{"id":9182,"date":"2024-08-15T19:37:41","date_gmt":"2024-08-15T19:37:41","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=9182"},"modified":"2024-08-15T19:37:41","modified_gmt":"2024-08-15T19:37:41","slug":"removing-blood-stasis","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/a-ver-pangasanak-megszuntetese\/","title":{"rendered":"A hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szat a v\u00e9r pang\u00e1s\u00e1nak elt\u00e1vol\u00edt\u00e1s\u00e1ra \u00e9s a kollater\u00e1lisok aktiv\u00e1l\u00e1s\u00e1ra jav\u00edtja a vese gyullad\u00e1s\u00e1t a cukorbetegs\u00e9gben szenved\u0151 nefrop\u00e1tia patk\u00e1nyokban a makrof\u00e1g besziv\u00e1rg\u00e1s \u00e9s aktiv\u00e1l\u00e1s g\u00e1tl\u00e1s\u00e1val a TAK1 \/ JNK \u00fatvonalon kereszt\u00fcl"},"content":{"rendered":"<p>A hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szat a v\u00e9r pang\u00e1s\u00e1nak elt\u00e1vol\u00edt\u00e1s\u00e1ra \u00e9s a kollater\u00e1lisok aktiv\u00e1l\u00e1s\u00e1ra jav\u00edtja a vese gyullad\u00e1s\u00e1t a cukorbetegs\u00e9gben szenved\u0151 nefrop\u00e1tia patk\u00e1nyokban a makrof\u00e1g besziv\u00e1rg\u00e1s \u00e9s aktiv\u00e1l\u00e1s g\u00e1tl\u00e1s\u00e1val a TAK1 \/ JNK \u00fatvonalon kereszt\u00fcl<br \/>\nA diab\u00e9teszes nefrop\u00e1tia (DN) a cukorbetegs\u00e9g gyakori \u00e9s s\u00falyos sz\u00f6v\u0151dm\u00e9nye, \u00e9s vil\u00e1gszerte a v\u00e9gst\u00e1dium\u00fa vesebetegs\u00e9g els\u0151dleges oka. Jelenleg a DN kezel\u00e9se els\u0151sorban a n\u00e1triumbevitel korl\u00e1toz\u00e1s\u00e1t, a v\u00e9rcukorszint szab\u00e1lyoz\u00e1s\u00e1t, a v\u00e9rnyom\u00e1s cs\u00f6kkent\u00e9s\u00e9t \u00e9s a renin-angiotenzin rendszer (RAS) blokkol\u00e1s\u00e1t foglalja mag\u00e1ban. B\u00e1r ez bizonyos m\u00e9rt\u00e9kig k\u00e9sleltetheti a DN progresszi\u00f3j\u00e1t, hat\u00e9konys\u00e1ga nem ide\u00e1lis. Egyre t\u00f6bb bizony\u00edt\u00e9k utal arra, hogy a gyullad\u00e1sos v\u00e1lasz fontos szerepet j\u00e1tszik a diab\u00e9teszes nefrop\u00e1tia kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben, \u00e9s a makrof\u00e1gok infiltr\u00e1ci\u00f3ja \u00e9s aktiv\u00e1ci\u00f3ja k\u00f6zponti l\u00e1ncszem a vese gyullad\u00e1s\u00e1ban. A TAK1\/JNK jel\u00e1tviteli \u00fatvonal fontos \u00fatvonal, amely szab\u00e1lyozza a makrof\u00e1gok besziv\u00e1rg\u00e1s\u00e1t \u00e9s aktiv\u00e1l\u00f3d\u00e1s\u00e1t. Ez\u00e9rt a TAK1\/JNK jel\u00e1tviteli \u00fatvonal blokkol\u00e1sa hat\u00e9kony strat\u00e9gia a DN megel\u0151z\u00e9s\u00e9re \u00e9s kezel\u00e9s\u00e9re.<\/p>\n<p>Kutat\u00f3csoportunk \u00fagy v\u00e9li, hogy a \"v\u00e9r pang\u00e1sa akad\u00e1lyozza a kollater\u00e1lisokat\" a diab\u00e9teszes nefrop\u00e1tia alapvet\u0151 patogenezise, \u00e9s a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s hozz\u00e1ad\u00e1sa a v\u00e9r pang\u00e1s\u00e1nak elt\u00e1vol\u00edt\u00e1s\u00e1ra \u00e9s a kollater\u00e1lisok el\u0151seg\u00edt\u00e9s\u00e9re a szindr\u00f3ma megk\u00fcl\u00f6nb\u00f6ztet\u00e9se \u00e9s kezel\u00e9se alapj\u00e1n a diab\u00e9teszes nefrop\u00e1tia kezel\u00e9s\u00e9nek alapelv\u00e9v\u00e9 v\u00e1lt. A v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re \u00e9s a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re szolg\u00e1l\u00f3 hagyom\u00e1nyos k\u00ednai orvosl\u00e1s sz\u00e1mos gy\u00f3gyszert tartalmaz. T\u00f6bb mint 20 \u00e9v klinikai gyakorlat \u00e9s ism\u00e9telt sz\u0171r\u00e9s ut\u00e1n kutat\u00f3csoportunk v\u00e9g\u00fcl \u00f6t k\u00ednai gy\u00f3gyszert, nevezetesen a Chuanxiong, Danshen, Dilong, Pi\u00f3ca \u00e9s Skorpi\u00f3t hat\u00e1rozta meg, mint a DN kezel\u00e9s\u00e9nek viszonylag r\u00f6gz\u00edtett alapgy\u00f3gyszereit. Kor\u00e1bbi kutat\u00e1saink meger\u0151s\u00edtett\u00e9k, hogy a v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re \u00e9s a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re szolg\u00e1l\u00f3 hagyom\u00e1nyos k\u00ednai gy\u00f3gyszerek g\u00e1tolj\u00e1k a vese RAS aktiv\u00e1l\u00f3d\u00e1s\u00e1t DN patk\u00e1nyokban, cs\u00f6kkentik a podocita p\u00f3rus membr\u00e1n feh\u00e9rje \u00e9s citoszkelet\u00e1lis feh\u00e9rje vesztes\u00e9g\u00e9t, \u00e9s k\u00e9sleltetik a DN progresszi\u00f3j\u00e1t. Jelenleg azonban nincs kutat\u00e1s ennek a gy\u00f3gyszernek a gyullad\u00e1sos v\u00e1lasz\u00e1ra vonatkoz\u00f3an DN \u00e1llapotban. Ennek f\u00e9ny\u00e9ben ez a tanulm\u00e1ny az SD patk\u00e1nyokat veszi kutat\u00e1si t\u00e1rgynak, hogy megfigyelje a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s hat\u00e1sait a v\u00e9r pang\u00e1s\u00e1nak elt\u00e1vol\u00edt\u00e1s\u00e1ra \u00e9s a kollater\u00e1lisok el\u0151seg\u00edt\u00e9s\u00e9re a makrof\u00e1gok besziv\u00e1rg\u00e1s\u00e1ra, aktiv\u00e1l\u00e1s\u00e1ra \u00e9s a TAK1 \/ JNK jel\u00e1tviteli \u00fatvonalra a DN patk\u00e1nyok vesesz\u00f6vet\u00e9ben, tov\u00e1bb tiszt\u00e1zva a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s c\u00e9lpontjait a v\u00e9r pang\u00e1s\u00e1nak elt\u00e1vol\u00edt\u00e1s\u00e1ra \u00e9s a kollater\u00e1lisok el\u0151seg\u00edt\u00e9s\u00e9re, \u00e9s k\u00eds\u00e9rleti alapot ny\u00fajtva a klinikai alkalmaz\u00e1shoz.<\/p>\n<p>40 SD patk\u00e1nyb\u00f3l 10 patk\u00e1nyt v\u00e9letlenszer\u0171en kiv\u00e1lasztottak norm\u00e1l csoportnak (C csoport), a t\u00f6bbi 30 patk\u00e1nyt pedig egyszeri intraperitone\u00e1lis sztreptozotocin (STZ, 40 mg\/kg) injekci\u00f3val etett\u00e9k, magas cukor- \u00e9s zs\u00edrtartalm\u00fa \u00e9trenddel kombin\u00e1lva, hogy cukorbetegs\u00e9g-modelleket hozzanak l\u00e9tre. A sikeresen modellezett patk\u00e1nyokat v\u00e9letlenszer\u0171en egy modellcsoportra (M csoport) \u00e9s egy k\u00ednai gy\u00f3gyn\u00f6v\u00e9nyes gy\u00f3gyszercsoportra (Z csoport) osztottuk. A Z csoport hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szati beavatkoz\u00e1st kapott. 16 h\u00e9t eltelt\u00e9vel 24 \u00f3r\u00e1s vizeletfeh\u00e9rje-kvantit\u00e1st (24 \u00f3r\u00e1s UTP) v\u00e9geztek minden patk\u00e1nycsoportban; ELISA-m\u00f3dszerrel kimutatt\u00e1k a monocita kemoattrakt\u00e1ns protein-1 (MCP-1), az interleukin-1 \u03b2 (IL-1 \u03b2) \u00e9s a tumor nekr\u00f3zis faktor - \u03b1 (TNF - \u03b1) expresszi\u00f3j\u00e1t a sz\u00e9rumban; Vese sz\u00f6vetet gy\u0171jt\u00f6tt\u00fcnk, \u00e9s immunfluoreszcenci\u00e1val kimutattuk a makrof\u00e1g marker feh\u00e9rje CD68 \u00e9s a klasszikus aktiv\u00e1lt makrof\u00e1g marker feh\u00e9rje, az induk\u00e1lhat\u00f3 nitrog\u00e9n-oxid szint\u00e1z (iNOS) expresszi\u00f3j\u00e1t. Western blotot haszn\u00e1ltunk a TAK1\/JNK jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3d\u00f3 feh\u00e9rj\u00e9k, k\u00f6zt\u00fck a transzform\u00e1l\u00f3 n\u00f6veked\u00e9si faktor aktiv\u00e1lt kin\u00e1z-1 (TAK1), p-TAK1, c-Jun N-termin\u00e1lis kin\u00e1z (JNK) \u00e9s p-JNK expresszi\u00f3j\u00e1nak kimutat\u00e1s\u00e1ra.<\/p>\n<p>Az elm\u00falt \u00e9vekben a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s m\u00e9lyebben meg\u00e9rtette a diab\u00e9teszes nefrop\u00e1ti\u00e1t, a legt\u00f6bb orvos a v\u00e9r pang\u00e1s\u00e1n alapulva \u00e9rvel. A szomj\u00fas\u00e1gt\u00f3l szenvedve a Qi hi\u00e1nya \u00e9s a v\u00e9r sz\u00e1ll\u00edt\u00e1s\u00e1nak k\u00e9ptelens\u00e9ge k\u00e9sleltetett v\u00e9r\u00e1raml\u00e1shoz vezet, ami id\u0151vel fokozatosan v\u00e9rstasishoz vezet; a Yin hi\u00e1nya \u00e9s a t\u00falzott t\u0171z a testnedvek szenved\u00e9s\u00e9t okozhatja, ami el\u00e9gtelen testnedveket \u00e9s rossz v\u00e9rkering\u00e9st eredm\u00e9nyez. Ez id\u0151vel v\u00e9r pang\u00e1shoz vezethet. A \"V\u00e9rszindr\u00f3ma elm\u00e9let: Blood Stasis\" (V\u00e9rst\u00e1zis) kimondja: \"Amikor a v\u00e9r pang\u00e1sa a meridi\u00e1nok \u00e9s a szervek k\u00f6z\u00f6tt jelentkezik, ez k\u00e9pezi a betegs\u00e9g gy\u00f6ker\u00e9t\". Az \"Orvosi iskola alapvet\u0151 olvasm\u00e1nyai\" kimondja: \"A v\u00e9r pang\u00e1s\u00e1nak felhalmoz\u00f3d\u00e1sa igazs\u00e1gos, az id\u0151 m\u00fal\u00e1s\u00e1val, \u00e9jjel-nappal felhalmoz\u00f3dik\". Ha a v\u00e9r pang\u00e1sa fenn\u00e1ll \u00e9s nem gy\u00f3gyul, azt meridi\u00e1n- \u00e9s j\u00e1rul\u00e9kos betegs\u00e9gek okozz\u00e1k. A DN lefoly\u00e1sa hosszadalmas, \u00edgy a lefoly\u00e1sa megfelel a hagyom\u00e1nyos k\u00ednai orvosl\u00e1sban szerepl\u0151 v\u00e1ltoz\u00e1soknak, mint p\u00e9ld\u00e1ul az aggreg\u00e1ci\u00f3 \u00e9s a kialakul\u00e1s, az id\u0151vel val\u00f3 felhalmoz\u00f3d\u00e1s, valamint a szt\u00e1zis \u00e9s a kollater\u00e1lisok elz\u00e1r\u00f3d\u00e1sa. A \"kollater\u00e1lisokat elz\u00e1r\u00f3 v\u00e9rst\u00e1zis\" elve a kezdetekt\u0151l a v\u00e9g\u00e9ig \u00e1thatja a DN-t, \u00e9s ez az alapvet\u0151 patogenezise. A v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9nek, a v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9nek \u00e9s a kollater\u00e1lisok elz\u00e1r\u00f3d\u00e1s\u00e1nak felold\u00e1s\u00e1nak m\u00f3dszere a DN alapvet\u0151 kezel\u00e9si elve lett. Ezt a v\u00e9r pang\u00e1s\u00e1t azonban neh\u00e9z feloldani a felhalmoz\u00f3d\u00e1sa miatt, ami a hagyom\u00e1nyos v\u00e9raktiv\u00e1l\u00f3 \u00e9s pang\u00e1st megsz\u00fcntet\u0151 gy\u00f3gyszerek hat\u00f3k\u00f6r\u00e9n k\u00edv\u00fcl esik. Ez\u00e9rt a kutat\u00f3csoportunk a hagyom\u00e1nyos v\u00e9raktiv\u00e1l\u00f3 \u00e9s szt\u00e1zis elt\u00e1vol\u00edt\u00f3 gy\u00f3gyszerek, mint a Danshen \u00e9s a Chuanxiong haszn\u00e1lata alapj\u00e1n pi\u00f3c\u00e1kat, f\u00f6ldigiliszt\u00e1kat, skorpi\u00f3kat \u00e9s m\u00e1s speci\u00e1lis gy\u00f3gyszereket adott hozz\u00e1 a meridi\u00e1nok kotr\u00e1s\u00e1ra \u00e9s a parazit\u00e1k elt\u00e1vol\u00edt\u00e1s\u00e1ra. A Danshen a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re \u00e9s a v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re szolg\u00e1l\u00f3 alapvet\u0151 gy\u00f3gyszer, amelynek f\u0151 hat\u00f3anyagai a szalvianolsavak \u00e9s a tansinonok. A modern farmakol\u00f3giai vizsg\u00e1latok kimutatt\u00e1k, hogy a Danshen k\u00e9pes szab\u00e1lyozni a gl\u00fck\u00f3z- \u00e9s lipidanyagcser\u00e9t DN-betegekben \u00e9s k\u00eds\u00e9rleti \u00e1llatokban, g\u00e1tolja az oxidat\u00edv stresszt, a gyullad\u00e1st \u00e9s a fibr\u00f3zist, valamint v\u00e9di a vesefunkci\u00f3t. A Chuanxiong a v\u00e9rkering\u00e9st \u00e9s a qi-kering\u00e9st el\u0151seg\u00edt\u0151 hat\u00e1s\u00fa. F\u0151 hat\u00f3anyagai a ligusztrazin \u00e9s a ferulasav. A modern farmakol\u00f3giai vizsg\u00e1latok kimutatt\u00e1k, hogy a Chuanxiong k\u00fcl\u00f6nb\u00f6z\u0151 biol\u00f3giai tev\u00e9kenys\u00e9gekkel rendelkezik, p\u00e9ld\u00e1ul g\u00e1tolja a v\u00e9rlemezk\u00e9k aggreg\u00e1ci\u00f3j\u00e1t \u00e9s a tromb\u00f3zist, cs\u00f6kkenti a v\u00e9r viszkozit\u00e1s\u00e1t, cs\u00f6kkenti a mezangiumsejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s g\u00e1tolja az endot\u00e9lsejtek prolifer\u00e1ci\u00f3j\u00e1t. A pi\u00f3c\u00e1k hat\u00e9konys\u00e1ga a v\u00e9r megt\u00f6r\u00e9se, a v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9se \u00e9s a menstru\u00e1ci\u00f3 el\u0151seg\u00edt\u00e9se. A pi\u00f3c\u00e1k f\u0151 hat\u00f3anyaga a hirudin, amely antikoagul\u00e1ns, antitrombotikus, lipidcs\u00f6kkent\u0151, gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1s\u00fa, g\u00e1tolja az epiteli\u00e1lis-mesenchim\u00e1lis \u00e1tmenetet, cs\u00f6kkenti a vese tubul\u00e1ris epit\u00e9lsejtek apopt\u00f3zis\u00e1t \u00e9s enyh\u00edti a vesefibr\u00f3zist. A f\u00f6ldigiliszt\u00e1knak a v\u00e9rkering\u00e9st \u00e9s a diur\u00e9zist el\u0151seg\u00edt\u0151 hat\u00e1sai vannak a vesebetegs\u00e9gek kezel\u00e9s\u00e9ben. A Lumbricus f\u00f6ldigiliszta kin\u00e1zt tartalmaz, amelynek hat\u00e1sai jav\u00edtj\u00e1k a fibrinolitikus rendszer egyens\u00falyhi\u00e1ny\u00e1t, g\u00e1tolj\u00e1k a v\u00e9rlemezke-aktiv\u00e1ci\u00f3t, szab\u00e1lyozz\u00e1k a lipidanyagcsere-zavarokat, \u00e9s g\u00e1tolj\u00e1k a glomerul\u00e1ris mezangiumsejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s az extracellul\u00e1ris m\u00e1trix t\u00falzott felhalmoz\u00f3d\u00e1s\u00e1t. A skorpi\u00f3 hat\u00e1s\u00e1ra eloszlatja a szelet, felszabad\u00edtja a meridi\u00e1nokat \u00e9s feloldja a csom\u00f3kat. A modern farmakol\u00f3giai vizsg\u00e1latok kimutatt\u00e1k, hogy a skorpi\u00f3 antikoagul\u00e1l, antitrombotikus, el\u0151seg\u00edti a fibrinol\u00edzist, n\u00f6veli a vese v\u00e9r\u00e1raml\u00e1s\u00e1t \u00e9s cs\u00f6kkenti a proteinuri\u00e1t. Ezen \u00f6t gy\u00f3gyn\u00f6v\u00e9ny kombin\u00e1ci\u00f3ja k\u00e9pes feloldani a meridi\u00e1nok elz\u00e1r\u00f3d\u00e1s\u00e1t \u00e9s megsz\u00fcntetni a v\u00e9r pang\u00e1s\u00e1t.<\/p>\n<p>A leg\u00fajabb vizsg\u00e1latok kimutatt\u00e1k, hogy a makrof\u00e1gok besziv\u00e1rg\u00e1sa a DN gyullad\u00e1sos v\u00e1lasz egyik jellegzetes megnyilv\u00e1nul\u00e1sa. Makrof\u00e1g infiltr\u00e1ci\u00f3t tal\u00e1ltak mind a DN betegekn\u00e9l, mind a DN \u00e1llatmodellekben, \u00e9s az infiltr\u00e1ci\u00f3 m\u00e9rt\u00e9ke pozit\u00edvan korrel\u00e1lt a DN proteinuri\u00e1val \u00e9s a vesefunkci\u00f3 zavar\u00e1val. A kutat\u00e1sok kimutatt\u00e1k, hogy a vesebetegs\u00e9g kialakul\u00e1s\u00e1nak ir\u00e1ny\u00e1t meghat\u00e1roz\u00f3 f\u0151 t\u00e9nyez\u0151 nem a makrof\u00e1g infiltr\u00e1ci\u00f3 mennyis\u00e9ge, hanem a makrof\u00e1gok aktiv\u00e1ci\u00f3s \u00e1llapota a helyi sz\u00f6vetekben. A vesek\u00e1rosod\u00e1st k\u00f6vet\u0151en a v\u00e9rben l\u00e9v\u0151 monocit\u00e1k a vesesz\u00f6vetbe v\u00e1ndorolnak \u00e9s makrof\u00e1gokk\u00e1 differenci\u00e1l\u00f3dnak. A makrof\u00e1gok egy adott mikrok\u00f6rnyezetben k\u00e9t k\u00fcl\u00f6nb\u00f6z\u0151 aktiv\u00e1ci\u00f3s fenot\u00edpusra tesznek szert, nevezetesen klasszikusan aktiv\u00e1lt makrof\u00e1gokra (M1) \u00e9s nem klasszikusan aktiv\u00e1lt makrof\u00e1gokra (M2). Az M1 makrof\u00e1gok k\u00f6zvet\u00edtik a vesegyullad\u00e1st \u00e9s a fibr\u00f3zist az iNOS, kemokinek (MCP-1, IL-8) \u00e9s pro-inflammatorikus faktorok (TNF - \u03b1, IL-1 \u03b2) szekr\u00e9ci\u00f3j\u00e1val; az M2 gyullad\u00e1sg\u00e1tl\u00f3 faktorokat termel, mint p\u00e9ld\u00e1ul az IL-1 \u00e9s IL-10, amelyek gyullad\u00e1sg\u00e1tl\u00f3 \u00e9s sz\u00f6vetjav\u00edt\u00f3 funkci\u00f3val rendelkeznek. Az INOS az M1 makrof\u00e1gok aktiv\u00e1l\u00f3d\u00e1s\u00e1nak markere. A vesek\u00e1rosod\u00e1s korai szakasz\u00e1ban els\u0151sorban az M1 makrof\u00e1gok infiltr\u00e1l\u00f3dnak, \u00e9s olyan gyullad\u00e1sos faktorokat szabad\u00edtanak fel, mint az MCP-1, IL-1 \u03b2, TNF - \u03b1, ROS stb., ami kiv\u00e1ltja \u00e9s fokozza a gyullad\u00e1sos v\u00e1laszt. Ebben a vizsg\u00e1latban a norm\u00e1l csoporttal \u00f6sszehasonl\u00edtva a patk\u00e1nyok modellcsoportja a CD68 pozit\u00edv makrof\u00e1gok aggreg\u00e1ci\u00f3j\u00e1nak n\u00f6veked\u00e9s\u00e9t mutatta a vesesz\u00f6vetben, az M1 makrof\u00e1g aktiv\u00e1ci\u00f3s marker iNOS expresszi\u00f3j\u00e1nak n\u00f6veked\u00e9s\u00e9t, \u00e9s a gyullad\u00e1sos faktorok, mint az MCP-1, IL-1 \u03b2, TNF - \u03b1 szintj\u00e9nek n\u00f6veked\u00e9s\u00e9t. A v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re \u00e9s a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re szolg\u00e1l\u00f3 k\u00ednai n\u00f6v\u00e9nyi gy\u00f3gyszer g\u00e1tolhatja a vese makrof\u00e1gok besziv\u00e1rg\u00e1s\u00e1t, aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s gyullad\u00e1sos faktorainak felszabadul\u00e1s\u00e1t DN patk\u00e1nyokban, ez\u00e1ltal cs\u00f6kkentve a vesegyullad\u00e1st.<\/p>\n<p>A makrof\u00e1gok besziv\u00e1rg\u00e1sa \u00e9s aktiv\u00e1ci\u00f3ja a DN vesesz\u00f6vetben szorosan \u00f6sszef\u00fcgg a TAK1\/JNK jel\u00e1tviteli \u00fatvonallal. A JNK a mitog\u00e9n aktiv\u00e1lt feh\u00e9rje kin\u00e1z csal\u00e1dba (MAPK) tartozik. Minden MAPK-csal\u00e1d h\u00e1rom kin\u00e1zb\u00f3l \u00e1ll, amelyek egym\u00e1s ut\u00e1n hatnak: MAPKK-kin\u00e1z (MAPKKK), MAPK-kin\u00e1z (MAPKK) \u00e9s MAPK. Az aktiv\u00e1lt MAPKKK k\u00e9pes foszforil\u00e1lni a MAPKK-t \u00e9s aktiv\u00e1lni azt. Az aktiv\u00e1lt MAPKK foszforil\u00e1lja a MAPK-t \u00e9s aktiv\u00e1lja azt. Az aktiv\u00e1lt MAPK transzlok\u00e1l\u00f3dhat a sejtmagba, hogy szab\u00e1lyozza a c\u00e9lg\u00e9nek transzkripci\u00f3j\u00e1t. Az elm\u00falt \u00e9vekben \u00e1llat- \u00e9s sejtk\u00eds\u00e9rletek meger\u0151s\u00edtett\u00e9k, hogy a JNK \u00fatvonal el\u0151seg\u00edti a vese gyullad\u00e1sos v\u00e1lasz\u00e1t. A TAK1 a MAPKKK csal\u00e1dba tartoz\u00f3 szerin\/treonin kin\u00e1z, amely a JNK el\u0151tt helyezkedik el, \u00e9s fontos jel\u00e1tviteli molekula a JNK jel\u00e1tvitelben. A TAK1\/JNK jel\u00e1tviteli \u00fatvonal aktiv\u00e1l\u00f3d\u00e1sa megfigyelhet\u0151 olyan vesebetegs\u00e9gekben, mint a DN, az IgA nefrop\u00e1tia \u00e9s a vese\u00e1t\u00fcltet\u00e9ses iszk\u00e9mia\/reperf\u00fazi\u00f3, \u00e9s szorosan \u00f6sszef\u00fcgg a gyullad\u00e1sos v\u00e1lasz progresszi\u00f3j\u00e1val. UUO egerekben a TAK1\/JNK jel\u00e1tviteli \u00fatvonal g\u00e1tl\u00e1sa cs\u00f6kkentheti a makrof\u00e1g infiltr\u00e1ci\u00f3t, g\u00e1tolhatja az M1 makrof\u00e1gok aktiv\u00e1l\u00f3d\u00e1s\u00e1t \u00e9s cs\u00f6kkentheti a gyullad\u00e1sos faktorok szintj\u00e9t. Ebben a vizsg\u00e1latban a norm\u00e1l csoporthoz k\u00e9pest a TAK1\/JNK jel\u00e1tviteli \u00fatvonal jelent\u0151sen aktiv\u00e1l\u00f3dott a DN patk\u00e1nyokban. A v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re \u00e9s a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re szolg\u00e1l\u00f3 k\u00ednai n\u00f6v\u00e9nyi gy\u00f3gyszer jelent\u0151sen cs\u00f6kkentheti a TAK1\/JNK jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3d\u00f3 feh\u00e9rj\u00e9k expresszi\u00f3j\u00e1t \u00e9s g\u00e1tolhatja a TAK1\/JNK jel\u00e1tviteli \u00fatvonal aktiv\u00e1l\u00f3d\u00e1s\u00e1t.<\/p>\n<p>\u00d6sszefoglalva, kutat\u00e1si eredm\u00e9nyeink azt mutatj\u00e1k, hogy a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s a v\u00e9r pang\u00e1s\u00e1nak megsz\u00fcntet\u00e9s\u00e9re \u00e9s a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9re jav\u00edthatja a proteinuri\u00e1t \u00e9s enyh\u00edtheti a vese gyullad\u00e1s\u00e1t DN patk\u00e1nyokn\u00e1l. A hat\u00e1smechanizmus a TAK1\/JNK jel\u00e1tviteli \u00fatvonal \u00e1ltal k\u00f6zvet\u00edtett makrof\u00e1g infiltr\u00e1ci\u00f3, aktiv\u00e1ci\u00f3 \u00e9s gyullad\u00e1sos faktorok felszabadul\u00e1s\u00e1nak g\u00e1tl\u00e1s\u00e1val f\u00fcgghet \u00f6ssze.<\/p>","protected":false},"excerpt":{"rendered":"<p>Traditional Chinese Medicine for Removing Blood Stasis and Activating Collaterals Improves Renal Inflammation in diabetes Nephropathy Rats by Inhibiting Macrophage Infiltration and Activation through TAK1\/JNK Pathway Diabetes nephropathy (DN) is a common and serious complication of diabetes and the primary cause of end-stage renal disease worldwide. At present, the treatment of DN mainly includes limiting [&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>Traditional Chinese Medicine for Removing Blood Stasis and Activating Collaterals Improves Renal Inflammation in diabetes Nephropathy Rats by Inhibiting Macrophage Infiltration and Activation through TAK1\/JNK Pathway - 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\/a-ver-pangasanak-megszuntetese\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Traditional Chinese Medicine for Removing Blood Stasis and Activating Collaterals Improves Renal Inflammation in diabetes Nephropathy Rats by Inhibiting Macrophage Infiltration and Activation through TAK1\/JNK Pathway - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Traditional Chinese Medicine for Removing Blood Stasis and Activating Collaterals Improves Renal Inflammation in diabetes Nephropathy Rats by Inhibiting Macrophage Infiltration and Activation through TAK1\/JNK Pathway Diabetes nephropathy (DN) is a common and serious complication of diabetes and the primary cause of end-stage renal disease worldwide. 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