{"id":7174,"date":"2024-08-06T18:53:17","date_gmt":"2024-08-06T18:53:17","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=7174"},"modified":"2024-08-06T18:53:17","modified_gmt":"2024-08-06T18:53:17","slug":"high-altitude-disease-model-rats","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/magaslati-betegseg-modell-patkanyok\/","title":{"rendered":"A Cistanche deserticola feniletanoid glikozid ter\u00e1pi\u00e1s hat\u00e1s\u00e1nak \u00e9s mechanizmus\u00e1nak vizsg\u00e1lata kr\u00f3nikus magashegyi betegs\u00e9g modell patk\u00e1nyokon"},"content":{"rendered":"

A Cistanche deserticola feniletanoid glikozid ter\u00e1pi\u00e1s hat\u00e1s\u00e1nak \u00e9s mechanizmus\u00e1nak vizsg\u00e1lata kr\u00f3nikus magashegyi betegs\u00e9g modell patk\u00e1nyokon
\nA magaslati betegs\u00e9g egy \u00e1ltal\u00e1nos kifejez\u00e9s a k\u00fcl\u00f6nb\u00f6z\u0151 klinikai megnyilv\u00e1nul\u00e1sokra, amelyeket az okoz, hogy a szervezet k\u00e9ptelen alkalmazkodni a nagy magass\u00e1gban uralkod\u00f3 alacsony nyom\u00e1s\u00fa hipoxi\u00e1hoz, ami a szervezetben egy sor patol\u00f3giai \u00e9s fiziol\u00f3giai v\u00e1ltoz\u00e1st eredm\u00e9nyez. Ezt a betegs\u00e9get \u00e1ltal\u00e1ban k\u00e9t kateg\u00f3ri\u00e1ra osztj\u00e1k: akut \u00e9s kr\u00f3nikus. A kr\u00f3nikus hegyibetegs\u00e9g (CMS) olyan \u00e1llapotra utal, amikor az akut hegyibetegs\u00e9g eredeti t\u00fcnetei fenn\u00e1llnak, vagy t\u00f6bb mint hat h\u00f3nappal a nagy magass\u00e1gba \u00e9rkez\u00e9s ut\u00e1n is jelentkeznek. A kutat\u00f3k meg\u00e1llap\u00edtott\u00e1k, hogy az Egl9 homol\u00f3g 1 (EGLN1) \u00e9s a peroxisz\u00f3ma prolifer\u00e1tor aktiv\u00e1lt receptor alfa (PPAR - \u03b1) g\u00e9nek a tibeti n\u00e9pess\u00e9gben elt\u00e9rnek az alacsony tengerszint feletti magass\u00e1g\u00fa ter\u00fcleteken \u00e9l\u0151k\u00e9t\u0151l, \u00e9s g\u00e1tolhatj\u00e1k a tibeti v\u00e9rben a hemoglobin alacsony koncentr\u00e1ci\u00f3ban tart\u00e1s\u00e1t. Ez is r\u00e9sze annak, hogy a tibetiek mi\u00e9rt tudnak nagy magass\u00e1gban is \u00e9letben maradni. Ez a tanulm\u00e1ny azt sugallja, hogy a fent eml\u00edtett k\u00e9t g\u00e9n a hipoxia v\u00e1lasz\u00fatvonal jel\u00f6lt g\u00e9njei, amelyek v\u00e9gs\u0151 soron a hipoxia induk\u00e1lhat\u00f3 faktor 1 alfa (HIF-1 alfa) \u00fatvonalon kereszt\u00fcl fejtik ki hat\u00e1sukat. Az EGLN1 a HIF-1 \u03b1 upstream g\u00e9nje, m\u00edg a PPAR - \u03b1 a HIF-1 \u03b1 downstream c\u00e9lpontja.
\nAz alacsony oxig\u00e9nszint blokkolhatja a HIF-1 \u03b1 hidroxil\u00e1l\u00e1s\u00e1t \u00e9s acetil\u00e1l\u00e1s\u00e1t, n\u00f6velheti stabilit\u00e1s\u00e1t, \u00e9s a g\u00e9n\u00e1t\u00edr\u00e1si inform\u00e1ci\u00f3\u00e1tvitelt induk\u00e1lhatja a downstream g\u00e9nek, p\u00e9ld\u00e1ul a vaszkul\u00e1ris endoteli\u00e1lis n\u00f6veked\u00e9si faktor (VEGF), az endotelin-1 (ET-1) stb. \u00e1t\u00edr\u00e1s\u00e1nak \u00e9s expresszi\u00f3j\u00e1nak szab\u00e1lyoz\u00e1s\u00e1val, ez\u00e1ltal t\u00fcd\u0151 \u00e9rrendszeri remodellinget okozva, ami t\u00fcd\u0151\u00f6d\u00e9m\u00e1hoz \u00e9s magaslati sz\u00edvbetegs\u00e9ghez vezet. Az ET-1 hat\u00e1s\u00e1val ellent\u00e9tben a nitrog\u00e9n-monoxid (NO) egy g\u00e1zjelz\u0151 molekula, amely a nitrog\u00e9n-monoxid-szint\u00e1z (NOS) \u00e1ltal kataliz\u00e1lt L-arginin termel\u00e9s\u00e9t kataliz\u00e1lja, \u00e9s sz\u00e9les k\u00f6r\u0171 hat\u00e1sai vannak.
\nEbben a tanulm\u00e1nyban egy speci\u00e1lis k\u00f6rnyezetben, \u00e9szaknyugaton tal\u00e1lhat\u00f3 mesters\u00e9ges k\u00eds\u00e9rleti kabinban szimul\u00e1lt\u00e1k a fenns\u00edk alacsony oxig\u00e9nszint\u0171 k\u00f6rnyezet\u00e9t. Figyelembe v\u00e9ve a fenns\u00edk \u00e9s a s\u00edkvid\u00e9ki ter\u00fcletek k\u00f6z\u00f6tti f\u0151 k\u00fcl\u00f6nbs\u00e9geket, egy magashegyi betegs\u00e9g \u00e1llatmodellt hoztunk l\u00e9tre, hogy megvizsg\u00e1ljuk a HIF-1 \u03b1 \u00fatvonal szerep\u00e9t \u00e9s bels\u0151 kapcsolat\u00e1t a magashegyi betegs\u00e9g patogenezis\u00e9ben. Ennek alapj\u00e1n megfigyelt\u00e9k a Cistanche-b\u00f3l sz\u00e1rmaz\u00f3 feniletanoid glikozidok (PhGC-k) magashegyi betegs\u00e9gekre gyakorolt megel\u0151z\u0151 \u00e9s ter\u00e1pi\u00e1s hat\u00e1sait \u00e9s azok mechanizmusait, elm\u00e9leti alapot szolg\u00e1ltatva a magashegyi betegs\u00e9gek patogenezis\u00e9nek tanulm\u00e1nyoz\u00e1s\u00e1hoz \u00e9s \u00faj magashegyi betegs\u00e9gek elleni gy\u00f3gyszerek kifejleszt\u00e9s\u00e9hez.<\/p>\n

 <\/p>\n

\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"A phGC-ket a Cistanche deserticola-b\u00f3l nyert\u00e9k ki a d\u00e9li Hszincsiangban, \u00e9s a kapcsol\u00f3d\u00f3 kutat\u00e1sok sor\u00e1n sikeresen izol\u00e1ltak k\u00fcl\u00f6nb\u00f6z\u0151 feniletanolos glikozidokat, k\u00f6zt\u00fck echinakozidot, verbaszkozidot, izoveraszkozidot, 2'-acetilverbaszkozidot, Cistanche deserticola glikozid A-t \u00e9s szalidrozidot. Sok \u00e9ven \u00e1t m\u00e9lyrehat\u00f3 kutat\u00e1sokat folytattak a PhGC-k farmakol\u00f3giai hat\u00e1sair\u00f3l, mint p\u00e9ld\u00e1ul az antioxid\u00e1ns, a szabadgy\u00f6k-lev\u00e1laszt\u00f3 \u00e9s az \u00f6reged\u00e9sg\u00e1tl\u00f3 hat\u00e1s. Ebben a k\u00eds\u00e9rletben a PhGCs-M csoport k\u00e9pes volt jelent\u0151sen cs\u00f6kkenteni a patk\u00e1nyok jobb kamrai hipertr\u00f3fia index\u00e9t, ami azt jelzi, hogy a Cistanche deserticola feniletanolsav jav\u00edthatja a hemodinamik\u00e1t \u00e9s a jobb kamrai hipertr\u00f3fia m\u00e9rt\u00e9k\u00e9t CMS patk\u00e1nyokn\u00e1l, \u00e9s bizonyos ter\u00e1pi\u00e1s hat\u00e1ssal rendelkezik a CMS-re. Ez a tanulm\u00e1ny a v\u00e9r oxig\u00e9ntel\u00edtetts\u00e9g\u00e9vel kapcsolatos mutat\u00f3kb\u00f3l arra k\u00f6vetkeztet, hogy a PhGC-k n\u00f6velik a v\u00e9r oxig\u00e9ntel\u00edtetts\u00e9g\u00e9t, cs\u00f6kkentik a hipoxia k\u00e1rosod\u00e1s\u00e1t a szervezetben, \u00e9s n\u00f6velik a szervezet toleranci\u00e1j\u00e1t a hipoxia k\u00e1rosod\u00e1s\u00e1val szemben azonos v\u00f6r\u00f6sv\u00e9rsejtsz\u00e1m \u00e9s hemoglobin tartalom mellett, ez\u00e1ltal el\u00e9rve a magass\u00e1gi betegs\u00e9g kezel\u00e9s\u00e9nek c\u00e9lj\u00e1t. A PhGC-vel t\u00f6rt\u00e9n\u0151 kezel\u00e9s ut\u00e1n a CMS-patk\u00e1nyokn\u00e1l jelent\u0151sen cs\u00f6kkent a hal\u00e1loz\u00e1si ar\u00e1ny \u00e9s a v\u00e9gtag\u00f6d\u00e9ma el\u0151fordul\u00e1sa, ami tov\u00e1bb bizony\u00edtja a CMS kezel\u00e9s\u00e9nek hat\u00e9konys\u00e1g\u00e1t.<\/p>\n

Az NO, mint endothelf\u00fcgg\u0151 \u00e9rt\u00e1g\u00edt\u00f3, fontos szerepet j\u00e1tszik az endothelialis \u00e9rt\u00e1g\u00edt\u00e1sban, mivel k\u00f6zvetlen\u00fcl ellaz\u00edtja a t\u00fcd\u0151\u00e9r simaizomzat\u00e1t, ami jelent\u0151s t\u00fcd\u0151\u00e9rt\u00e1gul\u00e1st eredm\u00e9nyez. K\u00e9pes tov\u00e1bb\u00e1 g\u00e1tolni a t\u00fcd\u0151 \u00e9rrendszeri simaizomsejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s migr\u00e1ci\u00f3j\u00e1t, elnyomja a v\u00e9rlemezk\u00e9k aggreg\u00e1ci\u00f3j\u00e1t, \u00e9s fontos szerepet j\u00e1tszik a t\u00fcd\u0151kering\u00e9s stabilit\u00e1s\u00e1nak fenntart\u00e1s\u00e1ban. Ez a vizsg\u00e1lat meg\u00e1llap\u00edtotta, hogy a Mod t\u00fcd\u0151sz\u00f6vet homogen\u00e1tum NO-tartalma cs\u00f6kkent, \u00e9s a T-NOS, iNOS \u00e9s eNOS aktivit\u00e1sa cs\u00f6kkent. A PhGC-k n\u00f6velhetik a t\u00fcd\u0151sz\u00f6vet NO-tartalm\u00e1t a TNOS, iNOS \u00e9s eNOS aktivit\u00e1s\u00e1nak fokoz\u00e1s\u00e1val, szerepet j\u00e1tszva a t\u00fcd\u0151art\u00e9ria simaizomzat\u00e1nak prolifer\u00e1ci\u00f3ja \u00e9s myometriz\u00e1ci\u00f3ja elleni k\u00fczdelemben \u00e9s a CMS kezel\u00e9s\u00e9ben.
\nAz ET-1 az eddig felfedezett leger\u0151sebb \u00e9r\u00f6sszeh\u00faz\u00f3, \u00e9s a hipoxia jelent\u0151sen megn\u00f6velheti az ET-1 szintj\u00e9t a v\u00e9rben. Rajput \u00e9s munkat\u00e1rsai \u00f6sszehasonl\u00edtott\u00e1k az ET-1 all\u00e9lok k\u00fcl\u00f6nbs\u00e9geit a magashegyi \u00e9s a s\u00edkvid\u00e9ki lakosok k\u00f6z\u00f6tt, \u00e9s azt tal\u00e1lt\u00e1k, hogy az ET-1 bizonyos all\u00e9ljai a magashegyi lakosokn\u00e1l t\u00falterjedtek, \u00e9s az ET-l all\u00e9l kifejez\u0151d\u00e9se szignifik\u00e1nsan korrel\u00e1lt a plazma ET-1 szintj\u00e9vel. Ebben a cikkben a Mod patk\u00e1nyok t\u00fcd\u0151sz\u00f6vet\u00e9nek ET-1 tartalma jelent\u0151sen megn\u0151tt, ami azt jelzi, hogy a hipoxia az ET-1 fokozott szekr\u00e9ci\u00f3j\u00e1t induk\u00e1lta a t\u00fcd\u0151sz\u00f6vetben, \u00f6sszhangban m\u00e1s vizsg\u00e1latokkal. A PhGC-k bead\u00e1sa cs\u00f6kkentheti az ET-1 tartalm\u00e1t a CMS patk\u00e1nyok t\u00fcd\u0151sz\u00f6vet\u00e9ben, ami azt jelzi, hogy a PhGC-k g\u00e1tolhatj\u00e1k az ET-1 \u00e1ltal induk\u00e1lt \u00e9rsz\u0171k\u00fcletet, cs\u00f6kkenthetik a t\u00fcd\u0151art\u00e9ria nyom\u00e1s\u00e1t, \u00e9s ter\u00e1pi\u00e1s hat\u00e1st gyakorolhatnak a CMS-re.
\nEzt k\u00f6vet\u0151en a PhGC-k HIF-1 \u03b1-ra, VEGF-re \u00e9s PPAR - \u03b1-ra gyakorolt hat\u00e1s\u00e1nak megfigyel\u00e9s\u00e9re \u00f6sszpontos\u00edtottunk a hipoxia induk\u00e1lta \u00fatvonalon. Az mRNS \u00e9s feh\u00e9rje expresszi\u00f3j\u00e1t az egyes csoportokba tartoz\u00f3 patk\u00e1nyok t\u00fcd\u0151sz\u00f6veteiben immunhisztok\u00e9miai, fluoreszcens kvantitat\u00edv PCR \u00e9s Western blot m\u00f3dszerekkel mutattuk ki. Az immunhisztok\u00e9miai eredm\u00e9nyek azt mutatt\u00e1k, hogy a VEGF expresszi\u00f3s szintje a Mod patk\u00e1nyok t\u00fcd\u0151art\u00e9ri\u00e1iban magasabb volt, mint a Con eset\u00e9ben, m\u00edg a PPAR - \u03b1 expresszi\u00f3s szintje alacsonyabb volt, mint a Con eset\u00e9ben. A VEGF expresszi\u00f3s szintje a PhGCs alacsony, k\u00f6zepes, PhGCs-H \u00e9s RC csoportok t\u00fcd\u0151art\u00e9ri\u00e1iban alacsonyabb volt, mint a Mod csoport\u00e9, m\u00edg a PPAR - \u03b1 expresszi\u00f3s szintje emelkedett. Ez azt jelzi, hogy a PhGCs \u00e9s a Rhodiola rosea k\u00e9pes g\u00e1tolni a hipoxia \u00e1ltal induk\u00e1lt VEGF expresszi\u00f3j\u00e1t, el\u0151seg\u00edteni a PPAR - \u03b1 expresszi\u00f3j\u00e1t, \u00e9s enyh\u00edteni a t\u00fcd\u0151 \u00e9rrendszeri prolifer\u00e1ci\u00f3t \u00e9s a myogenezist, \u00edgy ter\u00e1pi\u00e1s szerepet j\u00e1tszik a CMS-ben. A HIF-1 \u03b1 feh\u00e9rje \u00e9s mRNS expresszi\u00f3j\u00e1nak k\u00eds\u00e9rleti m\u00e9r\u00e9se r\u00e9v\u00e9n a t\u00fcd\u0151sz\u00f6vetben azt tal\u00e1lt\u00e1k, hogy a HIF-1 \u03b1 feh\u00e9rje expresszi\u00f3ja a CMS modellpatk\u00e1nyok t\u00fcd\u0151sz\u00f6vet\u00e9ben jelent\u0151sen megn\u0151tt, m\u00edg az mRNS \u00e9s a Con expresszi\u00f3ja nem mutatott k\u00fcl\u00f6nbs\u00e9get. Ez \u00f6sszhangban van a vonatkoz\u00f3 kutat\u00e1si eredm\u00e9nyekkel, amelyek szerint a hipoxia els\u0151sorban a HIF-1 \u03b1 feh\u00e9rje expresszi\u00f3j\u00e1t szab\u00e1lyozza. A PhGC-k jelent\u0151sen cs\u00f6kkenthetik a HIF-1 \u03b1 feh\u00e9rje \u00e9s az mRNS expresszi\u00f3s szintj\u00e9t, ami azt jelzi, hogy hat\u00e1ssal lehetnek a HIF-1 \u03b1 transzkripci\u00f3j\u00e1ra \u00e9s transzl\u00e1ci\u00f3j\u00e1ra. A Rhodiola rosea azonban nem volt jelent\u0151s hat\u00e1ssal a HIF-1 \u03b1 mRNS expresszi\u00f3j\u00e1ra, ami azt jelzi, hogy a hipoxi\u00e1hoz hasonl\u00f3an els\u0151sorban a feh\u00e9rje expresszi\u00f3j\u00e1t befoly\u00e1solja.
\n\u00d6sszess\u00e9g\u00e9ben a h\u00e1rom PhGCs-d\u00f3zis k\u00f6z\u00fcl a PhGCs-M csoport mutatta a legjobb hat\u00e1st a CMS-re, m\u00edg a PhGCs-H kezel\u00e9s nem mutatott jelent\u0151s javul\u00e1st, ami \u00f6sszef\u00fcgghet a PhGCs-H b\u00e9lrendszeri felsz\u00edv\u00f3d\u00e1si sebess\u00e9g\u00e9nek cs\u00f6kken\u00e9s\u00e9vel. A Rhodiola rosea-val \u00f6sszehasonl\u00edtva a PhGCs-M jobb ter\u00e1pi\u00e1s hat\u00e1st fejtett ki a HIF-1 \u03b1 mRNS \u00e9s a VEGF mRNS mutat\u00f3kra. Az er\u0151forr\u00e1s-el\u0151ny\u00f6kkel egy\u00fctt a PhGCs bizonyos fejleszt\u00e9si kil\u00e1t\u00e1sokkal rendelkezik.<\/p>","protected":false},"excerpt":{"rendered":"

Study on the therapeutic effect and mechanism of Cistanche deserticola phenylethanoid glycoside on chronic high altitude disease model rats High altitude disease is a general term for various clinical manifestations caused by the body’s inability to adapt to low-pressure hypoxia at high altitudes, resulting in a series of pathological and physiological changes in the body. 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