u00e1k, hogy az SA-AKI patogenezise t\u00f6bbt\u00e9nyez\u0151s \u00e9s \u00f6sszetett, \u00e9s mag\u00e1ban foglalja a gyullad\u00e1s, a mikrokering\u00e9si zavar \u00e9s a metabolikus \u00e1tprogramoz\u00e1s k\u00f6lcs\u00f6nhat\u00e1s\u00e1t. Patofiziol\u00f3gi\u00e1ja t\u00f6bb sejtt\u00edpus k\u00e1rosod\u00e1s\u00e1t \u00e9s diszfunkci\u00f3j\u00e1t foglalja mag\u00e1ban. A szepszis sor\u00e1n a bakt\u00e9riumok endotoxinokat vagy endotoxinszer\u0171 anyagokat bocs\u00e1tanak ki, amelyek a szervezetben l\u00e9v\u0151 gyullad\u00e1sos sejteket, p\u00e9ld\u00e1ul neutrofileket, monocit\u00e1kat \u00e9s endot\u00e9lsejteket aktiv\u00e1lj\u00e1k, \u00e9s nagy mennyis\u00e9g\u0171 endog\u00e9n gyullad\u00e1sos medi\u00e1tort bocs\u00e1tanak ki a v\u00e9r\u00e1ramba. Ez egyr\u00e9szt t\u00f6bb szervet, k\u00f6zt\u00fck a ves\u00e9t is k\u00e1ros\u00edtja, m\u00e1sr\u00e9szt m\u00e9g t\u00f6bb gyullad\u00e1sos sejtet aktiv\u00e1l a betegs\u00e9gben val\u00f3 r\u00e9szv\u00e9telre, rosszindulat\u00fa immunh\u00e1l\u00f3zati v\u00e1laszt k\u00e9pezve. A lipopoliszacharid (LPS) - induk\u00e1lta SA-AKI SD patk\u00e1ny modellj\u00e9ben a nerolidol az NF - \u03ba B \u00e9s a Toll like receptor 4 (TLR4) jel\u00e1tviteli \u00fatvonalak g\u00e1tl\u00e1s\u00e1val enyh\u00edti a SA-AKI-t. A TLR4\/NF - \u03ba B jel\u00e1tviteli \u00fatvonal bizony\u00edtottan r\u00e9szt vesz a vese gyullad\u00e1sos v\u00e1lasz\u00e1nak folyamat\u00e1ban, \u00e9s a TLR4\/NF - \u03ba B \u00e1ltal k\u00f6zvet\u00edtett gyullad\u00e1sos v\u00e1lasz g\u00e1tl\u00e1sa v\u00e9d\u0151 hat\u00e1s\u00fa az LPS-induk\u00e1lt AKI-ra. L\u00e1that\u00f3, hogy a gyullad\u00e1sos v\u00e1lasz fontos mechanizmus a SA-AKI patogenezis\u00e9ben, \u00e9s a gyullad\u00e1sos v\u00e1lasz \u00fatvonal\u00e1nak g\u00e1tl\u00e1sa fontos kezel\u00e9si lehet\u0151s\u00e9g a szepszisben, ami \u00faj \u00f6tleteket ny\u00fajt a SA-AKI betegek klinikai kezel\u00e9s\u00e9hez.<br \/>\nEz a tanulm\u00e1ny egy biol\u00f3giai adatb\u00e1zist haszn\u00e1lt fel az SA-AKI patogenezis\u00e9ben szerepet j\u00e1tsz\u00f3 2801 kulcsfontoss\u00e1g\u00fa c\u00e9lpont elemz\u00e9s\u00e9re. E c\u00e9lpontok KEGG-elemz\u00e9se \u00f6sszesen 5 kulcsfontoss\u00e1g\u00fa gyullad\u00e1sos v\u00e1lasz jel\u00e1tviteli \u00fatvonalat t\u00e1rt fel, amelyek k\u00f6z\u00fcl a TNF jel\u00e1tviteli \u00fatvonal \u00e9s az IL-17 jel\u00e1tviteli \u00fatvonal magasan rangsorolt, \u00e9s az NF - \u03ba B jel\u00e1tviteli \u00fatvonal mindk\u00e9t \u00fatvonal sz\u00e1m\u00e1ra hubk\u00e9nt szolg\u00e1lt a SA-AKI patogenezis\u00e9ben val\u00f3 r\u00e9szv\u00e9telhez. A TNF jel\u00e1tviteli \u00fatvonalban a TNF - \u03b1 nemcsak az NF - \u03ba B jel\u00e1tviteli \u00fatvonal kulcsfontoss\u00e1g\u00fa upstream aktiv\u00e1tora, hanem az NF - \u03ba B jel\u00e1tviteli \u00fatvonal downstream reag\u00e1l\u00f3 molekul\u00e1jak\u00e9nt is szolg\u00e1l, ami arra utal, hogy pozit\u00edv visszacsatol\u00e1ssal el\u0151seg\u00edti az NF - \u03ba B jel\u00e1tviteli \u00fatvonalat, \u00e9s a kett\u0151 kieg\u00e9sz\u00edti egym\u00e1st. Az IL-17 jel\u00e1tviteli \u00fatvonalban az IL-17A az IL-17 csal\u00e1d f\u0151 inici\u00e1l\u00f3 faktor\u00e1nak sz\u00e1m\u00edt, \u00e9s a Th17 sejtek a f\u0151 szekret\u00e1l\u00f3 sejtjei. A CLP induk\u00e1lt modellben azt tal\u00e1lt\u00e1k, hogy az IL-17A nagym\u00e9rt\u00e9kben expressz\u00e1l\u00f3dik a has\u00fcregben, \u00e9s kulcsszerepet j\u00e1tszik a s\u00falyos szepszist k\u00f6vet\u0151 gyullad\u00e1sos v\u00e1laszban. Az IL-17A semleges\u00edt\u00e9se a has\u00fcregben cs\u00f6kkentheti a pro-inflammatorikus citokinek termel\u0151d\u00e9s\u00e9t. Ek\u00f6zben vizsg\u00e1latok kimutatt\u00e1k, hogy a dendritikus sejtekben (DC-k) l\u00e9v\u0151 Toll-like receptor 9 (TLR9) kulcsszerepet j\u00e1tszhat a SA-AKI kialakul\u00e1s\u00e1ban az\u00e1ltal, hogy k\u00f6zvet\u00edti a gamma delta T-sejtek IL-17A termel\u00e9s\u00e9t; M\u00e1s vizsg\u00e1latok kimutatt\u00e1k, hogy az IL-17A ki\u00fct\u00e9se megakad\u00e1lyozhatja a SA-AKI kialakul\u00e1s\u00e1t. A fentiek arra utalnak, hogy a TNF - \u03b1 \u00e9s az IL-17A pro-inflammatorikus faktorok a szepszisben, \u00e9s a TNF jel\u00e1tviteli \u00fatvonal \u00e9s az IL-17 jel\u00e1tviteli \u00fatvonal sz\u00e9les k\u00f6rben r\u00e9szt vesz a szepszis kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben, ami \u00f6sszhangban van az adatelemz\u00e9s eredm\u00e9nyeivel.<\/p>\n<p>A szepszis emodinnal t\u00f6rt\u00e9n\u0151 kezel\u00e9s\u00e9r\u0151l sz\u00e1mos tanulm\u00e1ny k\u00e9sz\u00fclt, els\u0151sorban az agy, a v\u00e9r, a sz\u00edv, a b\u00e9l \u00e9s a t\u00fcd\u0151 sz\u00f6veteire \u00f6sszpontos\u00edtva. A szepszishez t\u00e1rsul\u00f3 enkefalop\u00e1ti\u00e1ban (SAE) az emodin jav\u00edthatja a kognit\u00edv k\u00e1rosod\u00e1st \u00e9s a k\u00f3ros k\u00e1rosod\u00e1st, \u00e9s g\u00e1tolhatja a CLP \u00e1ltal kiv\u00e1ltott gyullad\u00e1st egerekben a BDNF\/TrkB jel\u00e1tvitel felszab\u00e1lyoz\u00e1s\u00e1val. A v\u00e9rrendszerben az emodin lefel\u00e9 szab\u00e1lyozza a P-szelektint, jav\u00edtja a v\u00e9rlemezk\u00e9k sz\u00e1m\u00e1t \u00e9s aggreg\u00e1ci\u00f3s k\u00e9pess\u00e9g\u00e9t a szepszis k\u00e9s\u0151i szakasz\u00e1ban, valamint fokozza az endog\u00e9n v\u00e9ralvad\u00e1si faktorok aktivit\u00e1s\u00e1t \u00e9s a fibrinog\u00e9n funkci\u00f3j\u00e1t, gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejt ki. Szeptikus kardiomiop\u00e1ti\u00e1ban azt tal\u00e1lt\u00e1k, hogy az emodin visszaford\u00edthatja a sz\u00edvm\u0171k\u00f6d\u00e9si zavarokat \u00e9s jav\u00edthatja a sz\u00edvizom \u00e1llapot\u00e1t szeptikus patk\u00e1nyokn\u00e1l, ami \u00f6sszef\u00fcgg\u00e9sben lehet az inflammasz\u00f3ma aktiv\u00e1ci\u00f3j\u00e1nak g\u00e1tl\u00e1s\u00e1val. A szepszis okozta b\u00e9ls\u00e9r\u00fcl\u00e9sben az emodin jav\u00edthatja a b\u00e9lny\u00e1lkah\u00e1rtya k\u00e1rosod\u00e1s\u00e1t a gyullad\u00e1sos faktorok \u00e9s az oxidat\u00edv stressz markerek szintj\u00e9nek cs\u00f6kkent\u00e9s\u00e9vel, \u00e9s hat\u00e1smechanizmusa a VDR\/Nrf2\/HO-1 \u00fatvonalhoz kapcsol\u00f3dhat; \u00e9s a szoros k\u00f6t\u00e9s (TJ) feh\u00e9rje expresszi\u00f3s szintj\u00e9nek n\u00f6vel\u00e9s\u00e9vel v\u00e9di a b\u00e9lg\u00e1t integrit\u00e1s\u00e1t \u00e9s g\u00e1tolja a b\u00e9lg\u00e1t permeabilit\u00e1s\u00e1t. A gyullad\u00e1sos v\u00e1lasz \u00e9s a b\u00e9l barrier funkci\u00f3j\u00e1nak jav\u00edt\u00e1sa mellett az emodin megakad\u00e1lyozhatja az Escherichia coli kiszorul\u00e1s\u00e1t, megakad\u00e1lyozhatja a bakt\u00e9riumok terjed\u00e9s\u00e9t \u00e9s \u00e1tvitel\u00e9t, \u00e9s cs\u00f6kkentheti a bakt\u00e9riumok \u00e1ltal okozott m\u00e1sodlagos k\u00e1rokat. A szepszishez kapcsol\u00f3d\u00f3 akut t\u00fcd\u0151k\u00e1rosod\u00e1sban az emodin g\u00e1tolhatja az NF - \u03ba B \u00e9s a nagy mobilit\u00e1s\u00fa csoportbox 1 (HMGB1) \u00fatvonalakat, ez\u00e1ltal cs\u00f6kkentve a t\u00fcd\u0151 oxidat\u00edv stressz\u00e9t \u00e9s a gyullad\u00e1sos v\u00e1laszt. Egy m\u00e1sik, a t\u00fcd\u0151re vonatkoz\u00f3 tanulm\u00e1ny az autof\u00e1gia \u00fatvonal\u00e1n alapul, \u00e9s az emodin beavatkoz\u00e1sa hat\u00e9konyan megakad\u00e1lyozhatja az akut t\u00fcd\u0151k\u00e1rosod\u00e1s progresszi\u00f3j\u00e1t. Ezenk\u00edv\u00fcl m\u00e1s tanulm\u00e1nyok kimutatt\u00e1k, hogy az emodin hat\u00e9konyan enyh\u00edtheti a t\u00fcd\u0151sz\u00f6veti \u00f6d\u00e9m\u00e1t a szepszis \u00e1ltal kiv\u00e1ltott akut t\u00fcd\u0151s\u00e9r\u00fcl\u00e9sben az aquaporin (AQP), a TJ, a gyullad\u00e1sos faktorok \u00e9s a t\u00fcd\u0151sejt apopt\u00f3zis szab\u00e1lyoz\u00e1s\u00e1val. Az emodin SA-AKI-ra vonatkoz\u00f3 vizsg\u00e1lat\u00e1r\u00f3l m\u00e9g nem sz\u00e1moltak be. E vizsg\u00e1lat r\u00e9v\u00e9n meg\u00e1llap\u00edtott\u00e1k, hogy az emodinnal kezelt CLP modell patk\u00e1nyokn\u00e1l az ELISA eredm\u00e9nyek alapj\u00e1n cs\u00f6kkent a TNF - \u03b1, IL-17 \u00e9s IFN - \u03b3 expresszi\u00f3ja, ami \u00f6sszhangban van az emodin szepszis gyullad\u00e1sra gyakorolt g\u00e1tl\u00f3 hat\u00e1s\u00e1val.<br \/>\nAz emodin ugyanilyen hat\u00e1s\u00e1t a Th17\/Treg gyullad\u00e1sos tengelyre is megvizsg\u00e1lt\u00e1k. Az akut pancreatitis vizsg\u00e1lat\u00e1ban azt tal\u00e1lt\u00e1k, hogy az emodin g\u00e1tolja az immunv\u00e1laszt s\u00falyos akut pancreatitisben az IFN - \u03b3\/IL-17 ar\u00e1ny\u00e1nak szab\u00e1lyoz\u00e1s\u00e1val, ez\u00e1ltal enyh\u00edtve a b\u00e9lg\u00e1t diszfunkci\u00f3j\u00e1t. Ez a tanulm\u00e1ny pedig azt tal\u00e1lta, hogy SA-AKI-ban az emodin szint\u00e9n cs\u00f6kkentheti az IL-17A expresszi\u00f3j\u00e1t \u00e9s jav\u00edthatja a gyullad\u00e1sos v\u00e1laszt.<br \/>\n\u00d6sszefoglalva, ez a tanulm\u00e1ny adatb\u00e1ny\u00e1szattal 2801 kulcsfontoss\u00e1g\u00fa g\u00e9nt azonos\u00edtott, amelyek r\u00e9szt vesznek az emodin patogenezis\u00e9ben. A GO biol\u00f3giai folyamatok elemz\u00e9se arra utal, hogy e c\u00e9lpontok biol\u00f3giai funkci\u00f3i f\u0151k\u00e9nt a membr\u00e1n jel\u00e1tvitelt, az \u00e9rrendszeri szab\u00e1lyoz\u00e1st \u00e9s a sebgy\u00f3gyul\u00e1st \u00e9rintik. A KEGG \u00fatvonalak gazdagod\u00e1si elemz\u00e9se azt mutatta, hogy a TNF, IL-17, PI3K Akt, NF - \u03ba B \u00e9s MAPK jel\u00e1tviteli \u00fatvonalak a gyullad\u00e1ssal kapcsolatos jel\u00e1tviteli \u00fatvonalakban gazdagodtak. A k\u00eds\u00e9rleti ellen\u0151rz\u00e9s azt mutatta, hogy az emodin kezel\u00e9s jav\u00edtotta a vesefunkci\u00f3t SA-AKI-ban, \u00e9s cs\u00f6kkent az oxidat\u00edv stressz (MDA) \u00e9s a gyullad\u00e1sos citokinek (TNF - \u03b1, IL-17 \u00e9s IFN - \u03b3) szintje. Az IL-17A, TNF - \u03b1, TRAF6, NF - \u03ba Bp65 feh\u00e9rjeexpresszi\u00f3ja \u00e9s az I \u03ba B \u03b1 foszforil\u00e1ci\u00f3s szintje szignifik\u00e1nsan cs\u00f6kkent a CLP csoporthoz k\u00e9pest, ami \u00f6sszhangban van az adatelemz\u00e9s eredm\u00e9nyeivel. Ez azt sugallja, hogy az emodin jav\u00edthatja az SA-AKI-t patk\u00e1nyokban, ami \u00f6sszef\u00fcgghet az IL-17\/NF - \u03ba B \u00e9s a TNF\/NF - \u03ba B jel\u00e1tviteli \u00fatvonalakkal.<\/p>","protected":false},"excerpt":{"rendered":"<p>Exploring the mechanism of action of emodin in treating sepsis related acute kidney injury based on data mining and experimental verification Sepsis is a life-threatening organ dysfunction caused by an imbalance in the host&#8217;s response to infection. The kidneys are one of the most commonly affected organs in sepsis, and sepsis associated acute kidney injury [&hellip;]<\/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":"<!-- This site is optimized with the Yoast SEO plugin v23.0 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Exploring the mechanism of action of emodin in treating sepsis related acute kidney injury based on data mining and experimental verification - 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\/emodin\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Exploring the mechanism of action of emodin in treating sepsis related acute kidney injury based on data mining and experimental verification - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Exploring the mechanism of action of emodin in treating sepsis related acute kidney injury based on data mining and experimental verification Sepsis is a life-threatening organ dysfunction caused by an imbalance in the host&#8217;s response to infection. 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