{"id":7931,"date":"2024-08-11T09:50:54","date_gmt":"2024-08-11T09:50:54","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=7931"},"modified":"2024-08-11T09:50:54","modified_gmt":"2024-08-11T09:50:54","slug":"guanggancao-ding","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/guanggancao-ding\/","title":{"rendered":"A Guanggancao Ding hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a kasztr\u00e1ci\u00f3s rezisztens prosztatar\u00e1k kezel\u00e9s\u00e9ben a h\u00e1l\u00f3zati farmakol\u00f3gia \u00e9s a k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n"},"content":{"rendered":"

A Guanggancao Ding hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a kasztr\u00e1ci\u00f3s rezisztens prosztatar\u00e1k kezel\u00e9s\u00e9ben a h\u00e1l\u00f3zati farmakol\u00f3gia \u00e9s a k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n
\nA prosztatar\u00e1k (PCa) a leggyakoribb rosszindulat\u00fa daganat az id\u0151s f\u00e9rfiak reprodukt\u00edv rendszer\u00e9ben. Sok korai androg\u00e9nmegvon\u00e1sos kezel\u00e9s hat\u00e9kony, de a legt\u00f6bb esetben a hormon\u00e9rz\u00e9keny prosztatar\u00e1k v\u00e9g\u00fcl kasztr\u00e1ci\u00f3rezisztens prosztatar\u00e1kk\u00e1 (CRPC) alakul. A CRPC rendk\u00edv\u00fcl hal\u00e1los \u00e9s invaz\u00edv prosztatar\u00e1k. A CRPC-betegek t\u00f6bb mint 84%-j\u00e9n\u00e9l alakul ki \u00e1tt\u00e9t, \u00e9s a medi\u00e1n t\u00fal\u00e9l\u00e9s mind\u00f6ssze 20 h\u00f3nap. B\u00e1r az elm\u00falt \u00e9vekben \u00faj kemoter\u00e1pi\u00e1s gy\u00f3gyszerek \u00e9s endokrin gy\u00f3gyszerek jelentek meg, ezeknek a kemoter\u00e1pi\u00e1s gy\u00f3gyszereknek sok mell\u00e9khat\u00e1sa van, az endokrin gy\u00f3gyszereknek pedig rezisztenciaprobl\u00e9m\u00e1i vannak, amelyek ler\u00f6vid\u00edtik a gy\u00f3gyszer hat\u00f3idej\u00e9t. Ez\u00e9rt az \u00faj gy\u00f3gyszerek megtal\u00e1l\u00e1sa nagy jelent\u0151s\u00e9ggel b\u00edr a kasztr\u00e1ci\u00f3s rezisztencia folyamat\u00e1nak k\u00e9sleltet\u00e9se \u00e9s a CRPC kezel\u00e9se szempontj\u00e1b\u00f3l.
\nA glabridin egy \u00e9desgy\u00f6k\u00e9rb\u0151l kivont flavonoid vegy\u00fclet, amely sz\u00e1mos biol\u00f3giai hat\u00e1ssal rendelkezik, p\u00e9ld\u00e1ul gyullad\u00e1scs\u00f6kkent\u0151, antioxid\u00e1ns, daganatellenes, neuroprotekt\u00edv \u00e9s csontritkul\u00e1s elleni. A jelent\u00e9sek szerint a glicirrizin j\u00f3 hat\u00e1ssal van a tumorsejtek prolifer\u00e1ci\u00f3j\u00e1nak g\u00e1tl\u00e1s\u00e1ra \u00e9s az apopt\u00f3zis kiv\u00e1lt\u00e1s\u00e1ra mellr\u00e1kban, m\u00e1jr\u00e1kban, gyomorr\u00e1kban \u00e9s m\u00e9hnyakr\u00e1kban. A glicirrizinnek a CRPC-re gyakorolt molekul\u00e1ris mechanizmusa azonban nem teljesen ismert. A h\u00e1l\u00f3zati farmakol\u00f3gia a farmakol\u00f3gia, az informatika \u00e9s a rendszerbiol\u00f3gi\u00e1n alapul\u00f3 inform\u00e1ci\u00f3s h\u00e1l\u00f3zatok kombin\u00e1ci\u00f3ja, amely \u00faj \u00f6tleteket ny\u00fajt a komplex betegs\u00e9gekben a gy\u00f3gyszerek felfedez\u00e9s\u00e9hez \u00e9s kiv\u00e1laszt\u00e1s\u00e1hoz. A Guanggancao Ding CRPC-re gyakorolt hat\u00e1smechanizmus\u00e1nak tov\u00e1bbi vizsg\u00e1lat\u00e1hoz h\u00e1l\u00f3zati farmakol\u00f3gi\u00e1t, molekul\u00e1ris dokkol\u00e1st \u00e9s sejtk\u00eds\u00e9rleteket haszn\u00e1ltunk a hat\u00e1smechanizmus felt\u00e1r\u00e1s\u00e1ra, referenci\u00e1t ny\u00fajtva a j\u00f6v\u0151beli gy\u00f3gyszeralapkutat\u00e1shoz \u00e9s klinikai alkalmaz\u00e1sokhoz.<\/p>\n

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\nAz elm\u00falt \u00e9vekben jelent\u0151s el\u0151rel\u00e9p\u00e9s t\u00f6rt\u00e9nt a prosztatar\u00e1k hagyom\u00e1nyos k\u00ednai orvosl\u00e1ssal t\u00f6rt\u00e9n\u0151 kezel\u00e9s\u00e9ben, k\u00fcl\u00f6n\u00f6sen a CRPC eset\u00e9ben. A hagyom\u00e1nyos k\u00ednai orvosl\u00e1s m\u0171t\u00e9ttel vagy kemoter\u00e1pi\u00e1val val\u00f3 kombin\u00e1ci\u00f3ja cs\u00f6kkenti a tumor m\u00e9ret\u00e9t, cs\u00f6kkenti a PSA-t, cs\u00f6kkenti a ki\u00fajul\u00e1st \u00e9s meghosszabb\u00edtja a t\u00fal\u00e9l\u00e9si id\u0151t. Sz\u00e1mos kutat\u00e1si jelent\u00e9s arra utal, hogy az \u00e9desgy\u00f6k\u00e9r hat\u00f3anyagai jelent\u0151s daganatellenes hat\u00e1ssal vannak a CRPC-re. Gioti \u00e9s munkat\u00e1rsai meg\u00e1llap\u00edtott\u00e1k, hogy az \u00e9desgy\u00f6k\u00e9r-kivonat (GGE) \u00f6nmag\u00e1ban vagy doxorubicinnel kombin\u00e1lva antiproliferat\u00edv hat\u00e1ssal van az androg\u00e9nf\u00fcggetlen prosztatar\u00e1kos sejtekre (PC-3 sejtek), \u00e9s el\u0151seg\u00edtheti az autof\u00e1gi\u00e1val kapcsolatos g\u00e9nek, p\u00e9ld\u00e1ul az LC3A, ULK1 \u00e9s AMBRA1 expresszi\u00f3j\u00e1t. Zhang \u00e9s munkat\u00e1rsai in vivo \u00e1llatk\u00eds\u00e9rleteken kereszt\u00fcl meg\u00e1llap\u00edtott\u00e1k, hogy az izoliquiritigenin k\u00e9pes g\u00e1tolni a prosztatar\u00e1ksejtek (PC-3 \u00e9s 22RV1) prolifer\u00e1ci\u00f3j\u00e1t, apopt\u00f3zist induk\u00e1lni, blokkolni a G2\/M sejtciklust \u00e9s g\u00e1tolni a PC-3 xenotranszplant\u00e1tumok n\u00f6veked\u00e9s\u00e9t. Az \u00e9desgy\u00f6k\u00e9r kiv\u00e1l\u00f3 CRPC-ellenes aktivit\u00e1st mutat, \u00e9s az \u00e9desgy\u00f6k\u00e9rben l\u00e9v\u0151 glicirrizin egyike a sok flavonoidnak, amely nagy figyelmet keltett \u00e9s j\u00f3 daganatellenes aktivit\u00e1ssal rendelkezik. A CRPC hat\u00e1smechanizmusa tov\u00e1bbi felt\u00e1r\u00e1st \u00e9rdemel.
\nA hagyom\u00e1nyos farmakol\u00f3gi\u00e1val \u00f6sszehasonl\u00edtva a h\u00e1l\u00f3zati farmakol\u00f3gia \u00faj perspekt\u00edv\u00e1t k\u00edn\u00e1l az \u00faj gy\u00f3gyszerek fejleszt\u00e9s\u00e9hez. Annak \u00e9rdek\u00e9ben, hogy jobban meg\u00e9rts\u00fck a glicirrizinnek a CRPC-re gyakorolt hat\u00e1smechanizmus\u00e1t, h\u00e1l\u00f3zati farmakol\u00f3giai m\u00f3dszereket alkalmaztunk a glicirrizinnek 683 c\u00e9lpontj\u00e1nak \u00f6sszegy\u0171jt\u00e9s\u00e9re olyan adatb\u00e1zisokon kereszt\u00fcl, mint a TCMIO, a TCMSP \u00e9s a PharmMapper. A Venn-diagram eszk\u00f6z\u00f6k seg\u00edts\u00e9g\u00e9vel a glicirrizinnek a kasztr\u00e1ci\u00f3s rezisztens prosztatar\u00e1k 55 kulcsfontoss\u00e1g\u00fa c\u00e9lpontj\u00e1t kaptuk meg, \u00e9s a PPI feh\u00e9rje k\u00f6lcs\u00f6nhat\u00e1si h\u00e1l\u00f3zat elemz\u00e9s\u00e9vel 10 f\u0151 c\u00e9lpontot azonos\u00edtottunk, mint p\u00e9ld\u00e1ul az AKT1, TP53, ESR1, EGFR \u00e9s ALB. A GO-gazdagod\u00e1si elemz\u00e9s azt mutatta, hogy a glicirrizin els\u0151sorban a sejtek anyagcser\u00e9j\u00e9t \u00e9s az apopt\u00f3zist szab\u00e1lyozza a feh\u00e9rje-foszforil\u00e1ci\u00f3, az oxid\u00e1ci\u00f3s reakci\u00f3k \u00e9s a sejtciklus szab\u00e1lyoz\u00e1s\u00e1val. A molekul\u00e1ris dokkol\u00e1s tov\u00e1bb\u00e1 kimutatta, hogy a glicirrizinnek j\u00f3 dokkol\u00e1si aktivit\u00e1sa van 10 f\u0151 c\u00e9lponthoz. A glicirrizinnek a daganatellenes hat\u00e1sokat ezen alapvet\u0151 c\u00e9lfeh\u00e9rj\u00e9k expresszi\u00f3j\u00e1nak szab\u00e1lyoz\u00e1s\u00e1val lehet el\u00e9rni. Ezen alapvet\u0151 c\u00e9lpontok k\u00f6z\u00fcl az AKT1 feh\u00e9rje rendelkezik a legmagasabb dokkol\u00e1si aktivit\u00e1ssal. Az AKT1 az egyik fontos szab\u00e1lyoz\u00f3 faktor a PI3K\/AKT jel\u00e1tviteli \u00fatvonalban, amely r\u00e9szt vesz a daganatok k\u00fcl\u00f6nb\u00f6z\u0151 biol\u00f3giai folyamataiban. Prosztatar\u00e1kban a genom- \u00e9s transzkriptomprofilok alapj\u00e1n a PI3K\/AKT-\u00fatvonal komponenseinek genetikai vari\u00e1ci\u00f3it \u00e9s g\u00e9nexpresszi\u00f3s diszregul\u00e1ci\u00f3j\u00e1t 42% primer prosztatar\u00e1k \u00e9s 100% metasztatikus prosztatar\u00e1kmint\u00e1ban mutatt\u00e1k ki. Korai tanulm\u00e1nyokban azt felt\u00e9telezt\u00e9k, hogy az AKT alt\u00edpusok (AKT1, AKT2) el\u0151seg\u00edthetik az androg\u00e9n\u00e9rz\u00e9keny st\u00e1diumb\u00f3l a hormonrefrakter st\u00e1diumba val\u00f3 \u00e1tmenetet a prosztatar\u00e1kban. A CRPC betegek kezel\u00e9s\u00e9vel kapcsolatos alapkutat\u00e1sok alapj\u00e1n a vizsg\u00e1latok arr\u00f3l sz\u00e1moltak be, hogy az AKT1\/2 ki\u00fct\u00e9se kasztr\u00e1ci\u00f3s rezisztens prosztatar\u00e1k \u00e1llatmodellekben jelent\u0151sen cs\u00f6kkentette az in vivo \u00e9s in vitro metaszt\u00e1zisok kialakul\u00e1s\u00e1t. L\u00e1that\u00f3, hogy az AKT1 expresszi\u00f3j\u00e1nak g\u00e1tl\u00e1sa jav\u00edthatja a CRPC-betegek t\u00fal\u00e9l\u00e9si progn\u00f3zis\u00e1t, \u00e9s az AKT1-g\u00e1tl\u00f3k a CRPC-betegek potenci\u00e1lis kezel\u00e9s\u00e9t jelenthetik. Tanulm\u00e1nyunk elm\u00e9letileg azt sugallja, hogy a glicirrizin AKT1-g\u00e1tl\u00f3 lehet, de hogy a glicirrizin hat\u00e9kony AKT1-g\u00e1tl\u00f3v\u00e1 v\u00e1lhat-e a CRPC-betegek sz\u00e1m\u00e1ra, a j\u00f6v\u0151ben m\u00e9g tov\u00e1bbi k\u00eds\u00e9rleti ellen\u0151rz\u00e9sre szorul.
\nA KEGG \u00fatvonalak gazdagod\u00e1s\u00e1nak eredm\u00e9nyei azt mutatt\u00e1k, hogy a PI3K\/AKT jel\u00e1tviteli \u00fatvonal \u00e9s a proteoglik\u00e1nok 105 kapcsol\u00f3d\u00f3 jel\u00e1tviteli \u00fatvonalban vettek r\u00e9szt, bele\u00e9rtve a r\u00e1kot, a prosztatar\u00e1kot, a kemokinreceptorok aktiv\u00e1l\u00f3d\u00e1s\u00e1t, az endokrin rezisztenci\u00e1t \u00e9s az epiderm\u00e1lis n\u00f6veked\u00e9si faktor receptor tirozinkin\u00e1z inhibitorokkal szembeni rezisztenci\u00e1t (P<0,01). Ezek k\u00f6z\u00fcl a legink\u00e1bb \u00e9rintett a foszfatidil-3-kin\u00e1z (PI3K)\/szerin-treonin-protein-kin\u00e1z (AKT) jel\u00e1tviteli \u00fatvonal. A PI3K\/AKT jel\u00e1tviteli \u00fatvonal r\u00e9szt vesz a sejtek anyagcser\u00e9j\u00e9nek, n\u00f6veked\u00e9s\u00e9nek, prolifer\u00e1ci\u00f3j\u00e1nak, differenci\u00e1l\u00f3d\u00e1s\u00e1nak \u00e9s feh\u00e9rjeszint\u00e9zis\u00e9nek szab\u00e1lyoz\u00e1s\u00e1ban. A PI3K\/AKT jel\u00e1tviteli \u00fatvonal mut\u00e1ci\u00f3it sz\u00e1mos emberi daganatban kimutatt\u00e1k. A kutat\u00e1si adatok azt mutatj\u00e1k, hogy az el\u0151rehaladott prosztatar\u00e1kos betegek ak\u00e1r 70% - 100% eset\u00e9ben is el\u0151fordul a PI3K \u00fatvonal diszregul\u00e1ci\u00f3ja. \u00c9s meg\u00e1llap\u00edtott\u00e1k, hogy a PI3K\/AKT jel\u00e1tviteli \u00fatvonal fontos szerepet j\u00e1tszik a hormon\u00e9rz\u00e9keny prosztatar\u00e1k kasztr\u00e1ci\u00f3s rezisztens prosztatar\u00e1kk\u00e1 t\u00f6rt\u00e9n\u0151 progresszi\u00f3j\u00e1ban, \u00e9s hat\u00e1smechanizmusa \u00f6sszef\u00fcgghet az androg\u00e9nreceptor (AR) jel\u00e1tviteli \u00fatvonal szab\u00e1lyoz\u00e1s\u00e1val, ami a CRPC potenci\u00e1lis biomarkerek\u00e9nt szolg\u00e1lhat. Jelenleg a PI3K\/AKT jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3d\u00f3 inhibitorok, mint p\u00e9ld\u00e1ul az AZD5363, a klinikai vizsg\u00e1lati szakaszba l\u00e9ptek, \u00e9s jelent\u0151s ter\u00e1pi\u00e1s hat\u00e1st \u00e9rtek el. Az ehhez az \u00fatvonalhoz kapcsol\u00f3d\u00f3 inhibitorok tanulm\u00e1nyoz\u00e1sa jelent\u0151s \u00e9rt\u00e9kkel b\u00edr a CRPC kezel\u00e9s\u00e9ben.
\nCCK8 m\u00f3dszerrel meg\u00e1llap\u00edtottuk tov\u00e1bb\u00e1, hogy a glicirrizin jelent\u0151sen g\u00e1tolja a PC-3 sejtek prolifer\u00e1ci\u00f3j\u00e1t. Az \u00e1raml\u00e1si citometri\u00e1s \u00e9s DAPI fest\u00e9si k\u00eds\u00e9rletek azt mutatt\u00e1k, hogy k\u00e9pes a sejtek apopt\u00f3zis\u00e1t kiv\u00e1ltani, \u00e9s mikroszk\u00f3p alatt a sejtek sz\u00e1m\u00e1nak cs\u00f6kken\u00e9s\u00e9t \u00e9s morfol\u00f3giai zsugorod\u00e1s\u00e1t figyelt\u00fck meg. A daganatellenes gy\u00f3gyszerkoncentr\u00e1ci\u00f3k sz\u0171r\u00e9se sor\u00e1n azt tal\u00e1ltuk, hogy az IC50 \u00e9rt\u00e9k\u00fck kiss\u00e9 magasabb volt, ami a molekul\u00e1ris dokkol\u00e1shoz haszn\u00e1lt f\u00e9lig rugalmas dokkol\u00e1si m\u00f3dszerrel f\u00fcgg \u00f6ssze. A rugalmas dokkol\u00e1ssal \u00f6sszehasonl\u00edtva a f\u00e9lig rugalmas dokkol\u00e1ssal sz\u00e1m\u00edtott k\u00f6t\u00e9si energia alacsonyabb. Tov\u00e1bb\u00e1, mint term\u00e9szetes antioxid\u00e1ns, a glicirrizinnek er\u0151s antioxid\u00e1ns hat\u00e1sa van. A kis d\u00f3zis\u00fa term\u00e9szetes antioxid\u00e1nsok azonban nem mutattak j\u00f3 daganatellenes aktivit\u00e1st a daganatellenes k\u00eds\u00e9rletekben, m\u00edg a nagy d\u00f3zis\u00fa term\u00e9szetes antioxid\u00e1nsok toxikus hat\u00e1st gyakorolnak a sejtekre, \u00e9s a specifikus mechanizmus tov\u00e1bbi felt\u00e1r\u00e1st ig\u00e9nyel. A h\u00e1l\u00f3zati farmakol\u00f3gia \u00e1ltal megj\u00f3solt KEGG jel\u00e1tviteli \u00fatvonal alapj\u00e1n azt j\u00f3soljuk, hogy a glicirrizinnek a PC-3 sejtekre gyakorolt g\u00e1tl\u00f3 hat\u00e1sa els\u0151sorban a PI3K\/AKT jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3dhat. Tov\u00e1bbi Western blot k\u00eds\u00e9rleteket v\u00e9gezt\u00fcnk, hogy megvizsg\u00e1ljuk a glicirrizinnek a PI3K\/AKT jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3d\u00f3 feh\u00e9rj\u00e9k expresszi\u00f3j\u00e1ra gyakorolt hat\u00e1s\u00e1t a PC-3 sejtekben. Az eredm\u00e9nyek azt mutatt\u00e1k, hogy a glicirrizin jelent\u0151sen g\u00e1tolni tudja az AKT feh\u00e9rj\u00e9k foszforil\u00e1ci\u00f3s folyamat\u00e1t. K\u00eds\u00e9rlet\u00fcnkben megfigyelt\u00fck, hogy a glicirrizin jelent\u0151sen g\u00e1tolni tudja a foszforil\u00e1lt AKT feh\u00e9rje expresszi\u00f3j\u00e1t, de a foszforil\u00e1lt PI3K feh\u00e9rje expresszi\u00f3j\u00e1ra gyakorolt g\u00e1tl\u00f3 hat\u00e1sa nem volt a v\u00e1rtnak megfelel\u0151. A feh\u00e9rje bet\u00f6lt\u00e9si koncentr\u00e1ci\u00f3 \u00e9s ar\u00e1ny ism\u00e9telt be\u00e1ll\u00edt\u00e1sa \u00e9s a m\u0171velet szigor\u00faan standardiz\u00e1l\u00e1sa ut\u00e1n a feh\u00e9rje m\u00e9g mindig nem mutatott szignifik\u00e1ns hat\u00e1st. \u00dagy v\u00e9lj\u00fck, hogy ennek oka mag\u00e1nak a p-PI3K feh\u00e9rj\u00e9nek a min\u0151s\u00e9gi probl\u00e9m\u00e1j\u00e1val f\u00fcgghet \u00f6ssze, amely alacsony hat\u00e9konys\u00e1ggal rendelkezik. A vizsg\u00e1lat korl\u00e1tozott finansz\u00edroz\u00e1sa miatt azonban nem cser\u00e9lt\u00fck ki m\u00e1s term\u00e9kek feh\u00e9rj\u00e9it. A j\u00f6v\u0151beli k\u00eds\u00e9rletek sor\u00e1n a hipot\u00e9zis\u00fcnk ellen\u0151rz\u00e9se \u00e9rdek\u00e9ben az \u00fatvonal t\u00f6bb rokon feh\u00e9rj\u00e9t fogjuk elemezni.
\n\u00d6sszefoglalva, ez a tanulm\u00e1ny elemezte \u00e9s megj\u00f3solta a glicirrizin potenci\u00e1lis hat\u00e1smechanizmus\u00e1t a kasztr\u00e1ci\u00f3rezisztens prosztatar\u00e1kra a h\u00e1l\u00f3zati farmakol\u00f3gia seg\u00edts\u00e9g\u00e9vel, \u00e9s tov\u00e1bb igazolta azt molekul\u00e1ris dokkol\u00e1ssal \u00e9s in vitro sejtk\u00eds\u00e9rletekkel. Az eredm\u00e9nyek azt mutatt\u00e1k, hogy a glicirrizin k\u00e9pes g\u00e1tolni a PC-3 sejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s apopt\u00f3zist induk\u00e1lni, \u00e9s mechanizmusa az AKT feh\u00e9rje foszforil\u00e1ci\u00f3s folyamat\u00e1hoz kapcsol\u00f3dik. Ez\u00e9rt felt\u00e9telezz\u00fck, hogy a CRPC-ellenes mechanizmusa els\u0151sorban a PI3K\/AKT jel\u00e1tviteli \u00fatvonalhoz kapcsol\u00f3d\u00f3 feh\u00e9rj\u00e9k foszforil\u00e1ci\u00f3j\u00e1nak szab\u00e1lyoz\u00e1s\u00e1n kereszt\u00fcl t\u00f6rt\u00e9nhet. Ez a tanulm\u00e1ny nemcsak kutat\u00e1si \u00f6tleteket ny\u00fajt a Guanggancao Ding molekul\u00e1ris mechanizmus\u00e1nak felt\u00e1r\u00e1s\u00e1hoz a kasztr\u00e1ci\u00f3rezisztens prosztatar\u00e1k kezel\u00e9s\u00e9ben, hanem hat\u00e9kony m\u00f3dszert biztos\u00edt az \u00e9desgy\u00f6k\u00e9rben l\u00e9v\u0151 flavonoidokat tartalmaz\u00f3 daganatellenes gy\u00f3gyszerek fejleszt\u00e9s\u00e9hez \u00e9s klinikai alkalmaz\u00e1s\u00e1hoz.<\/p>","protected":false},"excerpt":{"rendered":"

Exploring the mechanism of action of Guanggancao Ding in treating castration resistant prostate cancer based on network pharmacology and experimental verification Prostate cancer (PCa) is the most common malignant tumor in the reproductive system of elderly men. Many early treatments for androgen deprivation are effective, but most eventually progress from hormone sensitive prostate cancer to […]<\/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":"\nExploring the mechanism of action of Guanggancao Ding in treating castration resistant prostate cancer based on network pharmacology 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\/guanggancao-ding\/\" \/>\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 Guanggancao Ding in treating castration resistant prostate cancer based on network pharmacology and experimental verification - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Exploring the mechanism of action of Guanggancao Ding in treating castration resistant prostate cancer based on network pharmacology and experimental verification Prostate cancer (PCa) is the most common malignant tumor in the reproductive system of elderly men. 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