{"id":4007,"date":"2024-08-04T08:07:05","date_gmt":"2024-08-04T08:07:05","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=4007"},"modified":"2024-08-04T08:07:05","modified_gmt":"2024-08-04T08:07:05","slug":"crocin","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/crocin\/","title":{"rendered":"Az NLRP3 \u00fatvonalat szab\u00e1lyoz\u00f3 \u00e9s az epithelialis-mesenchymalis \u00e1tmenetet g\u00e1tl\u00f3 crocin mechanizmusa a diabetes nephropathia kezel\u00e9s\u00e9ben"},"content":{"rendered":"

Az NLRP3 \u00fatvonalat szab\u00e1lyoz\u00f3 \u00e9s az epithelialis-mesenchymalis \u00e1tmenetet g\u00e1tl\u00f3 crocin mechanizmusa a diabetes nephropathia kezel\u00e9s\u00e9ben
\nA diab\u00e9teszes vesebetegs\u00e9g (DKD) a cukorbetegs\u00e9g gyakori sz\u00f6v\u0151dm\u00e9nye, amely a vese szerkezet\u00e9nek \u00e9s funkci\u00f3j\u00e1nak k\u00e1rosod\u00e1s\u00e1hoz vezet, ami f\u0151k\u00e9nt glomerul\u00e1ris mezangiumt\u00e1gulatban, tubulointerstitialis fibr\u00f3zisban, glomerul\u00e1ris baz\u00e1lis membr\u00e1n megvastagod\u00e1s\u00e1ban stb. nyilv\u00e1nul meg, \u00e9s v\u00e9g\u00fcl v\u00e9gst\u00e1dium\u00fa vesebetegs\u00e9gg\u00e9 alakul. A DKD rejtett kezdet\u0171, gyors progresszi\u00f3j\u00fa, \u00f6sszetett mechanizmus\u00fa \u00e9s rossz progn\u00f3zis\u00fa. A nyugati orvosl\u00e1s kezel\u00e9se els\u0151sorban a v\u00e9rcukorszint, a v\u00e9rnyom\u00e1s \u00e9s a v\u00e9rzs\u00edrok szab\u00e1lyoz\u00e1s\u00e1ra \u00f6sszpontos\u00edt, de a DKD progresszi\u00f3ja nem lassul, ami s\u00falyosan befoly\u00e1solja a betegek \u00e9letmin\u0151s\u00e9g\u00e9t. Tov\u00e1bb\u00e1, mivel a DKD el\u0151fordul\u00e1si ar\u00e1nya \u00e9vr\u0151l \u00e9vre n\u0151 K\u00edn\u00e1ban, a DKD hatalmas gazdas\u00e1gi \u00e9s t\u00e1rsadalmi terhet jelent, \u00e9s s\u00fcrg\u0151sen hat\u00e9kony gy\u00f3gyszereket kell kifejleszteni a DKD kezel\u00e9s\u00e9re.
\nA hagyom\u00e1nyos k\u00ednai orvosl\u00e1s hat\u00f3anyagai jelent\u0151s el\u0151ny\u00f6kkel rendelkeznek a DKD progresszi\u00f3j\u00e1nak k\u00e9sleltet\u00e9s\u00e9ben. Az epimedium glikozid a nukle\u00e1ris faktor kappaB (NF - \u03ba B) \u00fatvonal g\u00e1tl\u00e1s\u00e1val enyh\u00edtheti a gyullad\u00e1st a vesesz\u00f6vetben \u00e9s k\u00e9sleltetheti a diab\u00e9teszes vesebetegs\u00e9g (DKD) progresszi\u00f3j\u00e1t. A szilimarin aktiv\u00e1lhatja a protein kin\u00e1z B (Akt) \u00fatvonalat a DKD jav\u00edt\u00e1sa \u00e9rdek\u00e9ben. A hipericin jav\u00edthatja az eg\u00e9r DKD-t az\u00e1ltal, hogy el\u0151seg\u00edti a makrof\u00e1gok M1-r\u0151l M2 fenot\u00edpusra val\u00f3 polariz\u00e1ci\u00f3j\u00e1t \u00e9s a CD4+T sejtek differenci\u00e1l\u00f3d\u00e1s\u00e1t seg\u00edt\u0151 T-sejt 2 (Th2) \u00e9s szab\u00e1lyoz\u00f3 T-sejt (Treg) popul\u00e1ci\u00f3kk\u00e1. Az \u00e9desgy\u00f6k\u00e9r bioakt\u00edv \u00f6sszetev\u0151je, az \u00e9desgy\u00f6k\u00e9r flavonoidok jav\u00edthatj\u00e1k a diab\u00e9teszes vesebetegs\u00e9get (DKD) a vashi\u00e1ny \u00e9s a vaszkul\u00e1ris endoteli\u00e1lis n\u00f6veked\u00e9si faktor (VEGF)\/Akt\/extracellul\u00e1ris jel szab\u00e1lyozott kin\u00e1z (ERK) \u00fatvonal g\u00e1tl\u00e1s\u00e1val. A paeoniflorin g\u00e1tolhatja a k\u00fcl\u00f6nb\u00f6z\u0151 gyullad\u00e1sos faktorokat, mint p\u00e9ld\u00e1ul az interleukin-1 b\u00e9ta (IL-1 \u03b2), lecs\u00f6kkentheti a foszforil\u00e1lt Janus kin\u00e1z 2 (p-JAK2) \u00e9s a foszforil\u00e1lt jel\u00e1tviv\u0151 \u00e9s transzkripci\u00f3s aktiv\u00e1tor 3 (p-STAT3) feh\u00e9rjeexpresszi\u00f3j\u00e1t a vesesejtekben, enyh\u00edtheti a vesesz\u00f6veti gyullad\u00e1st \u00e9s az autof\u00e1gia v\u00e1laszt, \u00e9s v\u00e9di a ves\u00e9ket.
\nA krocin (CRO) a hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szatban haszn\u00e1lt s\u00e1fr\u00e1ny f\u0151 hat\u00f3anyaga, amely k\u00fcl\u00f6nb\u00f6z\u0151 hat\u00e1sokkal rendelkezik, p\u00e9ld\u00e1ul gyullad\u00e1scs\u00f6kkent\u0151 \u00e9s antioxid\u00e1ns hat\u00e1s\u00fa. Tanulm\u00e1nyok meg\u00e1llap\u00edtott\u00e1k, hogy a CRO az oxidat\u00edv stressz \u00e9s a gyullad\u00e1sos v\u00e1lasz g\u00e1tl\u00e1s\u00e1val enyh\u00edtheti a DKD-t. Vannak olyan vizsg\u00e1latok is, amelyek azt tal\u00e1lt\u00e1k, hogy a CRO g\u00e1tolja az NLRP3 \u00fatvonal aktiv\u00e1l\u00f3d\u00e1s\u00e1t a kardiomiocit\u00e1kban. Nem vil\u00e1gos azonban, hogy a NOD-szer\u0171 receptorhoz hasonl\u00f3 termikus feh\u00e9rje dom\u00e9nhez kapcsol\u00f3d\u00f3 feh\u00e9rje 3 (NLRP3) aktiv\u00e1ci\u00f3j\u00e1nak g\u00e1tl\u00e1s\u00e1val \u00e9s az epithelialis-mesenchym\u00e1lis \u00e1tmenet (EMT) elfojt\u00e1s\u00e1val kezelheti-e a DKD-t. Ez\u00e9rt ez a tanulm\u00e1ny DKD eg\u00e9rmodellt hozott l\u00e9tre a CRO DKD egerekre gyakorolt ter\u00e1pi\u00e1s hat\u00e1s\u00e1nak vizsg\u00e1lat\u00e1ra, \u00e9s tanulm\u00e1nyozta a CRO mechanizmus\u00e1t a DKD kezel\u00e9s\u00e9ben az EMT \u00e9s az NLRP3 \u00fatvonalak szempontj\u00e1b\u00f3l.<\/p>\n

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\nA DKD a cukorbetegs\u00e9g okozta mikrovaszkul\u00e1ris betegs\u00e9g, amely glomeruloszkler\u00f3zishoz, a baz\u00e1lmembr\u00e1n megvastagod\u00e1s\u00e1hoz \u00e9s a vese interstitium fibr\u00f3zis\u00e1hoz vezet. A v\u00e9gst\u00e1dium\u00fa vesebetegs\u00e9g egyik fontos oka. Az \u00e9vr\u0151l \u00e9vre n\u00f6vekv\u0151 el\u0151fordul\u00e1si ar\u00e1ny komoly orvosi teherr\u00e9 v\u00e1lt. A DKD tanulm\u00e1nyoz\u00e1s\u00e1ra szolg\u00e1l\u00f3 \u00e1llatmodellek alkalmaz\u00e1sa el\u0151seg\u00edti az \u00faj gy\u00f3gyszerek kifejleszt\u00e9s\u00e9t, ez\u00e1ltal jav\u00edtja a betegek \u00e9letmin\u0151s\u00e9g\u00e9t \u00e9s cs\u00f6kkenti a t\u00e1rsadalmi terheket. A HFD di\u00e9ta \u00e9s az STZ injekci\u00f3 indukci\u00f3j\u00e1nak kombin\u00e1ci\u00f3ja klasszikus m\u00f3dszer a DKD modellez\u00e9s\u00e9re, \u00e9s a sikeres modellez\u00e9s ut\u00e1n a t\u00fcnetek hasonl\u00f3ak a DKD betegek\u00e9hez. Az elv els\u0151sorban az egerek HFD di\u00e9t\u00e1val t\u00f6rt\u00e9n\u0151 inzulinrezisztencia indukci\u00f3j\u00e1hoz \u00e9s az STZ injekci\u00f3val t\u00f6rt\u00e9n\u0151 hasny\u00e1lmirigy b\u00e9ta-sejt nekr\u00f3zis \u00e9s vesek\u00e1rosod\u00e1s indukci\u00f3j\u00e1hoz kapcsol\u00f3dik. A 24 \u00f3r\u00e1s UTP, Cr \u00e9s BUN \u00e9rt\u00e9keket \u00e1ltal\u00e1ban a glomerul\u00e1ris filtr\u00e1ci\u00f3s funkci\u00f3 \u00e9rt\u00e9kel\u00e9s\u00e9re haszn\u00e1lj\u00e1k, \u00e9s az emelkedett szintek veseel\u00e9gtelens\u00e9gre utalnak. Ebben a vizsg\u00e1latban a DKD egerek s\u00falyos veseelv\u00e1ltoz\u00e1sokat mutattak, bele\u00e9rtve a megn\u00f6vekedett glomerulusokat, a vese tubulointerstitialis sz\u00f6vet\u00e9nek gyullad\u00e1sos infiltr\u00e1ci\u00f3j\u00e1t, amelyet fibr\u00f3zis k\u00eds\u00e9rt, ami a sikeres modellez\u00e9sre utal. A CRO beavatkoz\u00e1s ut\u00e1n a fenti t\u00fcnetek javultak, a nagy d\u00f3zis\u00fa CRO mutatta a legjelent\u0151sebb jav\u00edt\u00f3 hat\u00e1st, \u00e9s a javul\u00e1s m\u00e9rt\u00e9ke hasonl\u00f3 volt, mint a pozit\u00edv MCC950 gy\u00f3gyszer\u00e9. M\u00e1s vizsg\u00e1latok kimutatt\u00e1k, hogy a CRO beavatkoz\u00e1s 25mg\/kg d\u00f3zisban hat\u00e9konyan jav\u00edtja a bleomicin induk\u00e1lta t\u00fcd\u0151fibr\u00f3zist.
\nAz EMT a vesefibr\u00f3zis \u00e9s a proteinuria k\u00f6zvetlen oka, \u00e9s fontos szerepet j\u00e1tszik a DKD kialakul\u00e1s\u00e1ban. Tanulm\u00e1nyok kimutatt\u00e1k, hogy a CRO g\u00e1tolhatja az EMT-t a m\u00e1jban a m\u00e1jfibr\u00f3zis jav\u00edt\u00e1sa \u00e9rdek\u00e9ben. Ez\u00e9rt ez a tanulm\u00e1ny tov\u00e1bb vizsg\u00e1lja, hogy a CRO jav\u00edthatja-e a vese EMT-t. Ebben a vizsg\u00e1latban a DKD egerek ves\u00e9iben az E-cad expresszi\u00f3ja lecs\u00f6kkent, m\u00edg a VIM, \u03b1 - SMA \u00e9s TGF - \u03b2 1 expresszi\u00f3ja felfel\u00e9 szab\u00e1lyoz\u00f3dott, ami az EMT s\u00falyosbod\u00e1s\u00e1t jelzi a DKD egerek ves\u00e9iben. Az E-cad az epit\u00e9lsejtek f\u0151 markere, amely szerepet j\u00e1tszik az epit\u00e9lsejtek polarit\u00e1s\u00e1nak \u00e9s az intercellul\u00e1ris adh\u00e9zi\u00f3nak a fenntart\u00e1s\u00e1ban. Az interstitialis sejtek els\u0151sorban VIM-et, \u03b1 - SMA-t \u00e9s TGF - \u03b2 1-t expressz\u00e1lnak, amelyek k\u00f6z\u00fcl a TGF - \u03b2 1 er\u0151s profibrotikus hat\u00e1ssal b\u00edr. Sz\u00e1mos tanulm\u00e1ny meger\u0151s\u00edtette, hogy a TGF - \u03b2 1 nagym\u00e9rt\u00e9kben expressz\u00e1l\u00f3dik a DKD vesesz\u00f6vetben. Az EMT folyamat sor\u00e1n az epit\u00e9lsejtek adh\u00e9zi\u00f3s molekul\u00e1inak \u00e9s citoszkelet\u00e1lis komponenseinek cs\u00f6kken\u00e9se vagy elt\u0171n\u00e9se az epit\u00e9lsejtek fenot\u00edpusos \u00e1talakul\u00e1s\u00e1hoz vezet, a stromasejtek markereinek megszerz\u00e9s\u00e9hez. K\u00fcl\u00f6nb\u00f6z\u0151 s\u00e9r\u00fcl\u00e9si ingerek hat\u00e1s\u00e1ra a differenci\u00e1lt epit\u00e9lsejtek fenot\u00edpusos \u00e1talakul\u00e1son mennek kereszt\u00fcl, \u00e9s nagysz\u00e1m\u00fa fibroblasztot \u00e9s myofibroblasztot k\u00e9peznek, el\u0151seg\u00edtve a vesefibr\u00f3zis kialakul\u00e1s\u00e1t. E vizsg\u00e1lat eredm\u00e9nyei szerint a CRO k\u00e9pes felszab\u00e1lyozni az E-cad expresszi\u00f3j\u00e1t, lefel\u00e9 szab\u00e1lyozni a VIM, \u03b1 - SMA \u00e9s TGF - \u03b2 1 expresszi\u00f3j\u00e1t, \u00e9s j\u00f3 g\u00e1tl\u00f3 szerepet j\u00e1tszik a vese EM kialakul\u00e1s\u00e1ban. Ezenk\u00edv\u00fcl a CRO a MAPK\/ERK \u00fatvonalon kereszt\u00fcl g\u00e1tolja az EMT-t a tumorsejtekben. A MAPK\/ERK szint\u00e9n fontos t\u00e9nyez\u0151, amely a diab\u00e9teszes vesebetegs\u00e9gben a vesefibr\u00f3zishoz vezet. A j\u00f6v\u0151ben tov\u00e1bbi kutat\u00e1sokat lehet v\u00e9gezni a CRO MAPK\/ERK \u00e1ltal kiv\u00e1ltott vesefibr\u00f3zisra gyakorolt g\u00e1tl\u00f3 hat\u00e1s\u00e1val kapcsolatban, hogy \u00faj c\u00e9lpontokat tal\u00e1ljunk a CRO sz\u00e1m\u00e1ra az EMT g\u00e1tl\u00e1s\u00e1ra.
\nAz EMT elv\u00e1ltoz\u00e1sai dinamikusak \u00e9s reverzibilisek, \u00e9s vizsg\u00e1latok kimutatt\u00e1k, hogy az NLRP3 \u00fatvonal r\u00e9szt vesz a fenot\u00edpus-\u00e1tmenet szab\u00e1lyoz\u00e1s\u00e1ban. Ebben a vizsg\u00e1latban az NLRP3 inflammasz\u00f3ma nagym\u00e9rt\u00e9kben kifejez\u0151d\u00f6tt a DKD egerek ves\u00e9iben, s\u00falyosb\u00edtva a gyullad\u00e1sos v\u00e1laszt a DKD egerek ves\u00e9iben. Az NLRP3 inflammasz\u00f3ma egy multifeh\u00e9rje komplex, amely NLRP3-b\u00f3l, ASC-b\u0151l \u00e9s kaszp\u00e1z-1-b\u0151l \u00e1ll. Az aktiv\u00e1lt NLRP3 inflammasz\u00f3ma fontos szerepet j\u00e1tszik a DKD el\u0151ret\u00f6r\u00e9s\u00e9ben. Amikor az NLRP3 aktiv\u00e1l\u00f3dik, el\u0151seg\u00edti az NLRP3 inflammasz\u00f3ma komponenseinek (NLRP3, ASC, kaszp\u00e1z-1) \u00f6sszeszerel\u0151d\u00e9s\u00e9t, ez\u00e1ltal aktiv\u00e1lja a pro-kaszp\u00e1z-1-et, hogy akt\u00edv tiszt\u00edtott kaszp\u00e1z-1-et k\u00e9pezzen, amely has\u00edtja \u00e9s \u00e9rleli az IL-1 \u03b2 \u00e9s IL-18 gyullad\u00e1sos faktorokat. Az \u00e9rett-IL-1 \u03b2 serkentheti a TGF - \u03b2 1 szint\u00e9zis\u00e9t, amely kulcsfontoss\u00e1g\u00fa t\u00e9nyez\u0151 az EMT kialakul\u00e1s\u00e1ban. A TGF - \u03b2 1 el\u0151seg\u00edtheti az extracellul\u00e1ris m\u00e1trix k\u00fcl\u00f6nb\u00f6z\u0151 feh\u00e9rjekomponenseinek szint\u00e9zis\u00e9t \u00e9s megakad\u00e1lyozhatja azok leboml\u00e1s\u00e1t, ez\u00e1ltal s\u00falyosb\u00edtva a vese EMT folyamat\u00e1t \u00e9s felgyors\u00edtva a vesefibr\u00f3zis kialakul\u00e1s\u00e1t. Emellett vizsg\u00e1latok kimutatt\u00e1k, hogy az NLRP3 knockout egerekben az \u03b1 - SMA expresszi\u00f3ja jelent\u0151sen le van szab\u00e1lyozva. Az NLRP3 t\u00falterjed\u00e9se g\u00e1tolja az E-cad expresszi\u00f3j\u00e1t \u00e9s el\u0151seg\u00edti az \u03b1 - SMA expresszi\u00f3j\u00e1t, m\u00edg a VIM-r\u0151l kimutatt\u00e1k, hogy el\u0151seg\u00edti az NLRP3 aktiv\u00e1l\u00f3d\u00e1s\u00e1t. Mindezek arra utalnak, hogy az NLRP3 \u00e9s az EMT k\u00f6z\u00f6tt k\u00f6lcs\u00f6n\u00f6s szab\u00e1lyoz\u00f3 hat\u00e1s van, \u00e9s az NLRP3 g\u00e1tl\u00e1sa jelent\u0151sen enyh\u00edtheti a vese EMT-t. \u00c9s ez a tanulm\u00e1ny meg\u00e1llap\u00edtotta, hogy a CRO beavatkoz\u00e1s hat\u00e9konyan g\u00e1tolja az NLRP3 inflammasz\u00f3m\u00e1val kapcsolatos faktorok expresszi\u00f3j\u00e1t, j\u00f3 gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejt ki, mik\u00f6zben EMT-ellenes hat\u00e1st is kifejt. Az NLRP3 aktiv\u00e1l\u00e1s\u00e1hoz kett\u0151s jelek bevon\u00e1s\u00e1ra van sz\u00fcks\u00e9g. El\u0151sz\u00f6r is, az NF - \u03ba B transzkripci\u00f3s faktor aktiv\u00e1l\u00f3dik \u00e9s bel\u00e9p a sejtmagba, el\u0151seg\u00edtve az NLRP3 \u00e9s az IL-1 \u03b2 g\u00e9nek expresszi\u00f3j\u00e1t (els\u0151 jel); Ezt k\u00f6vet\u0151en olyan faktorok, mint a K+ \u00e9s a ROS stimul\u00e1l\u00e1sa mellett megindul az NLRP3 inflammasz\u00f3ma \u00f6sszeszerel\u0151d\u00e9se (m\u00e1sodik jel). \u00c9rdekes m\u00f3don kor\u00e1bbi tanulm\u00e1nyok kimutatt\u00e1k a CRO g\u00e1tl\u00f3 hat\u00e1s\u00e1t az NF - \u03ba B-re. \u00cdgy a j\u00f6v\u0151beni kutat\u00e1si ir\u00e1ny lehet, hogy a CRO k\u00e9pes-e elnyomni az NLRP3 \u00e1ltal induk\u00e1lt EMT-t \u00e9s jav\u00edtani a DKD-t az NF - \u03ba B (az els\u0151 jel) g\u00e1tl\u00e1s\u00e1val. A CRO g\u00e1tolhatja az NLRP3 aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s jav\u00edthatja a peritonitist a mitokondri\u00e1lis reakt\u00edv oxig\u00e9nfajok termel\u00e9s\u00e9nek cs\u00f6kkent\u00e9s\u00e9vel. Ek\u00f6zben a CRO antioxid\u00e1ns \u00e9s mitokondri\u00e1lis jav\u00edt\u00f3 funkci\u00f3ir\u00f3l k\u00fcl\u00f6nb\u00f6z\u0151 modellekben sz\u00e1moltak be. Teh\u00e1t tov\u00e1bbi kutat\u00e1sokra van sz\u00fcks\u00e9g annak meger\u0151s\u00edt\u00e9s\u00e9re, hogy a CRO jav\u00edthatja-e a DKD modell EMT-j\u00e9t a mitokondri\u00e1lis ROS-termel\u00e9s cs\u00f6kkent\u00e9s\u00e9vel, ez\u00e1ltal blokkolva az NLRP3 m\u00e1sodik jel\u00e9nek aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s g\u00e1tolva annak aktiv\u00e1l\u00f3d\u00e1s\u00e1t. Ezenk\u00edv\u00fcl ez a tanulm\u00e1ny pozit\u00edv kontrollk\u00e9nt az MCC950 NLRP3-inhibitort v\u00e1lasztotta, \u00e9s meg\u00e1llap\u00edtotta, hogy a CRO az MCC950-hez hasonl\u00f3 gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejtett ki. \u00d6sszefoglalva, a CRO v\u00e9gs\u0151 soron enyh\u00edtheti a DKD-t az NLRP3 \u00fatvonal g\u00e1tl\u00e1s\u00e1val az EMT elnyom\u00e1sa \u00e9rdek\u00e9ben.<\/p>","protected":false},"excerpt":{"rendered":"

Mechanism of crocin regulating NLRP3 pathway and inhibiting epithelial mesenchymal transition in the treatment of diabetes nephropathy Diabetes kidney disease (DKD) is a common complication of diabetes, which will lead to damage to the structure and function of the kidney, mainly manifested as glomerular mesangial dilatation, tubulointerstitial fibrosis, glomerular basement membrane thickening, etc., and eventually […]<\/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":"\nMechanism of crocin regulating NLRP3 pathway and inhibiting epithelial mesenchymal transition in the treatment of diabetes nephropathy - 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\/crocin\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Mechanism of crocin regulating NLRP3 pathway and inhibiting epithelial mesenchymal transition in the treatment of diabetes nephropathy - 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