{"id":3768,"date":"2024-08-03T07:54:10","date_gmt":"2024-08-03T07:54:10","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=3768"},"modified":"2024-08-03T07:54:10","modified_gmt":"2024-08-03T07:54:10","slug":"curcuma-zedoaria-and-turtle-shell-medicine","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/tr\/curcuma-zedoaria-and-turtle-shell-medicine\/","title":{"rendered":"Curcuma zedoaria ve Biejia ilac\u0131n\u0131n karaci\u011fer fibrozuyla m\u00fccadeledeki etki mekanizmas\u0131n\u0131n a\u011f farmakolojisi, molek\u00fcler yerle\u015ftirme ve deneysel do\u011frulamaya dayal\u0131 olarak ara\u015ft\u0131r\u0131lmas\u0131"},"content":{"rendered":"

Curcuma zedoaria ve Biejia ilac\u0131n\u0131n karaci\u011fer fibrozuyla m\u00fccadeledeki etki mekanizmas\u0131n\u0131n a\u011f farmakolojisi, molek\u00fcler yerle\u015ftirme ve deneysel do\u011frulamaya dayal\u0131 olarak ara\u015ft\u0131r\u0131lmas\u0131
\nKaraci\u011fer fibrozu, \u00e7e\u015fitli patojenik fakt\u00f6rlerin s\u00fcrekli etkisinin neden oldu\u011fu karaci\u011fer h\u00fccrelerinin kronik enflamasyonu ve nekrozunu ifade eder. Karaci\u011ferdeki baz\u0131 parankimal olmayan h\u00fccreler aktive olur, bu da karaci\u011ferde yayg\u0131n ekstrasel\u00fcler matriks proliferasyonu, fibr\u00f6z proliferasyon ve dengesiz lif ayr\u0131\u015fmas\u0131 ile sonu\u00e7lanarak karaci\u011ferde fibr\u00f6z ba\u011f dokusu proliferasyonuna yol a\u00e7ar ve karaci\u011fer fibrozu s\u00fcrecini ba\u015flat\u0131r. Daha sonraki a\u015famada, karaci\u011fer lob\u00fcl\u00fc yeniden \u015fekillenmesi ve ps\u00f6dolob\u00fcl olu\u015fumu meydana gelir ve karaci\u011fer dokusu sertle\u015ferek siroz ad\u0131 verilen karaci\u011fer fonksiyon bozuklu\u011funa yol a\u00e7ar; Karaci\u011fer fibrozu ba\u011f\u0131ms\u0131z bir hastal\u0131k de\u011fil, bir\u00e7ok kronik karaci\u011fer hastal\u0131\u011f\u0131nda ortak bir patolojik s\u00fcre\u00e7tir. Bir ara\u015ft\u0131rma, d\u00fcnya \u00e7ap\u0131nda 50 milyondan fazla yeti\u015fkinin kronik karaci\u011fer hastal\u0131\u011f\u0131ndan muzdarip oldu\u011funu g\u00f6stermektedir; \u00c7in'de yakla\u015f\u0131k 300 milyon insan karaci\u011fer hastal\u0131\u011f\u0131ndan etkilenmektedir ve sirozdan kaynaklanan k\u00fcresel \u00f6l\u00fcmlerin 11%'sini olu\u015fturmaktad\u0131r. Bu nedenle, karaci\u011fer fibrozunu \u00f6nleyecek ve tedavi edecek ila\u00e7lar\u0131n bulunmas\u0131, karaci\u011fer fibrozu gibi karaci\u011fer hastal\u0131klar\u0131 olan hastalar i\u00e7in b\u00fcy\u00fck \u00f6nem ta\u015f\u0131maktad\u0131r. Ara\u015ft\u0131rmalara g\u00f6re, geleneksel \u00c7in t\u0131bb\u0131 ve bile\u015fik preparatlar (Bile\u015fik Biejia Ruangan Tabletleri\/Kaps\u00fclleri, Fuzheng Huayu Tabletleri\/Kaps\u00fclleri, Dahuang Zhechong Haplar\u0131 vb. gibi) karaci\u011fer fibrozunu \u00f6nlemede ve tedavi etmede iyi terap\u00f6tik etkilere sahiptir ve \u00e7oklu bile\u015fen ve hedef avantajlar\u0131na sahiptir.
\nKaraci\u011fer fibrozu, geleneksel \u00c7in t\u0131bb\u0131nda \"a\u011fr\u0131 kesici\", \"karaci\u011fer t\u0131kan\u0131kl\u0131\u011f\u0131\", \"karaci\u011fer birikimi\" ve \"birikim\" kategorilerine aittir. Curcumae Rhizoma (CR) ve Trionycis Carapax (TC) geleneksel \u00c7in t\u0131bb\u0131nda karaci\u011fer fibrozunun klinik tedavisinde yayg\u0131n olarak kullan\u0131lan ila\u00e7lard\u0131r. TC karaci\u011fere girer, sertli\u011fi yumu\u015fat\u0131r ve nod\u00fclleri da\u011f\u0131t\u0131r, kan staz\u0131n\u0131 giderir ve semptomlar\u0131 ortadan kald\u0131r\u0131r. CR kan dola\u015f\u0131m\u0131n\u0131 te\u015fvik eder ve kan staz\u0131n\u0131 giderir, sertli\u011fi yumu\u015fat\u0131r ve durgunlu\u011fu te\u015fvik eder ve semptomlar\u0131 ve nod\u00fclleri ortadan kald\u0131r\u0131r. Kan dola\u015f\u0131m\u0131n\u0131 te\u015fvik etme, kan staz\u0131n\u0131 giderme, sertli\u011fi yumu\u015fatma ve nod\u00fclleri da\u011f\u0131tma etkisini art\u0131rmak i\u00e7in ikisi birlikte kullan\u0131l\u0131r. Modern farmakolojik \u00e7al\u0131\u015fmalar, CR'nin anti karaci\u011fer fibrozu etkilerini \u00e7oklu etki mekanizmalar\u0131 yoluyla g\u00f6sterebilece\u011fini g\u00f6stermi\u015ftir. Buna ek olarak, TC'den olu\u015fan \u00e7e\u015fitli geleneksel \u00c7in t\u0131bb\u0131 bile\u015fik preparatlar\u0131 hastalar\u0131n karaci\u011fer fonksiyonlar\u0131n\u0131 iyile\u015ftirebilir ve fibroz s\u00fcrecini hafifletebilir. Klinik ve deneysel \u00e7al\u0131\u015fmalar, hem CR hem de TC'nin net karaci\u011fer fibrozu kar\u015f\u0131t\u0131 etkilere sahip oldu\u011funu g\u00f6stermektedir, ancak bir ila\u00e7 olarak birle\u015ftirildiklerinde sinerjik karaci\u011fer fibrozu kar\u015f\u0131t\u0131 etkilerinin spesifik mekanizmas\u0131 ayd\u0131nlat\u0131lmam\u0131\u015ft\u0131r. Bu \u00e7al\u0131\u015fma, CRTC'nin anti karaci\u011fer fibrozu \u00fczerine modern ara\u015ft\u0131rmalar i\u00e7in belirli bir temel ve referans sa\u011flamay\u0131 umarak, bile\u015fenler, hedefler, biyolojik i\u015flevler, sinyal yollar\u0131 vb. a\u00e7\u0131lardan CRTC'nin anti karaci\u011fer fibrozundaki geleneksel ila\u00e7lar\u0131n rol\u00fcn\u00fc ve olas\u0131 mekanizmalar\u0131n\u0131 ara\u015ft\u0131rmak i\u00e7in a\u011f farmakolojisi, molek\u00fcler yerle\u015ftirme teknolojisi ve deneysel do\u011frulama gibi \u00e7e\u015fitli ara\u015ft\u0131rma y\u00f6ntemlerini benimsemektedir.<\/p>\n

\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"Geleneksel \u00c7in t\u0131bb\u0131n\u0131n modern \u00f6zelliklerinin ve mekanizmalar\u0131n\u0131n incelenmesi, geleneksel \u00c7in t\u0131bb\u0131ndaki modern ara\u015ft\u0131rmalar\u0131n her zaman \u00f6nemli bir odak noktas\u0131 olmu\u015ftur. Biejia ve Curcuma zedoaria, geleneksel \u00c7in t\u0131bb\u0131nda karaci\u011fer fibrozunun klinik tedavisinde yayg\u0131n olarak kullan\u0131lan ila\u00e7lard\u0131r. Klinik uygulamada, kan dola\u015f\u0131m\u0131n\u0131 te\u015fvik etme, kan staz\u0131n\u0131 giderme, nod\u00fclleri yumu\u015fatma ve da\u011f\u0131tma ve net bir anti karaci\u011fer fibrozu etkisine sahip olma etkilerini g\u00f6steren bu ikisi genellikle birbirinin yerine kullan\u0131l\u0131r. Bununla birlikte, bu iki ilac\u0131n sinerjik anti karaci\u011fer fibrozu etkilerinin spesifik mekanizmas\u0131 uzun s\u00fcredir net de\u011fildir.
\nBu makale, \u00f6nce CRTC ve karaci\u011fer fibrozunun kesi\u015fme hedeflerini taramak ve ard\u0131ndan IL-6, AKT1, STAT3, PPARG gibi \u00e7ekirdek hedefleri taramak i\u00e7in bir PPI a\u011f\u0131 olu\u015fturmak i\u00e7in modern a\u011f farmakolojisini kullanmaktad\u0131r. Bunlar aras\u0131nda, IL-6 en y\u00fcksek derece s\u0131ralamas\u0131na sahip anahtar hedeftir. IL-6, pro-inflamatuar sitokin ailesinin bir \u00fcyesidir ve akut faz protein \u00fcretimi (C-reaktif protein, ferritin vb.), inflamasyon, antijene \u00f6zg\u00fc imm\u00fcn yan\u0131t, hematopoez, h\u00fccre apoptozu, farkl\u0131la\u015fma ve h\u00fccre metabolizmas\u0131 gibi \u00e7e\u015fitli imm\u00fcn ve fizyolojik s\u00fcre\u00e7leri etkileyebilir. Buna ek olarak, \u00e7al\u0131\u015fmalar karaci\u011fer h\u00fccrelerinde STAT3 sinyalinin aktivasyonunun genellikle karaci\u011fer iltihab\u0131n\u0131 iyile\u015ftirdi\u011fini ve karaci\u011fer h\u00fccresi hasar\u0131n\u0131 \u00f6nleyerek ve STAT1 sinyalini inhibe ederek karaci\u011fer fibroz s\u00fcrecini d\u00fczenledi\u011fini bulmu\u015ftur; STAT3 ayr\u0131ca fibroblastlardan miyofibroblastlara ge\u00e7i\u015fi ve matris metaloproteinazlar\u0131n ve bunlar\u0131n homolog inhibit\u00f6r proteinlerinin transkripsiyonunu d\u00fczenleyebilir, b\u00f6ylece h\u00fccre d\u0131\u015f\u0131 matris bozulmas\u0131 d\u00fczeyinde karaci\u011fer fibrozunu iyile\u015ftirebilir. Analizler IL-6 ve STAT3'\u00fcn karaci\u011fer fibrozuyla m\u00fccadelede CRTC i\u00e7in b\u00fcy\u00fck \u00f6neme sahip oldu\u011funu g\u00f6stermektedir. \u200d
\nTopolojik analiz kullan\u0131larak a\u011f modelinin daha ileri analizi, CRTC'nin \u00e7ok bile\u015fenli \u00e7oklu hedefinin farmakolojik etkilerinin karma\u015f\u0131k bir a\u011f olu\u015fturdu\u011funu ortaya koymu\u015ftur. Be\u015f temel fonksiyonel bile\u015fen tan\u0131mlanm\u0131\u015ft\u0131r: 9,12-oktadesadienoik asit, hederagenin, 8-oktadesadienoik asit, 9-oktadesadienoik asit ve 11 oktadesadienoik asit. Karaci\u011fer fibrozunu \u00f6nleyici etkisinde rol oynayan ana biyolojik s\u00fcre\u00e7ler aras\u0131nda hormon yan\u0131t\u0131, fosfat metabolizmas\u0131n\u0131n pozitif d\u00fczenlenmesi ve fosfat metabolizmas\u0131n\u0131n pozitif d\u00fczenlenmesi yer almaktad\u0131r. H\u00fccresel bile\u015fenler resept\u00f6r kompleksleri, membran sallar\u0131, membran mikro b\u00f6lgeleri vb. i\u00e7erir. Molek\u00fcler fonksiyonlar temel olarak transkripsiyon fakt\u00f6r\u00fc ba\u011flanmas\u0131, kinaz ba\u011flanmas\u0131, kinaz aktivitesi vb. i\u00e7erir; \u00c7ekirdek sinyal yollar\u0131 EGFR tirozin kinaz inhibit\u00f6r direnci, PI3K Akt sinyal yolu vb. i\u00e7erir. KEGG yolak zenginle\u015ftirme analizinde, EGFR tirozin kinaz inhibit\u00f6r direncinin P-de\u011ferinin nispeten k\u00fc\u00e7\u00fck oldu\u011funu ve bu yolakta zenginle\u015ftirilmi\u015f daha fazla gen oldu\u011funu bulduk. \u00c7ekirdek hedefler IL-6, AKT1, STAT3, vb. hepsi EGFR tirozin kinaz inhibit\u00f6r\u00fc diren\u00e7 yolunda zenginle\u015ftirilmi\u015ftir. EGFR tirozin kinaz inhibit\u00f6r\u00fc diren\u00e7 yolu, CRTC'nin karaci\u011fer fibrozunu \u00f6nleyici etkisi i\u00e7in b\u00fcy\u00fck \u00f6nem ta\u015f\u0131maktad\u0131r ve etki mekanizmas\u0131nda JAK-STAT, PI3K Akt ve di\u011fer yollarla etkile\u015fiminin olu\u015fturdu\u011fu sinyal a\u011f\u0131 g\u00f6z ard\u0131 edilemez. \u00c7ok say\u0131da \u00e7al\u0131\u015fma, IL-6\/EGFR\/STAT sinyal ekseninin h\u00fccre b\u00fcy\u00fcmesi, \u00e7o\u011falmas\u0131, farkl\u0131la\u015fmas\u0131, apoptoz ve ba\u011f\u0131\u015f\u0131kl\u0131k d\u00fczenlemesi gibi \u00e7e\u015fitli \u00f6nemli biyolojik s\u00fcre\u00e7lerde yer ald\u0131\u011f\u0131n\u0131 g\u00f6stermi\u015ftir. IL-6, v\u00fccudun ba\u011f\u0131\u015f\u0131kl\u0131k tepkisinde \u00f6nemli bir enflamatuar arac\u0131 olarak, JAK\/STAT sinyalinin aktivasyonunu te\u015fvik edebilir. Resept\u00f6rlere ba\u011fland\u0131\u011f\u0131nda, JAK1'in aktivasyonunu ve STAT3'\u00fcn fosforilasyonunu ve transkripsiyonunu te\u015fvik edebilir. \u00c7o\u011fu \u00e7al\u0131\u015fma, STAT3'\u00fcn neredeyse t\u00fcm fibrotik sistemlerde s\u0131kl\u0131kla aktive oldu\u011funu g\u00f6stermi\u015ftir; Karaci\u011ferde STAT3 sinyali, karaci\u011fer iltihab\u0131n\u0131 kontrol eden \u00f6nemli bir anti-enflamatuar sinyaldir ve aktivasyonu, karaci\u011fer fibrozu s\u00fcrecinde anti-enflamatuar ve imm\u00fcn d\u00fczenleyici roller oynayabilir. Buna ek olarak, klinik \u00f6ncesi hayvan modellerinde STAT3 inhibit\u00f6rlerinin kullan\u0131m\u0131 iyi bir anti fibrotik aktivite g\u00f6stermi\u015ftir, bu da STAT3'\u00fcn hastalarda fibrotik hastal\u0131klar\u0131n tedavisi i\u00e7in ger\u00e7ek hedef oldu\u011funu g\u00f6stermektedir. EGFR'nin karaci\u011fer rejenerasyonunun ilk a\u015famas\u0131nda karaci\u011fer h\u00fccresi proliferasyonu i\u00e7in kilit bir d\u00fczenleyici fakt\u00f6r oldu\u011fu bilinmektedir; t\u00fcm dokular aras\u0131nda EGFR, yeti\u015fkin karaci\u011fer h\u00fccrelerinde en y\u00fcksek oranda ifade edilir ve bu da karaci\u011fer fonksiyonunun s\u00fcrd\u00fcr\u00fclmesindeki \u00f6nemli rol\u00fcn\u00fc g\u00f6sterir. \u0130lk olarak, EGF, HSC aktivasyonunda yer alan bilinen bir \u00e7\u00f6z\u00fcn\u00fcr arac\u0131d\u0131r ve EGFR, HSC aktivasyonuna arac\u0131l\u0131k edebilir ve pro fibrotik bir fenotipi te\u015fvik edebilir. Kesin mekanizmas\u0131 karaci\u011fer dokusunda reaktif oksijen t\u00fcrlerinin \u00fcretimini i\u00e7erebilir. \u0130kinci olarak, Fuchs ve arkada\u015flar\u0131 \u00e7al\u0131\u015fmalar\u0131nda EGFR inhibit\u00f6rlerinin \u00e7oklu karaci\u011fer fibroz modellerinde bilinen birka\u00e7 pro fibrotik genin ekspresyonunu inhibe edebildi\u011fini bulmu\u015flard\u0131r ki bu da EGFR'nin inhibe edilmesinin karaci\u011fer fibrozunu tersine \u00e7evirebilece\u011fine dair ilk kan\u0131tt\u0131r. Son olarak, EGFR dimerler olu\u015fturmak i\u00e7in spesifik ligandlar\u0131na ba\u011flanabilir, \u00e7e\u015fitli efekt\u00f6r proteinlerin fosforilasyonunu tetikleyebilir ve sinyal d\u00f6n\u00fc\u015ft\u00fcr\u00fcc\u00fc ve transkripsiyonel aktivat\u00f6r (STAT) yollar\u0131 gibi \u00e7oklu klasik a\u015fa\u011f\u0131 ak\u0131\u015f sinyal yollar\u0131n\u0131 aktive edebilir; EGFR, yaralanmaya karaci\u011fer yan\u0131t\u0131n\u0131n t\u00fcm a\u015famalar\u0131nda kilit bir kat\u0131l\u0131mc\u0131 olarak, klasik STAT3 Tyr705 fosforilasyonunu ind\u00fckleyebilir, b\u00f6ylece sitokin \u00e7o\u011falmas\u0131n\u0131 ve farkl\u0131la\u015fmas\u0131n\u0131 kontrol edebilir ve fibroz olu\u015fumunu inhibe edebilir. Bu nedenle, a\u011f farmakolojisi yoluyla temel hedeflerin ve yolaklar\u0131n tahmin edilmesi ve tahmin edilen IL-6\/EGFR\/STAT3 sinyal ekseninin karaci\u011fer fibrozu \u00fczerindeki d\u00fczenleyici etkisinin deneyler yoluyla daha fazla do\u011frulanmas\u0131, CRTC'nin anti karaci\u011fer fibrozu etkisinin mekanizmas\u0131n\u0131 anlamam\u0131za yard\u0131mc\u0131 olacakt\u0131r.
\nHayvan deneylerinde, HE boyama sonu\u00e7lar\u0131, uygulamadan sonra inflamasyon ve infiltrasyon gibi patolojik morfolojide iyile\u015fme g\u00f6stermi\u015ftir, bu da CRTC'nin domuz serumunun neden oldu\u011fu karaci\u011fer fibrozunu hafifletebilece\u011fini g\u00f6stermektedir. Di\u011fer ELISA sonu\u00e7lar\u0131, model grup s\u0131\u00e7anlar\u0131n serumundaki IL-6, EGFR ve STAT3 seviyelerinin \u00f6nemli \u00f6l\u00e7\u00fcde artt\u0131\u011f\u0131n\u0131 ve doz ba\u011f\u0131ml\u0131 bir ili\u015fki g\u00f6stererek uygulamadan sonra hepsinin \u00f6nemli \u00f6l\u00e7\u00fcde a\u015fa\u011f\u0131 reg\u00fcle edildi\u011fini g\u00f6stermi\u015ftir. Bu \u00e7al\u0131\u015fma, karaci\u011fer fibrozunun tedavisinde CRTC'nin etki mekanizmas\u0131n\u0131n IL-6\/EGFR\/STAT3 sinyal ekseniyle ili\u015fkili olabilece\u011fini, karaci\u011fer fibrozunun geleneksel CRTC tedavisinin modern mekanizmas\u0131n\u0131 ortaya \u00e7\u0131karmak i\u00e7in belirli bir temel sa\u011flad\u0131\u011f\u0131n\u0131 ve ayr\u0131ca geleneksel ila\u00e7lar i\u00e7in a\u011f farmakolojisi ve molek\u00fcler yerle\u015ftirme teknolojisinin molek\u00fcler mekanizma ara\u015ft\u0131rmas\u0131 i\u00e7in yararl\u0131 referanslar sa\u011flad\u0131\u011f\u0131n\u0131 g\u00f6stermektedir.<\/p>","protected":false},"excerpt":{"rendered":"

Exploring the mechanism of action of Curcuma zedoaria and Biejia medicine in combating liver fibrosis based on network pharmacology, molecular docking, and experimental verification Liver fibrosis refers to the chronic inflammation and necrosis of liver cells caused by the continuous action of various pathogenic factors. Some non parenchymal cells in the liver are activated, resulting […]<\/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 Curcuma zedoaria and Biejia medicine in combating liver fibrosis based on network pharmacology, molecular docking, 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\/tr\/curcuma-zedoaria-and-turtle-shell-medicine\/\" \/>\n<meta property=\"og:locale\" content=\"tr_TR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Exploring the mechanism of action of Curcuma zedoaria and Biejia medicine in combating liver fibrosis based on network pharmacology, molecular docking, and experimental verification - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Exploring the mechanism of action of Curcuma zedoaria and Biejia medicine in combating liver fibrosis based on network pharmacology, molecular docking, and experimental verification Liver fibrosis refers to the chronic inflammation and necrosis of liver cells caused by the continuous action of various pathogenic factors. 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