{"id":4718,"date":"2024-08-04T15:16:25","date_gmt":"2024-08-04T15:16:25","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=4718"},"modified":"2024-08-04T15:16:25","modified_gmt":"2024-08-04T15:16:25","slug":"icariin","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/icariin\/","title":{"rendered":"Az icariin szab\u00e1lyoz\u00f3 hat\u00e1sa a mikroglia fenot\u00edpus \u00e1talakul\u00e1s\u00e1ra depresszi\u00f3s modellben"},"content":{"rendered":"

Az icariin szab\u00e1lyoz\u00f3 hat\u00e1sa a mikroglia fenot\u00edpus \u00e1talakul\u00e1s\u00e1ra depresszi\u00f3s modellben
\nA depresszi\u00f3 egyfajta \u00e9rzelmi ment\u00e1lis zavar, amelynek el\u0151fordul\u00e1si ar\u00e1nya magas, k\u00f6nnyen ki\u00fajul\u00f3, s\u00falyos esetben ak\u00e1r \u00e9letvesz\u00e9lyes is lehet. Glob\u00e1lis k\u00f6zeg\u00e9szs\u00e9g\u00fcgyi probl\u00e9m\u00e1v\u00e1 v\u00e1lt. A depresszi\u00f3s betegek klinikai megnyilv\u00e1nul\u00e1sai k\u00f6z\u00e9 tartoznak els\u0151sorban a depresszi\u00f3s \u00e9rzelmek, a cs\u00f6kkent \u00f6r\u00f6m\u00e9rzet, az \u00e9rt\u00e9ktelens\u00e9g vagy b\u0171ntudat \u00e9rz\u00e9se \u00e9s az \u00f6ngyilkoss\u00e1gi gondolatok. Az \u00f6sszetett biol\u00f3giai mechanizmusok \u00e9s a sz\u00e1mos rendszer \u00e9rintetts\u00e9ge miatt a depresszi\u00f3 patogenezise nem teljesen ismert, \u00e9s az antidepressz\u00e1nsok kutat\u00e1sa vil\u00e1gszerte kiemelt figyelmet kap, de a fejl\u0151d\u00e9s lass\u00fa. A depresszi\u00f3 kezel\u00e9s\u00e9re szolg\u00e1l\u00f3 \u00faj megk\u00f6zel\u00edt\u00e9sek \u00e9s gy\u00f3gyszerc\u00e9lpontok megtal\u00e1l\u00e1sa s\u00fcrg\u0151s k\u00e9rd\u00e9ss\u00e9 v\u00e1lt.
\nA stressz okozta neuroinflammatorikus v\u00e1laszt egyre ink\u00e1bb felismerik a depresszi\u00f3 patogenezis\u00e9ben. A mikroglia a velesz\u00fcletett immunsejtek egy t\u00edpusa a k\u00f6zponti idegrendszerben, amely szorosan kapcsol\u00f3dik az agy neuroinflammatorikus v\u00e1laszaihoz, \u00e9s potenci\u00e1lisan \u00faj ter\u00e1pi\u00e1s c\u00e9lpont lehet. A klasszikus M1 polariz\u00e1ci\u00f3 gyullad\u00e1sos faktorokat, p\u00e9ld\u00e1ul interleukin-6 (IL6), interleukin-1 (IL-1), tumor nekr\u00f3zis faktor alfa (TNF - \u03b1) stb. szabad\u00edt fel, neuroinflammatorikus reakci\u00f3kat okozva; Helyettes\u00edtse az aktiv\u00e1lt M2 polariz\u00e1ci\u00f3t, interleukin-10 (interle, ukin-10, IL-10), transzform\u00e1l\u00f3 n\u00f6veked\u00e9si faktor b\u00e9ta (TGF - \u03b2) stb. szekret\u00e1l, sz\u00f6veti jav\u00edt\u00e1st induk\u00e1l, \u00e9s neuroprotekt\u00edv hat\u00e1st fejt ki. A mikroglia fenot\u00edpus-\u00e1talakul\u00e1s\u00e1nak szab\u00e1lyoz\u00e1sa az egyik fontos beavatkoz\u00e1si lehet\u0151s\u00e9g a depresszi\u00f3 kialakul\u00e1s\u00e1ba \u00e9s fejl\u0151d\u00e9s\u00e9be. A hagyom\u00e1nyos k\u00ednai orvosl\u00e1s mindig is jelent\u0151s el\u0151ny\u00f6kkel rendelkezett a depresszi\u00f3 megel\u0151z\u00e9s\u00e9ben \u00e9s kezel\u00e9s\u00e9ben. A hagyom\u00e1nyos k\u00ednai orvosl\u00e1sban a vese jang hi\u00e1nya a depresszi\u00f3 egyik fontos mechanizmusa, \u00e9s a depresszi\u00f3 kezel\u00e9se a veseelm\u00e9let szemsz\u00f6g\u00e9b\u0151l ad \u00f6tleteket. A klinikai gyakorlatban az Epimediumot, a vese-jang toniz\u00e1l\u00e1s\u00e1ra szolg\u00e1l\u00f3 hagyom\u00e1nyos k\u00ednai gy\u00f3gyszert gyakran kombin\u00e1lj\u00e1k m\u00e1s k\u00ednai gy\u00f3gyszerekkel, mint p\u00e9ld\u00e1ul a Xianmao, a Morinda officinalis \u00e9s a Yejiaoteng, a vese-jang hi\u00e1nyt\u00edpus\u00fa depresszi\u00f3 kezel\u00e9s\u00e9re. Kor\u00e1bbi tanulm\u00e1nyokban megfigyelt\u00e9k, hogy az Epimedium brevicomu Maxim, a vese-jang toniz\u00e1l\u00e1s\u00e1ra szolg\u00e1l\u00f3 hagyom\u00e1nyos k\u00ednai gy\u00f3gyszer, az icariin hat\u00f3anyaga j\u00f3 antidepressz\u00e1ns hat\u00e1ssal rendelkezik, de a mechanizmusa m\u00e9g mindig nem vil\u00e1gos. Ez a tanulm\u00e1ny egy kr\u00f3nikus, kisz\u00e1m\u00edthatatlan, enyhe stressz \u00e1ltal kiv\u00e1ltott depresszi\u00f3s modellt k\u00edv\u00e1n haszn\u00e1lni, kombin\u00e1lva egy lipopoliszacharid (LPS) - induk\u00e1lt BV-2 sejtpolariz\u00e1ci\u00f3s modellel, hogy felt\u00e1rja az icariin antidepressz\u00e1ns hat\u00e1s\u00e1nak mechanizmus\u00e1t.<\/p>\n

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\nA depresszi\u00f3 s\u00falyos ment\u00e1lis betegs\u00e9g, amelynek komplex patogenezise miatt nincsenek ide\u00e1lis kezel\u00e9si m\u00f3dszerei. A hagyom\u00e1nyos k\u00ednai orvosl\u00e1snak megvannak a maga saj\u00e1toss\u00e1gai \u00e9s el\u0151nyei a depresszi\u00f3 kezel\u00e9s\u00e9ben. Jelenleg a depresszi\u00f3 patogenezise nem teljesen ismert. A jelenleg kialakult hipot\u00e9zisek f\u0151k\u00e9nt a k\u00f6vetkez\u0151k: gyullad\u00e1sos immunit\u00e1s hipot\u00e9zis, hipotalamusz-hipof\u00edzis-mell\u00e9kvese (HPA) tengely diszfunkci\u00f3 hipot\u00e9zis, monoamin neurotranszmitter hipot\u00e9zis, neurotr\u00f3fikus faktor hipot\u00e9zis stb. A kutat\u00e1sok elm\u00e9ly\u00fcl\u00e9s\u00e9vel a gyullad\u00e1sos immunit\u00e1s hipot\u00e9zis sz\u00e9les k\u00f6r\u0171 figyelmet kapott mind hazai, mind nemzetk\u00f6zi szinten. A kutat\u00e1sok kimutatt\u00e1k, hogy a depresszi\u00f3s betegekn\u00e9l nemcsak perif\u00e9ri\u00e1s gyullad\u00e1sos reakci\u00f3kat tapasztalnak, hanem a k\u00f6zponti idegrendszer immunaktiv\u00e1ci\u00f3j\u00e1t is. A mikroglia a k\u00f6zponti idegrendszer fontos immunsejtt\u00edpusa, amely szorosan kapcsol\u00f3dik a k\u00f6zponti idegrendszer gyullad\u00e1sos v\u00e1lasz\u00e1hoz. Hossz\u00fa t\u00e1v\u00fa stressz hat\u00e1s\u00e1ra szerkezet\u00fck \u00e9s m\u0171k\u00f6d\u00e9s\u00fck abnorm\u00e1lis, ami az \u00e9rzelmek \u00e9s a ment\u00e1lis \u00e1llapotok megv\u00e1ltoz\u00e1s\u00e1hoz vezet, ami fontos t\u00e9nyez\u0151 a depresszi\u00f3 kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben.
\nA klasszikus aktiv\u00e1ci\u00f3s t\u00edpus (M1 t\u00edpus) \u00e9s az alternat\u00edv aktiv\u00e1ci\u00f3s t\u00edpus (M2 t\u00edpus) a mikroglia k\u00e9t f\u0151 polariz\u00e1ci\u00f3s fenot\u00edpusa. Az M1 t\u00edpus teszi ki az aktiv\u00e1lt sejtek t\u00falnyom\u00f3 t\u00f6bbs\u00e9g\u00e9t, \u00e9s k\u00e9pes pro-inflammatorikus medi\u00e1torok, mint a TNF - \u03b1, IL-1, IL-6 \u00e9s a nitrog\u00e9n-oxid-szint\u00e1z iNOS szint\u00e9zis szintetiz\u00e1l\u00e1s\u00e1ra \u00e9s szekr\u00e9ci\u00f3j\u00e1ra, immungyullad\u00e1sos kaszk\u00e1dreakci\u00f3t kiv\u00e1ltva; M2 t\u00edpus (h\u00e1rom alt\u00edpus M2a, M2b immunfenot\u00edpus, M2c inakt\u00edv fenot\u00edpus) stimul\u00e1lhat\u00f3 interleukin-4 (IL-4), interleukin-13 (IL-13) \u00e9s m\u00e1s faktorok \u00e1ltal, gyullad\u00e1scs\u00f6kkent\u0151 faktorokat, p\u00e9ld\u00e1ul IL-10-et \u00e9s CD206-ot szabad\u00edt fel, gyullad\u00e1scs\u00f6kkent\u0151 \u00e9s neuroprotekt\u00edv funkci\u00f3kat fejt ki, \u00e9s fontos szerepet j\u00e1tszik az agyi idegek jav\u00edt\u00e1s\u00e1ban \u00e9s plaszticit\u00e1s\u00e1ban. \u00c1llatk\u00eds\u00e9rletek kimutatt\u00e1k, hogy a CUMS-nak kitett egerek \u00e9s patk\u00e1nyok prefront\u00e1lis k\u00e9reg\u00e9ben a mikroglia er\u0151sen aktiv\u00e1l\u00f3dik, \u00e9s a kapcsol\u00f3d\u00f3 gyullad\u00e1sos medi\u00e1torok magas expresszi\u00f3ja k\u00eds\u00e9ri, ami a depresszi\u00f3val \u00f6sszef\u00fcgg\u0151 gyullad\u00e1sos neuron\u00e1lis degener\u00e1ci\u00f3hoz vezethet. A post mortem vizsg\u00e1lat azt mutatta, hogy s\u00falyos depresszi\u00f3ban szenved\u0151 betegekn\u00e9l a mikroglia s\u0171r\u0171s\u00e9ge az el\u00fcls\u0151 cingul\u00e1ris k\u00e9regben \u00e9s a ventr\u00e1lis prefront\u00e1lis lebeny feh\u00e9r\u00e1llom\u00e1ny\u00e1nak ter\u00fclet\u00e9n jelent\u0151sen megn\u00f6vekedett \u00e9s aktiv\u00e1lt \u00e1llapotot mutatott, de az M2 mikroglia jellegzetes markere, a CD206 jelent\u0151sen le volt szab\u00e1lyozva. A fenti kutat\u00e1sok arra utalnak, hogy a mikroglia t\u00falzott aktiv\u00e1ci\u00f3ja \u00e9s az M1 \u00e9s M2 mikroglia polariz\u00e1ci\u00f3ja fontos szerepet j\u00e1tszik a depresszi\u00f3 kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben.<\/p>\n

Ez a tanulm\u00e1ny meg\u00e1llap\u00edtotta, hogy a CUMS \u00e1ltal kiv\u00e1ltott depresszi\u00f3s egerek hippokampusz\u00e1ban a pro-inflammatorikus citokin IL-6 szintje emelkedett, \u00e9s az IL-6 mRNS, az iNOS mRNS \u00e9s az iNOS feh\u00e9rje t\u00falterjedt, ami a depresszi\u00f3hoz hasonl\u00f3 viselked\u00e9s n\u00f6veked\u00e9s\u00e9vel j\u00e1rt egy\u00fctt (megn\u00f6vekedett k\u00e9nyszer\u00edtett \u00fasz\u00e1si mozdulatlans\u00e1gi id\u0151, cs\u00f6kkent cukros v\u00edzfogyaszt\u00e1s \u00e9s edz\u00e9st\u00e1vols\u00e1g), ami a depresszi\u00f3s egerek hippokampusz\u00e1ban a klasszikus aktiv\u00e1lt M1 mikroglia jelent\u0151s n\u00f6veked\u00e9s\u00e9re utal. Az epimedium glikozid k\u00e9pes g\u00e1tolni a mikroglia M1 t\u00edpus\u00fa aktiv\u00e1l\u00f3d\u00e1s\u00e1t, cs\u00f6kkenteni az IL-6 pro-inflammatorikus citokin szintj\u00e9t, cs\u00f6kkenteni az IL-6 mRNS, az iNOS mRNS \u00e9s az iNOS feh\u00e9rje t\u00falterjed\u00e9s\u00e9t, \u00e9s elnyomni az agyi gyullad\u00e1st modell egerekben; M\u00e1sr\u00e9szt az icariin el\u0151seg\u00edtheti a mikroglia M2 aktiv\u00e1ci\u00f3j\u00e1t, n\u00f6velheti az IL-10 szintj\u00e9t a CUMS-nak kitett egerek hippokampusz\u00e1ban, el\u0151seg\u00edtheti az IL-10 mRNS, CD206 mRNS \u00e9s CD206 feh\u00e9rje expresszi\u00f3j\u00e1t, ez\u00e1ltal g\u00e1tolja a depresszi\u00f3hoz hasonl\u00f3 viselked\u00e9st a modell egerekben. In vitro k\u00eds\u00e9rletek azt is kimutatt\u00e1k, hogy LPS stimul\u00e1ci\u00f3 alatt a mikroglia M1 polariz\u00e1ci\u00f3ja megn\u00f6vekedett, \u00e9s az icariin k\u00e9pes volt g\u00e1tolni a mikroglia M1 polariz\u00e1ci\u00f3j\u00e1t \u00e9s el\u0151seg\u00edteni az M2 polariz\u00e1ci\u00f3t. Ez arra utal, hogy az icariin a mikroglia fenot\u00edpusos \u00e1talakul\u00e1s\u00e1nak szab\u00e1lyoz\u00e1s\u00e1val enyh\u00edti a t\u00falzott neuroinflamm\u00e1ci\u00f3t.<\/p>\n

Az 5-HT, DA \u00e9s NE monoamin neurotranszmitterek anyagcserezavarai szorosan \u00f6sszef\u00fcggnek a neurol\u00f3giai \u00e9s pszichi\u00e1triai rendelleness\u00e9gek, p\u00e9ld\u00e1ul a depresszi\u00f3 megjelen\u00e9s\u00e9vel \u00e9s kialakul\u00e1s\u00e1val. Az 5-HT, DA \u00e9s NE monoamin neurotranszmitterek szintje a CUMS \u00e1ltal kiv\u00e1ltott depresszi\u00f3s modellpatk\u00e1nyok agy\u00e1ban jelent\u0151sen cs\u00f6kkent. A Rehmannia glutinosa k\u00e9pes cs\u00f6kkenteni az 5-HT, DA \u00e9s NE szintj\u00e9t a modellpatk\u00e1nyok hippokampusz\u00e1ban \u00e9s jav\u00edtani a depresszi\u00f3hoz hasonl\u00f3 viselked\u00e9st. A Danshen polifenolsav hat\u00e9konyan jav\u00edthatja a patk\u00e1nyok depresszi\u00f3hoz hasonl\u00f3 viselked\u00e9s\u00e9t, val\u00f3sz\u00edn\u0171leg a nem receptor tirozinkin\u00e1z 2 (Janus kin\u00e1z 2)\/szign\u00e1ltranszducer \u00e9s a transzkripci\u00f3 3 (STAT3) jel\u00e1tviteli \u00fatvonal g\u00e1tl\u00e1s\u00e1val, a neuroinflamm\u00e1ci\u00f3 enyh\u00edt\u00e9s\u00e9vel \u00e9s a monoamin neurotranszmitterek szintj\u00e9nek szab\u00e1lyoz\u00e1s\u00e1val. Egyre t\u00f6bb immunsejt - mikroglia. Az aktiv\u00e1lt mikroglia sz\u00e1mos gyullad\u00e1sos faktor, p\u00e9ld\u00e1ul interleukin-1 \u03b2 (IL-1 \u03b2), TNF - \u03b1, TGF - \u03b2 stb. felszabadul\u00e1s\u00e1t induk\u00e1lja. Ezek a gyullad\u00e1sos faktorok befoly\u00e1solhatj\u00e1k a monoamin neuronok m\u0171k\u00f6d\u00e9s\u00e9t, \u00e9s oxidat\u00edv stressz r\u00e9v\u00e9n a monoamin neurotranszmisszi\u00f3 cs\u00f6kken\u00e9s\u00e9t id\u00e9zhetik el\u0151, amit a depresszi\u00f3 fontos t\u00e9nyez\u0151j\u00e9nek tartanak. Meger\u0151s\u00edt\u00e9st nyert, hogy a monoamin gy\u00f3gyszerek k\u00e9pesek blokkolni a mikroglia aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s valamilyen m\u00f3don visszaford\u00edtani a depresszi\u00f3t. A kutat\u00e1sok meg\u00e1llap\u00edtott\u00e1k, hogy a tetrahidrobiopterin (BH4), mint a depresszi\u00f3 elismert biomarkere, az 5-HT, DA \u00e9s NE szint\u00e9zis\u00e9hez sz\u00fcks\u00e9ges kulcsfontoss\u00e1g\u00fa enzimatikus kofaktor. A BH4 hi\u00e1nya depresszi\u00f3hoz vezethet. Az M1 t\u00edpus\u00fa mikroglia a BH4 katabolizmus\u00e1hoz vezethet. A mikroglia M1-polariz\u00e1ci\u00f3j\u00e1nak g\u00e1tl\u00e1sa korl\u00e1tozhatja a BH4-katabolizmust, \u00e9s el\u0151seg\u00edtheti a monoamin neurotranszmitterek szint\u00e9zis\u00e9t \u00e9s szekr\u00e9ci\u00f3j\u00e1t. A vizsg\u00e1lat eredm\u00e9nyei azt mutatt\u00e1k, hogy a monoamin neurotranszmitterek cs\u00f6kken\u00e9se a CUMS induk\u00e1lt eg\u00e9r depresszi\u00f3s modell hippokampusz\u00e1ban a depresszi\u00f3hoz hasonl\u00f3 viselked\u00e9s n\u00f6veked\u00e9s\u00e9vel j\u00e1rt egy\u00fctt. Az epimedium glikozid k\u00e9pes n\u00f6velni a monoamin neurotranszmitterek szintj\u00e9t a modell egerek hippokampusz\u00e1ban, ami az antidepressz\u00e1ns hat\u00e1s\u00e1nak egyik mechanizmusa lehet, \u00f6sszhangban a kor\u00e1bbi jelent\u00e9sekkel. Azt azonban, hogy az icariin el\u0151seg\u00edti-e a monoamin neurotranszmitterek szint\u00e9zis\u00e9t \u00e9s szekr\u00e9ci\u00f3j\u00e1t a depresszi\u00f3s modell egerek hippokampusz\u00e1ban a mikroglia fenot\u00edpus \u00e1talakul\u00e1s\u00e1nak szab\u00e1lyoz\u00e1s\u00e1val, m\u00e9g tov\u00e1bb kell vizsg\u00e1lni.<\/p>\n

\u00d6sszefoglalva, ebben a tanulm\u00e1nyban a CUMS seg\u00edts\u00e9g\u00e9vel a depresszi\u00f3 eg\u00e9rmodellj\u00e9t \u00e9s a mikroglia LPS \u00e1ltal induk\u00e1lt polariz\u00e1ci\u00f3s modellj\u00e9t hozt\u00e1k l\u00e9tre. Meg\u00e1llap\u00edtottuk, hogy az ikariin, az Epimedium hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szatban a vese-jang toniz\u00e1l\u00e1s\u00e1ra szolg\u00e1l\u00f3 hat\u00f3anyag, g\u00e1tolja az M1 polariz\u00e1ci\u00f3t \u00e9s el\u0151seg\u00edti a mikroglia M2 polariz\u00e1ci\u00f3j\u00e1t, cs\u00f6kkenti a gyullad\u00e1st a depresszi\u00f3s egerek hippokampusz\u00e1ban, \u00e9s el\u0151seg\u00edti a monoamin neurotranszmitterek termel\u00e9s\u00e9t, ami az antidepressz\u00e1ns hat\u00e1s egyik mechanizmusa.<\/p>","protected":false},"excerpt":{"rendered":"

Regulatory effect of icariin on phenotype transformation of microglia in depression model Depression is a kind of emotional mental disorder, with a high incidence of incidence rate, which is easy to recur, and even life-threatening in serious cases. It has become a global public health problem. The clinical manifestations of depression patients mainly include depressive […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"video","meta":{"footnotes":""},"categories":[20],"tags":[],"yoast_head":"\nRegulatory effect of icariin on phenotype transformation of microglia in depression model - 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\/icariin\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Regulatory effect of icariin on phenotype transformation of microglia in depression model - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Regulatory effect of icariin on phenotype transformation of microglia in depression model Depression is a kind of emotional mental disorder, with a high incidence of incidence rate, which is easy to recur, and even life-threatening in serious cases. 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