{"id":4156,"date":"2024-08-04T08:37:17","date_gmt":"2024-08-04T08:37:17","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=4156"},"modified":"2024-08-04T08:37:17","modified_gmt":"2024-08-04T08:37:17","slug":"sophoridine","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/sophoridin\/","title":{"rendered":"A szofokarpin hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a prosztatar\u00e1k kezel\u00e9s\u00e9ben in vitro sejtk\u00eds\u00e9rletek \u00e9s h\u00e1l\u00f3zati farmakol\u00f3gia alapj\u00e1n"},"content":{"rendered":"

A szofokarpin hat\u00e1smechanizmus\u00e1nak felt\u00e1r\u00e1sa a prosztatar\u00e1k kezel\u00e9s\u00e9ben in vitro sejtk\u00eds\u00e9rletek \u00e9s h\u00e1l\u00f3zati farmakol\u00f3gia alapj\u00e1n
\nA prosztatar\u00e1k (PCa) vil\u00e1gszerte az egyik leggyakoribb rosszindulat\u00fa daganat a k\u00f6z\u00e9pkor\u00fa \u00e9s id\u0151s f\u00e9rfiak h\u00fagy\u00fati rendszer\u00e9ben. 2020-ban vil\u00e1gszerte 10,06 milli\u00f3 \u00faj f\u00e9rfi r\u00e1kos megbeteged\u00e9s \u00e9s 5,53 milli\u00f3 hal\u00e1leset volt, k\u00f6zt\u00fck 1,41 milli\u00f3 \u00faj PCa megbeteged\u00e9s \u00e9s 380000 hal\u00e1leset, a hal\u00e1loz\u00e1s \u00e9s az incidencia ar\u00e1nya 27%. K\u00edn\u00e1ban 120000 \u00faj PCa megbeteged\u00e9s \u00e9s 50000 hal\u00e1leset volt, a PCa hal\u00e1loz\u00e1si \u00e9s el\u0151fordul\u00e1si ar\u00e1nya 41,7%. Az Amerikai R\u00e1kellenes T\u00e1rsas\u00e1g 2023-as kutat\u00e1si adatai szerint a PCa el\u0151fordul\u00e1sa az els\u0151 helyen \u00e1ll a f\u00e9rfiak rosszindulat\u00fa daganatai k\u00f6z\u00f6tt, mintegy 29%-t tesz ki. Jelenleg a PCa f\u0151 kezel\u00e9si lehet\u0151s\u00e9gei a klinikai gyakorlatban az androg\u00e9nmegvon\u00f3 ter\u00e1pia, a radik\u00e1lis prosztatekt\u00f3mia, a sug\u00e1rkezel\u00e9s, a kemoter\u00e1pia \u00e9s a molekul\u00e1ris c\u00e9lzott ter\u00e1pia. Ezeknek a kezel\u00e9si m\u00f3dszereknek azonban sz\u00e1mos mell\u00e9khat\u00e1sa van, \u00e9s hajlamosak a gy\u00f3gyszerrezisztenci\u00e1ra, ami rossz progn\u00f3zist \u00e9s egyes betegekn\u00e9l ki\u00fajul\u00e1st vagy progresszi\u00f3t eredm\u00e9nyez. Ez\u00e9rt nagy jelent\u0151s\u00e9ggel b\u00edr a biztons\u00e1gos \u00e9s hat\u00e9kony \u00faj gy\u00f3gyszerek keres\u00e9se a PCa kezel\u00e9s\u00e9re.
\nA szoforidin (SRI) egy tetraciklusos kinolin alkaloid, amelyet f\u0151k\u00e9nt a Sophora alopecuroides L-b\u0151l izol\u00e1ltak. A kutat\u00e1sok kimutatt\u00e1k, hogy az SRI sz\u00e1mos farmakol\u00f3giai hat\u00e1ssal rendelkezik, bele\u00e9rtve a gyullad\u00e1scs\u00f6kkent\u0151, v\u00edrusellenes \u00e9s daganatellenes hat\u00e1sokat. 2005-ben a szofokarpin-hidroklorid injekci\u00f3t az \u00c1llami \u00c9lelmiszer- \u00e9s Gy\u00f3gyszer\u00fcgyi Hivatal j\u00f3v\u00e1hagyta a rosszindulat\u00fa trofoblasztos daganatok klinikai kezel\u00e9s\u00e9re. Jelenleg az SRI-t a gyomor-b\u00e9lrendszeri daganatok m\u00e1jmetaszt\u00e1zisainak kezel\u00e9s\u00e9ben pr\u00f3b\u00e1lt\u00e1k ki. Ugyanakkor sz\u00e1mos jelent\u00e9s meger\u0151s\u00edtette, hogy az SRI j\u00f3 g\u00e1tl\u00f3 hat\u00e1ssal van a vastagb\u00e9lr\u00e1kra, a t\u00fcd\u0151r\u00e1kra, a hasny\u00e1lmirigyr\u00e1kra \u00e9s m\u00e1s daganatokra. Az SRI hat\u00e1sa a PCa-ra \u00e9s lehets\u00e9ges hat\u00e1smechanizmusa azonban m\u00e9g mindig nem tiszt\u00e1zott.
\nA h\u00e1l\u00f3zati farmakol\u00f3gia a klasszikus farmakol\u00f3gi\u00e1n, bioinformatikai \u00e9s informatikai elm\u00e9leteken alapul\u00f3, felt\u00f6rekv\u0151 tudom\u00e1ny\u00e1g, amelyet sz\u00e9les k\u00f6rben alkalmaznak a gy\u00f3gyszerfejleszt\u00e9sben \u00e9s a gy\u00f3gyszerek hat\u00e1smechanizmus\u00e1nak kutat\u00e1s\u00e1ban. Ez a cikk in vitro sejtk\u00eds\u00e9rleteken kereszt\u00fcl vizsg\u00e1lja az SRI hat\u00e1s\u00e1t a DU-145 sejtek prolifer\u00e1ci\u00f3j\u00e1ra \u00e9s apopt\u00f3zis\u00e1ra, \u00e9s a h\u00e1l\u00f3zati farmakol\u00f3gi\u00e1t \u00e9s a molekul\u00e1ris dokkol\u00e1si technik\u00e1kat kombin\u00e1lja a lehets\u00e9ges hat\u00e1smechanizmus felt\u00e1r\u00e1sa \u00e9rdek\u00e9ben, hogy elm\u00e9leti alapot \u00e9s adatt\u00e1mogat\u00e1st ny\u00fajtson a PCa SRI-vel t\u00f6rt\u00e9n\u0151 klinikai kezel\u00e9s\u00e9hez.<\/p>\n

\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"<\/p>\n

A PCa a leggyakoribb rosszindulat\u00fa daganat a k\u00f6z\u00e9pkor\u00fa \u00e9s id\u0151s f\u00e9rfiak k\u00f6r\u00e9ben, amely hajlamos a gy\u00f3gyszerrezisztenci\u00e1ra \u00e9s az \u00e1tt\u00e9tk\u00e9pz\u0151d\u00e9sre, ami rossz progn\u00f3zishoz \u00e9s magas ki\u00fajul\u00e1si ar\u00e1nyhoz vezet. Ez\u00e9rt nagyon s\u00fcrg\u0151ss\u00e9 v\u00e1lt a PCa kezel\u00e9s\u00e9re szolg\u00e1l\u00f3 \u00faj ter\u00e1pi\u00e1k keres\u00e9se. A hagyom\u00e1nyos k\u00ednai orvosl\u00e1s term\u00e9szetes k\u00e9miai hat\u00f3anyagai fontos szerepet j\u00e1tszanak a rosszindulat\u00fa daganatok megel\u0151z\u00e9s\u00e9ben \u00e9s kezel\u00e9s\u00e9ben. Az SRI f\u0151k\u00e9nt a Sophora alopecuroides hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szatb\u00f3l izol\u00e1lt akt\u00edv alkaloid, amely k\u00fcl\u00f6nb\u00f6z\u0151 farmakol\u00f3giai tev\u00e9kenys\u00e9gekkel rendelkezik, amelyek k\u00f6z\u00fcl a daganatellenes aktivit\u00e1s k\u00fcl\u00f6n\u00f6sen kiemelked\u0151. 2005-ben a szofokarpin-hidroklorid injekci\u00f3t a K\u00ednai \u00c9lelmiszer- \u00e9s Gy\u00f3gyszer\u00fcgyi Hivatal r\u00e1kellenes gy\u00f3gyszerk\u00e9nt enged\u00e9lyezte. Az SRI j\u00f3 daganatellenes hat\u00e1st mutatott a gyomorr\u00e1k, m\u00e1jr\u00e1k, t\u00fcd\u0151r\u00e1k, vastagb\u00e9lr\u00e1k, hasny\u00e1lmirigyr\u00e1k \u00e9s m\u00e1s daganatok eset\u00e9ben in vivo \u00e9s in vitro. Az SRI k\u00e9pes g\u00e1tolni a k\u00fcl\u00f6nb\u00f6z\u0151 tumorsejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s inv\u00e1zi\u00f3j\u00e1t, el\u0151seg\u00edti a r\u00e1kos sejtek apopt\u00f3zis\u00e1t \u00e9s autof\u00e1gi\u00e1j\u00e1t. Funkci\u00f3ja olyan \u00fatvonalakhoz kapcsol\u00f3dik, mint a PI3K\/AKT, Wnt\/B-katenin, MAPK\/ERK \u00e9s a sejtciklus. A jelenlegi kutat\u00e1sok szerint az SRI szerepe \u00e9s pontos mechanizmusa a PCa eset\u00e9ben m\u00e9g mindig nem teljesen ismert. Ez a tanulm\u00e1ny a PCa SRI ter\u00e1pi\u00e1j\u00e1nak molekul\u00e1ris mechanizmus\u00e1t vizsg\u00e1lja in vitro sejtk\u00eds\u00e9rletek, h\u00e1l\u00f3zati farmakol\u00f3gia \u00e9s molekul\u00e1ris dokkol\u00e1si technik\u00e1k seg\u00edts\u00e9g\u00e9vel, bizonyos kutat\u00e1si alapot \u00e9s elm\u00e9leti alapot biztos\u00edtva a klinikai alkalmaz\u00e1shoz.
\nA magas prolifer\u00e1ci\u00f3s r\u00e1ta a rosszindulat\u00fa daganatos sejtek v\u00e9gtelen n\u00f6veked\u00e9s\u00e9nek fontos jellemz\u0151je, ez\u00e9rt a sejtprolifer\u00e1ci\u00f3 g\u00e1tl\u00e1sa hat\u00e9kony strat\u00e9gia a r\u00e1k kezel\u00e9s\u00e9re. Ebben a vizsg\u00e1latban azt tal\u00e1lt\u00e1k, hogy az SRI koncentr\u00e1ci\u00f3j\u00e1nak n\u00f6vel\u00e9s\u00e9vel a DU-145 sejtek n\u00f6veked\u00e9se jelent\u0151sen g\u00e1tolt a sejtek \u00e9letk\u00e9pess\u00e9g\u00e9nek \u00e9s a sejtkl\u00f3nok k\u00e9pz\u0151d\u00e9s\u00e9nek kimutat\u00e1s\u00e1val, ami azt jelzi, hogy az SRI k\u00e9pes g\u00e1tolni a DU-145 sejtek prolifer\u00e1ci\u00f3j\u00e1t. A Ki67 \u00e9s a PCNA prolifer\u00e1l\u00f3 sejtmagfeh\u00e9rj\u00e9k a sejtprolifer\u00e1ci\u00f3 markerfeh\u00e9rj\u00e9i, amelyeket \u00e1ltal\u00e1ban predikt\u00edv \u00e9s prognosztikai markerk\u00e9nt haszn\u00e1lnak a r\u00e1k diagn\u00f3zis\u00e1ban \u00e9s kezel\u00e9s\u00e9ben. Ez a tanulm\u00e1ny immunfluoreszcencia \u00e9s qPCR seg\u00edts\u00e9g\u00e9vel kimutatta a Ki67 expresszi\u00f3j\u00e1t a DU-145 sejtekben, \u00e9s meg\u00e1llap\u00edtotta, hogy az SRI jelent\u0151sen g\u00e1tolni tudja a Ki67 expresszi\u00f3j\u00e1t. qPCR \u00e9s Western blot elemz\u00e9s kimutatta, hogy az SRI jelent\u0151sen cs\u00f6kkenteni tudja a PCNA expresszi\u00f3j\u00e1t a DU-145 sejtekben, ami tov\u00e1bb bizony\u00edtja, hogy az SRI k\u00e9pes g\u00e1tolni a DU-145 sejtek prolifer\u00e1ci\u00f3j\u00e1t.
\nAz apopt\u00f3zis a tumorsejtek pusztul\u00e1s\u00e1nak f\u0151 oka, ez\u00e9rt az apopt\u00f3zis elker\u00fcl\u00e9se rezisztenci\u00e1hoz vezethet a tumor kezel\u00e9s\u00e9ben. A Bcl-2, mint az apopt\u00f3zis g\u00e1tl\u00f3ja, d\u00f6nt\u0151 szerepet j\u00e1tszik a sejtek apopt\u00f3zis\u00e1nak szab\u00e1lyoz\u00e1s\u00e1ban. A Bax a Bcl-2 homol\u00f3g konjug\u00e1ltja \u00e9s egy pro apoptotikus feh\u00e9rje. A Bcl-2 \u00e9s a Bax ar\u00e1nya fontos indik\u00e1tor a sejt apopt\u00f3zis hat\u00e1s\u00e1nak m\u00e9r\u00e9s\u00e9re. A kaszp\u00e1z-3 \u00e9s a kaszp\u00e1z-7 a sejt apopt\u00f3zis v\u00e9grehajt\u00f3i. Az apopt\u00f3zis bek\u00f6vetkez\u00e9sekor a kaszp\u00e1z-3 \u00e9s a kaszp\u00e1z-7 egym\u00e1s ut\u00e1n hasad \u00e9s aktiv\u00e1l\u00f3dik a feljebb l\u00e9v\u0151 kaszp\u00e1z feh\u00e9rj\u00e9k \u00e1ltal. Ezut\u00e1n az aktiv\u00e1lt kaszp\u00e1z-3 \u00e9s kaszp\u00e1z-7 t\u00f6bb downstream szubsztr\u00e1tot has\u00edt, v\u00e9g\u00fcl egy apoptotikus kaszk\u00e1dreakci\u00f3t ind\u00edt el. Ez a vizsg\u00e1lat a DU-145 sejtek apopt\u00f3zis\u00e1t 48 \u00f3r\u00e1s SRI-kezel\u00e9st k\u00f6vet\u0151en \u00e1raml\u00e1si citometri\u00e1s k\u00eds\u00e9rletekkel mutatta ki, \u00e9s az eredm\u00e9nyek azt mutatt\u00e1k, hogy az SRI jelent\u0151sen el\u0151seg\u00edtheti a DU-145 sejtek apopt\u00f3zis\u00e1t. Ez\u00e9rt tov\u00e1bb vizsg\u00e1ltuk az apopt\u00f3zissal kapcsolatos faktorok expresszi\u00f3j\u00e1t. A qPCR eredm\u00e9nyek azt mutatt\u00e1k, hogy az SRI k\u00e9pes volt felszab\u00e1lyozni a kaszp\u00e1z-3 \u00e9s a kaszp\u00e1z-7 mRNS expresszi\u00f3j\u00e1t, lefel\u00e9 szab\u00e1lyozni a Bcl-2 mRNS expresszi\u00f3j\u00e1t, \u00e9s lefel\u00e9 szab\u00e1lyozni a Bax mRNS expresszi\u00f3s szintj\u00e9t, de a Bcl-2\/Bax ar\u00e1ny szignifik\u00e1nsan cs\u00f6kkent (P<0,05). Ezenk\u00edv\u00fcl a Western blot eredm\u00e9nyek azt mutatt\u00e1k, hogy az SRI k\u00e9pes felszab\u00e1lyozni a tiszt\u00edtott-Kaszp\u00e1z-3 feh\u00e9rje expresszi\u00f3j\u00e1t \u00e9s lefel\u00e9 szab\u00e1lyozni a Bcl-2 feh\u00e9rje expresszi\u00f3j\u00e1t. B\u00e1r a Bax feh\u00e9rje expresszi\u00f3j\u00e1nak felszab\u00e1lyoz\u00e1s\u00e1ban nem volt szignifik\u00e1ns k\u00fcl\u00f6nbs\u00e9g, a Bcl-2\/Bax feh\u00e9rje expresszi\u00f3s ar\u00e1nya szignifik\u00e1nsan cs\u00f6kkent (P<0,05). Ezek az eredm\u00e9nyek arra utalnak, hogy az SRI k\u00e9pes szab\u00e1lyozni az apopt\u00f3zissal kapcsolatos faktorok expresszi\u00f3j\u00e1t, aktiv\u00e1lni az apopt\u00f3zis jel\u00e1tviteli \u00fatvonalakat \u00e9s apopt\u00f3zist induk\u00e1lni a DU-145 sejtekben.
\nEzenk\u00edv\u00fcl a DU-145 sejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s apopt\u00f3zis\u00e1t befoly\u00e1sol\u00f3 SRI mechanizmus\u00e1nak vizsg\u00e1lata \u00e9rdek\u00e9ben ez a tanulm\u00e1ny h\u00e1l\u00f3zati farmakol\u00f3giai kutat\u00e1si m\u00f3dszerekkel elemezte azt. A HERB, TCMSP, Pharm Mapper \u00e9s Swiss Target Prediction adatb\u00e1zisokon kereszt\u00fcl \u00f6sszesen 127 SRI c\u00e9lpontot gy\u0171jt\u00f6tt\u00fcnk \u00f6ssze, \u00e9s a Venny 2.1.0 online eszk\u00f6zzel a PCa-ra hat\u00f3 SRI 60 k\u00f6z\u00f6s c\u00e9lpontj\u00e1t kaptuk. A PPI-h\u00e1l\u00f3zat elemz\u00e9s\u00e9vel 16 k\u00f6zponti c\u00e9lpontot azonos\u00edtottunk (a 10 legmagasabb fok\u00fa \u00e9rt\u00e9kek), k\u00f6zt\u00fck az ALB, TNF, IL6, CASP3, MAPK1, PPARG, MDM2, PGR, MAPK8, NR3C1, ABL1, MAPK14, PARP1, HDAC2, CDK2, GSK3B stb. c\u00e9lpontokat. A MAPK8, CASP3, MAPK1, MAPK14 \u00e9s TNF core targetek a MAPK jel\u00e1tviteli \u00fatvonalban gazdagodnak. A GO-gazdagod\u00e1si elemz\u00e9s 158 bejegyz\u00e9st eredm\u00e9nyezett (P<0,01), ami azt jelzi, hogy az SRI els\u0151sorban a g\u00e9nexpresszi\u00f3, az apopt\u00f3zisfolyamat, a feh\u00e9rje-foszforil\u00e1ci\u00f3 \u00e9s a feh\u00e9rje szerin\/treonin\/tirozin-kin\u00e1z aktivit\u00e1s szab\u00e1lyoz\u00e1s\u00e1val fejthet ki ter\u00e1pi\u00e1s hat\u00e1st a PCa-ra. A KEGG \u00fatvonalak d\u00fas\u00edt\u00e1si elemz\u00e9s\u00e9nek eredm\u00e9nyei 84 jel\u00e1tviteli \u00fatvonalat mutattak, bele\u00e9rtve a r\u00e1k jel\u00e1tviteli \u00fatvonalat, a proteoglik\u00e1nokat a r\u00e1kban, a MAPK jel\u00e1tviteli \u00fatvonalat, a kemokarcinogenezis reakt\u00edv oxig\u00e9n specieseket, a PI3K-AKT jel\u00e1tviteli \u00fatvonalat, az apopt\u00f3zist stb. (P<0,01). A legink\u00e1bb aggaszt\u00f3 szempont a MAPK jel\u00e1tviteli \u00fatvonal szerepe az SRI PCa-ellenes folyamat\u00e1ban. A mitog\u00e9n aktiv\u00e1lt feh\u00e9rje kin\u00e1z (MAPK) k\u00e9pes extracellul\u00e1ris inform\u00e1ci\u00f3t tov\u00e1bb\u00edtani a sejtmagba, \u00e9s fontos szerepet j\u00e1tszik a fiziol\u00f3giai \u00e9s patol\u00f3gi\u00e1s folyamatokban. Az eml\u0151ssejtekben a MAPK csal\u00e1d h\u00e1romf\u00e9le tagja l\u00e9tezik: az extracellul\u00e1ris szign\u00e1l szab\u00e1lyozott kin\u00e1z (ERK), a c-JunN-termin\u00e1lis protein kin\u00e1z\/stressz aktiv\u00e1lt protein kin\u00e1z (JNK\/SAPK) \u00e9s a p38 mitog\u00e9n aktiv\u00e1lt protein kin\u00e1z (p38MAPK, m\u00e1s n\u00e9ven MAPK14).
\nA P38MAPK egy aktiv\u00e1lt feh\u00e9rjekin\u00e1z, amely sz\u00e1mos biol\u00f3giai folyamatban, p\u00e9ld\u00e1ul a sejtprolifer\u00e1ci\u00f3ban, a differenci\u00e1l\u00f3d\u00e1sban \u00e9s az apopt\u00f3zisban vesz r\u00e9szt. Aktiv\u00e1l\u00e1sa g\u00e1tolhatja a sejtprolifer\u00e1ci\u00f3t \u00e9s el\u0151seg\u00edtheti az apopt\u00f3zist. A kutat\u00e1sok azt tal\u00e1lt\u00e1k, hogy a p38 \u00fatvonal aktiv\u00e1l\u00e1sa cs\u00f6kkentheti a BGC-823 gyomorr\u00e1ksejtek prolifer\u00e1ci\u00f3s aktivit\u00e1s\u00e1t \u00e9s blokkolhatja \u0151ket a G2\/M f\u00e1zisban. A p38MAPK aktiv\u00e1l\u00e1sa g\u00e1tolhatja az SMMC-7721 sejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s elind\u00edthatja az intracellul\u00e1ris Caspase jel\u00e1tviteli kaszk\u00e1dot, ami v\u00e9g\u00fcl apopt\u00f3zist induk\u00e1l. Ezenk\u00edv\u00fcl vizsg\u00e1latok kimutatt\u00e1k, hogy a hagyom\u00e1nyos k\u00ednai gy\u00f3gyszerkivonatok k\u00e9pesek aktiv\u00e1lni a p38MAPK-t, kiv\u00e1ltani a kaszp\u00e1z \u00e1ltal k\u00f6zvet\u00edtett apoptotikus kaszk\u00e1dreakci\u00f3kat, \u00e9s apopt\u00f3zist induk\u00e1lni Lewis t\u00fcd\u0151r\u00e1ksejtekben, valamint HSC-3 \u00e9s SCC-9 sz\u00e1j\u00fcregi r\u00e1ksejtekben. A P38MAPK kin\u00e1z fontos szerepet j\u00e1tszik a PCa kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben is. A kutat\u00e1sok azt tal\u00e1lt\u00e1k, hogy a p38MAPK aktiv\u00e1l\u00e1sa ellen\u00e1ll a sejtprolifer\u00e1ci\u00f3nak, el\u0151seg\u00edti az apopt\u00f3zist \u00e9s tumoros nyugalmi \u00e1llapotot induk\u00e1l a prosztata epit\u00e9l rosszindulat\u00fa \u00e1talakul\u00e1s\u00e1ban vagy a csontmetasztatikus prosztatar\u00e1kban. Ek\u00f6zben m\u00e1s vizsg\u00e1latok kimutatt\u00e1k, hogy az \u00f6sszetev\u0151k, mint p\u00e9ld\u00e1ul a docetaxel \u00e9s az ursolsav n\u00f6velhetik a p38MAPK foszforil\u00e1ci\u00f3s szintj\u00e9t, induk\u00e1lhatj\u00e1k a PCa sejtek \u00f6reged\u00e9s\u00e9t, g\u00e1tolhatj\u00e1k a k\u00fcl\u00f6nb\u00f6z\u0151 PCa sejtek, p\u00e9ld\u00e1ul a PC-3 \u00e9s a 22Rv1 prolifer\u00e1ci\u00f3j\u00e1t, \u00e9s el\u0151seg\u00edthetik apopt\u00f3zisukat. Ez\u00e9rt ez a tanulm\u00e1ny a p38MAPK feh\u00e9rje kin\u00e1z szerep\u00e9re \u00f6sszpontos\u00edt az SRI anti PCa-ban. Az SRI p38MAPK feh\u00e9rj\u00e9hez val\u00f3 k\u00f6t\u0151d\u00e9s\u00e9nek ellen\u0151rz\u00e9s\u00e9re molekul\u00e1ris dokkol\u00e1si technol\u00f3gi\u00e1t alkalmazva az eredm\u00e9nyek azt mutatt\u00e1k, hogy az SRI stabilan k\u00e9pes k\u00f6t\u0151dni a p38MAPK feh\u00e9rj\u00e9hez, k\u00f6t\u00e9si energi\u00e1ja -6,83 kcal\/mol. A p-p38MAPK \u00e9s a p38MAPK feh\u00e9rje expresszi\u00f3s szintj\u00e9nek kimutat\u00e1si eredm\u00e9nyei azt mutatj\u00e1k, hogy az SRI k\u00e9pes aktiv\u00e1lni a p38MAPK feh\u00e9rj\u00e9t, \u00e9s a p38MAPK feh\u00e9rje foszforil\u00e1ci\u00f3s szintje felszab\u00e1lyozott, ami arra utal, hogy az SRI a p38MAPK feh\u00e9rje aktiv\u00e1l\u00e1s\u00e1val \u00e9s az apopt\u00f3zis \u00fatvonal induk\u00e1l\u00e1s\u00e1val PCa-ellenes hat\u00e1st fejthet ki.
\n\u00d6sszefoglalva, az SRI k\u00e9pes g\u00e1tolni a DU-145 sejtek prolifer\u00e1ci\u00f3j\u00e1t \u00e9s el\u0151seg\u00edteni apopt\u00f3zisukat, ami a p38MAPK aktiv\u00e1l\u00e1s\u00e1hoz kapcsol\u00f3dhat. Ez a tanulm\u00e1ny azonban csak az SRI DU-145 sejtekre gyakorolt hat\u00e1s\u00e1t vizsg\u00e1lta in vitro. A k\u00f6vetkez\u0151 l\u00e9p\u00e9s az in vivo \u00e1llatk\u00eds\u00e9rletek elv\u00e9gz\u00e9se lesz az SRI PCa-ellenes hat\u00e1s\u00e1nak mechanizmus\u00e1nak tov\u00e1bbi vizsg\u00e1lata \u00e9rdek\u00e9ben.<\/p>","protected":false},"excerpt":{"rendered":"

Exploring the mechanism of action of sophocarpine in the treatment of prostate cancer based on in vitro cell experiments and network pharmacology Prostate cancer (PCa) is one of the most common malignant tumors in the urinary system of middle-aged and elderly men worldwide. 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