{"id":6682,"date":"2024-08-06T14:03:48","date_gmt":"2024-08-06T14:03:48","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=6682"},"modified":"2024-08-06T14:03:48","modified_gmt":"2024-08-06T14:03:48","slug":"er-zhi-wan-in-combating","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/tr\/er-zhi-wan-in-combating\/","title":{"rendered":"Er Zhi Wan'\u0131n serum metabolomi\u011fi ve a\u011f farmakolojisine dayal\u0131 olarak Alzheimer hastal\u0131\u011f\u0131yla m\u00fccadelede etki mekanizmas\u0131 \u00fczerine \u00e7al\u0131\u015fma"},"content":{"rendered":"

Er Zhi Wan'\u0131n serum metabolomi\u011fi ve a\u011f farmakolojisine dayal\u0131 olarak Alzheimer hastal\u0131\u011f\u0131yla m\u00fccadelede etki mekanizmas\u0131 \u00fczerine \u00e7al\u0131\u015fma
\nEr Zhi Wan, klasik Ming Hanedanl\u0131\u011f\u0131 re\u00e7etesi \"Yi Bian\" Cilt 1'den gelmektedir ve b\u00f6brek \u00f6z\u00fcn\u00fc besleyici, kanamay\u0131 durdurucu, v\u00fccudu ve kemikleri g\u00fc\u00e7lendirici etkilere sahiptir. Er Zhi Wan, \u00e7obanp\u00fcsk\u00fcl\u00fc tohumlar\u0131 ve kurak lotus otundan olu\u015fur. Farmakolojik \u00e7al\u0131\u015fmalar Er Zhi Wan'\u0131n ya\u015flanma kar\u015f\u0131t\u0131, iltihap \u00f6nleyici ve t\u00fcm\u00f6r kar\u015f\u0131t\u0131 etkilere sahip oldu\u011funu g\u00f6stermi\u015ftir. \u0130lgili \u00e7al\u0131\u015fmalar, Er Zhi Wan'\u0131n D-galaktoz kaynakl\u0131 ya\u015flanan s\u0131\u00e7anlar\u0131n \u00f6\u011frenme ve haf\u0131za yeteneklerini geli\u015ftirebildi\u011fini, ya\u015flanma kar\u015f\u0131t\u0131 i\u015flevlere sahip oldu\u011funu, beyindeki serbest radikalleri temizledi\u011fini ve n\u00f6ronlar\u0131 korudu\u011funu ortaya koymu\u015ftur. Er Zhi Wan'\u0131n quercetin, geraniol, \u03b2 - sitosterol, naringenin ve icarium gibi aktif bile\u015fenleri Alzheimer hastal\u0131\u011f\u0131n\u0131 (AD) iyile\u015ftirebilir ve bu bile\u015fiklerin etki mekanizmas\u0131 PI3K\/Akt sinyal yola\u011f\u0131 ile yak\u0131ndan ili\u015fkilidir. \u015eu anda, Er Zhi Wan \u00fczerine yap\u0131lan ara\u015ft\u0131rmalar yaln\u0131zca genel terap\u00f6tik d\u00fczeyde y\u00fcr\u00fct\u00fclm\u00fc\u015ft\u00fcr ve AD kar\u015f\u0131t\u0131 mekanizmas\u0131 ayd\u0131nlat\u0131lmam\u0131\u015ft\u0131r, bu da klinik uygulamas\u0131n\u0131 b\u00fcy\u00fck \u00f6l\u00e7\u00fcde engellemektedir.
\nAH, \u015fu anda d\u00fcnya \u00e7ap\u0131nda 50 milyondan fazla insan\u0131 etkileyen ilerleyici bir n\u00f6rodejeneratif hastal\u0131kt\u0131r ve ya\u015flanan n\u00fcfus i\u00e7in \u00f6nemli bir sorun haline gelerek hastalar, aileler ve sa\u011fl\u0131k sistemleri \u00fczerinde b\u00fcy\u00fck bir y\u00fck olu\u015fturmas\u0131 beklenmektedir. AH ya\u015fa ba\u011fl\u0131 demanslar aras\u0131nda en yayg\u0131n olan\u0131d\u0131r ve t\u00fcm demans vakalar\u0131n\u0131n yakla\u015f\u0131k 70%'sini olu\u015fturur. AD'nin kesin pozitif tan\u0131s\u0131 hala beyin dokusunun post-mortem analizini gerektirse de, beyin omurilik s\u0131v\u0131s\u0131, kan ve pozitron emisyon tomografi g\u00f6r\u00fcnt\u00fclemesi i\u00e7in giderek artan say\u0131da biyobelirte\u00e7 \u00f6nerilmi\u015ftir ve klinik standartlar ve de\u011ferlendirmelerin birle\u015ftirilmesiyle ya\u015fayan hastalar i\u00e7in erken tan\u0131, hassasiyet ve spesifik tan\u0131 sa\u011flamas\u0131 beklenmektedir. AD'nin \u00f6zellikleri h\u00fccre d\u0131\u015f\u0131 amiloid beta (A \u03b2) plaklar\u0131, mikrot\u00fcb\u00fcl stabilize edici protein tau'nun kesilmi\u015f ve fosforile edilmi\u015f formlar\u0131ndan olu\u015fan n\u00f6ronal inkl\u00fczyonlar (n\u00f6rofibriler yumaklar), k\u00f6t\u00fc beslenmi\u015f n\u00f6ral s\u00fcre\u00e7ler, sinaps ve n\u00f6ron kayb\u0131 ve mikroglia ve astrositlerin morfolojisi ve i\u015flevindeki de\u011fi\u015fiklikleri i\u00e7eren belirgin bir gliozistir. Son y\u0131llarda, kan metabolomik teknolojisi, AD'nin tan\u0131 ve mekanizma ara\u015ft\u0131rmalar\u0131nda b\u00fcy\u00fck bir rol oynam\u0131\u015ft\u0131r ve hatta AD'nin taranmas\u0131 i\u00e7in spesifik bir tespit arac\u0131 olarak kullan\u0131labilir. AD'nin metabolik temeli tam olarak anla\u015f\u0131lamam\u0131\u015ft\u0131r ve metabolik sistem anormallikleri ile AD patogenezi aras\u0131ndaki ili\u015fki hala belirsizdir. Genel metabolik bozukluklar\u0131n AD n\u00f6ropatolojisinin \u015fiddeti ve y\u00fcksek riskli pop\u00fclasyonlarda AD semptomlar\u0131n\u0131n nihai ifadesi ile nas\u0131l ili\u015fkili oldu\u011funu anlamak, etkili hastal\u0131k iyile\u015ftirme tedavileri geli\u015ftirmek i\u00e7in \u00e7ok \u00f6nemlidir. A\u011f farmakolojisi, ila\u00e7lar\u0131n sistematik olarak incelenmesi i\u00e7in yapay zeka ve b\u00fcy\u00fck veri \u00e7a\u011f\u0131nda ortaya \u00e7\u0131kan, disiplinler aras\u0131 ve son teknoloji bir disiplindir. Sistem seviyesi ve biyolojik a\u011flar perspektifinden ila\u00e7lar ve tedavi hedefleri aras\u0131ndaki molek\u00fcler ili\u015fkilerin analizini vurgular. \u0130la\u00e7larda ve geleneksel \u00c7in t\u0131bb\u0131nda aktif bile\u015fiklerin ke\u015ffinde, genel etki mekanizmalar\u0131n\u0131n yorumlanmas\u0131nda ve ila\u00e7 kombinasyonlar\u0131n\u0131n ve form\u00fcl uyumluluk kurallar\u0131n\u0131n analizinde yayg\u0131n olarak kullan\u0131lmaktad\u0131r. Geleneksel \u00c7in t\u0131bb\u0131ndaki karma\u015f\u0131k sistemlerin incelenmesi i\u00e7in yeni fikirler ve klinik rasyonel ila\u00e7 kullan\u0131m\u0131 ve yeni ila\u00e7 geli\u015ftirme i\u00e7in yeni teknolojik destek sa\u011flar. Bu nedenle, bu \u00e7al\u0131\u015fmada, hastal\u0131kla ilgili potansiyel bile\u015fenleri ve \u00e7ekirdek metabolitleri ke\u015ffetmek ve ilac\u0131n etki mekanizmas\u0131n\u0131 a\u00e7\u0131kl\u0131\u011fa kavu\u015fturmak i\u00e7in a\u011f farmakolojisi teknikleriyle birlikte y\u00fcksek verimli metabolomik kullan\u0131lm\u0131\u015ft\u0131r.<\/p>\n

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\nBu \u00e7al\u0131\u015fmada, metabolomik teknikler arac\u0131l\u0131\u011f\u0131yla AD ile yak\u0131ndan ili\u015fkili 15 kan biyobelirteci ke\u015ffedilmi\u015ftir ve bunlar\u0131n metabolik mekanizmalar\u0131 ve fizyolojik \u00f6nemi farkl\u0131 a\u015famalardaki AD geli\u015fimi ile ili\u015fkilidir. A\u015fa\u011f\u0131da bir a\u00e7\u0131klama yer almaktad\u0131r.<\/p>\n

V\u00fccudun \u00f6\u011frenme ve haf\u0131za mekanizmas\u0131 5-HT gibi metabolitlerle yak\u0131ndan ili\u015fkilidir. Tirozin, insanlarda ve hayvanlarda fenilalaninin hidroksilasyonu ile \u00fcretilen esansiyel olmayan bir amino asittir. Adrenalin, norepinefrin ve dopamin gibi monoamin n\u00f6rotransmitterlerinin \u00f6nc\u00fcs\u00fcd\u00fcr. Dopamin, orta beyin marjini, orta beyin korteksi, substantia nigra striatum ve nod\u00fcl huni yolu arac\u0131l\u0131\u011f\u0131yla psikolojik aktiviteyi, duygular\u0131, tan\u0131may\u0131, d\u00fc\u015f\u00fcnmeyi ve muhakemeyi d\u00fczenler ve dolayl\u0131 olarak haf\u0131zay\u0131 etkiler. 3-metoksi-4-hidroksifeniletilen glikol s\u00fclfat ve homovanillik asit, dopamin metabolik yol sisteminin metabolitleridir. Bu \u00e7al\u0131\u015fmada, model gruptaki s\u0131\u00e7anlar\u0131n serumundaki 3-metoksi-4-hidroksifenilen glikol s\u00fclfat ve N-asetil5-hidroksitriptamin seviyeleri sahte operasyon grubundakilerden \u00f6nemli \u00f6l\u00e7\u00fcde y\u00fcksekken, model gruptaki vanilik asit ve vanil mandelik asit seviyeleri sahte operasyon grubundakilerden daha d\u00fc\u015f\u00fckt\u00fc. Er Zhi Wan, AD s\u0131\u00e7anlar\u0131nda endojen metabolitlerin seviyelerini d\u00fczenleyebilir (P<0.05), bu da Er Zhi Wan'\u0131n monoamin n\u00f6rotransmitterlerinin ve metabolitlerinin seviyelerini d\u00fczenleyerek AD s\u0131\u00e7anlar\u0131n\u0131n \u00f6\u011frenme ve haf\u0131za yeteneklerini art\u0131rabilece\u011fini d\u00fc\u015f\u00fcnd\u00fcrmektedir.<\/p>\n

Sinir sistemindeki ana inhibit\u00f6r amino asit n\u00f6rotransmitteri gama aminob\u00fctirik asidin de bili\u015fsel i\u015flevle ili\u015fkili oldu\u011funa inan\u0131lmaktad\u0131r. Gama aminob\u00fctirik asit, beyin uyar\u0131m dengesinin korunmas\u0131nda ve sinir iletiminin engellenmesinde \u00f6nemli bir rol oynar. Otopsi ve hayvan modeli \u00e7al\u0131\u015fmalar\u0131, AD'nin patolojik s\u00fcrecinde gama aminob\u00fctirik asit sisteminde i\u015flev bozuklu\u011fu oldu\u011funu g\u00f6stermi\u015ftir. 4-Guanidob\u00fctirik asit, gama aminob\u00fctirik asidin bir \u00f6nc\u00fcs\u00fcd\u00fcr. Arginaz eksikli\u011fi olan hastalarda, y\u00fcksek 4-guanidinob\u00fctirik asit seviyeleri zihinsel engellilik, n\u00f6rogeli\u015fimsel duraklama ve epilepsi gibi \u00e7e\u015fitli klinik sendromlara yol a\u00e7ar. Bu \u00e7al\u0131\u015fmada, Er Zhi Wan'\u0131n AD s\u0131\u00e7anlar\u0131n\u0131n kan\u0131ndaki 4-guanidinob\u00fctirik asit i\u00e7eri\u011fini azaltt\u0131\u011f\u0131 ve hipokamp\u00fcsteki gama aminob\u00fctirik asit i\u00e7eri\u011fini art\u0131rd\u0131\u011f\u0131 g\u00f6r\u00fclm\u00fc\u015ft\u00fcr; bu da Er Zhi Wan'\u0131n gama aminob\u00fctirik asit sentezini te\u015fvik edebilece\u011fini, hiperammoneminin sinir sisteminde neden oldu\u011fu hasar\u0131 azaltabilece\u011fini ve b\u00f6ylece n\u00f6roprotektif etkiler g\u00f6sterebilece\u011fini g\u00f6stermektedir.<\/p>\n

Glutamik asit ve aspartik asit, sinir sisteminde uyar\u0131c\u0131 bilgilerin iletilmesinde \u00f6nemli rol oynayan iki ana uyar\u0131c\u0131 amino asit n\u00f6rotransmitteridir. N\u00f6ronlar\u0131n hayatta kalmas\u0131, sinaptik olu\u015fumu ve plastisitesi ile ilgilidirler. Glutamat ve aspartat presinaptik membrandan sal\u0131nan uyar\u0131c\u0131 amino asitlerdir, G proteini arac\u0131l\u0131 glutamat resept\u00f6rlerine ve N-metil-D-aspartat (NMDA) resept\u00f6rlerine se\u00e7ici olarak ba\u011flanarak kalsiyum kanallar\u0131n\u0131n a\u00e7\u0131lmas\u0131na yol a\u00e7ar. Bu, postsinaptik membrana Ca2+ ak\u0131\u015f\u0131n\u0131 art\u0131r\u0131r ve sinaptik iletimin uzun vadeli g\u00fc\u00e7lenmesinin (LTP) olu\u015fumuna ve s\u00fcrd\u00fcr\u00fclmesine kat\u0131l\u0131r. LTP, haf\u0131za olu\u015fumu ve konsolidasyonu s\u00fcrecinde n\u00f6ronal fizyolojik aktivitenin bir g\u00f6stergesi olarak kabul edilir. Model grubundaki glisin ve aspartik asit i\u00e7eri\u011fi \u00f6nemli \u00f6l\u00e7\u00fcde artarken (P<0.01), tedavi grubundaki glisin ve aspartik asit i\u00e7eri\u011fi \u00f6nemli \u00f6l\u00e7\u00fcde azalm\u0131\u015ft\u0131r (P<0.01). Sonu\u00e7lar, Er Zhi Wan'\u0131n beyindeki uyar\u0131c\u0131 amino asitlerin sentezini inhibe edebilece\u011fini ve b\u00f6ylece sinir h\u00fccreleri \u00fczerinde koruyucu bir etki g\u00f6sterebilece\u011fini g\u00f6stermektedir.<\/p>\n

Taurin, \u00f6zellikle serebral korteks, hipokampus ve serebellumda da\u011f\u0131l\u0131m g\u00f6steren \u015fartl\u0131 esansiyel bir amino asittir. Merkezi sinir sisteminde, en bol bulunan ikinci endojen amino asit olan taurin, n\u00f6ral d\u00fczenleme, ozmotik d\u00fczenleme, kalsiyum homeostaz\u0131n\u0131n korunmas\u0131, membran stabilitesi, antioksidan fonksiyon, anti-inflamatuar s\u00fcre\u00e7 ve n\u00f6roproteksiyonda rol oynar. Taurin ayr\u0131ca AD ve Huntington hastal\u0131\u011f\u0131 gibi bir\u00e7ok patolojik durumda n\u00f6roprotektif etkiler g\u00f6stermi\u015ftir. AD'nin ilerlemesi s\u0131ras\u0131nda, A \u03b2 monomerleri n\u00f6rotoksik \u00e7\u00f6z\u00fcn\u00fcr oligomerler A \u03b2 halinde toplanarak bili\u015fsel bozulmaya yol a\u00e7ar. Raporlara g\u00f6re, AD hastalar\u0131n\u0131n beynindeki taurin i\u00e7eri\u011fi azal\u0131r ve taurin A \u03b2 birikimini engelleyebilir. Ayr\u0131ca, taurinin s\u0131\u00e7anlar\u0131n entelekt\u00fcel geli\u015fimi \u00fczerinde \u00f6nemli bir etkisi vard\u0131r. Taurinin v\u00fccuda enjekte edilmesi beyindeki asetilkolin i\u00e7eri\u011fini art\u0131rabilir ve uzun s\u00fcreli taurin kullan\u0131m\u0131n\u0131n toksisitesi veya ba\u015fka yan etkileri yoktur. Bu \u00e7al\u0131\u015fmada, Er Zhi Wan'\u0131n uygulanmas\u0131ndan sonra, model grup s\u0131\u00e7anlarda kan taurin konsantrasyonu azal\u0131rken, Er Zhi Wan ile tedaviden sonra \u00f6nemli \u00f6l\u00e7\u00fcde artm\u0131\u015ft\u0131r. Bu sonu\u00e7, Er Zhi Wan'\u0131n taurin metabolizmas\u0131n\u0131 d\u00fczenleyerek A \u03b2 proteininin birikimini engelleyebilece\u011fini g\u00f6stermektedir.<\/p>\n

Adenozin, n\u00f6ronal aktivitenin d\u00fczenlenmesinden, entegre edilmesinden ve ince ayar\u0131n\u0131n yap\u0131lmas\u0131ndan ve uyku ve uyan\u0131kl\u0131k, bili\u015f ve haf\u0131za gibi ilgili beyin fonksiyonlar\u0131n\u0131n yan\u0131 s\u0131ra n\u00f6ronal hasar ve dejenerasyonu etkilemekten sorumludur. Membran fosfolipid biyosentezinin bir \u00f6nc\u00fcs\u00fc olan \u00fcridinin, yenido\u011fanlarda erken apoptotik h\u00fccre \u00f6l\u00fcm\u00fcn\u00fc azaltarak beyin sinapslar\u0131n\u0131n say\u0131s\u0131n\u0131 art\u0131rd\u0131\u011f\u0131 ve uzun vadede \u00f6\u011frenme ve haf\u0131zay\u0131 geli\u015ftirdi\u011fi g\u00f6sterilmi\u015ftir. Sham cerrahisi ile kar\u015f\u0131la\u015ft\u0131r\u0131ld\u0131\u011f\u0131nda, model gruptaki adenozin ve \u00fcridin seviyeleri \u00f6nemli \u00f6l\u00e7\u00fcde artarken, tedavi grubundaki adenozin ve \u00fcridin seviyeleri model gruptakilerden \u00e7ok daha d\u00fc\u015f\u00fckt\u00fc. Adenozin ve \u00fcridinin sa\u011fl\u0131kl\u0131 seviyelere geri getirilmesi, Er Zhi Wan'daki n\u00f6ronlar\u0131n yap\u0131s\u0131n\u0131 ve i\u015flevini etkileyerek AD s\u0131\u00e7anlar\u0131n\u0131n \u00f6\u011frenme ve haf\u0131zas\u0131n\u0131 iyile\u015ftirebilir.<\/p>\n

Triptofan, proteinlerin ve baz\u0131 \u00f6nemli aktif maddelerin (serotonin, nikotinamid adenin din\u00fckleotid ve niasin) sentezinde yer alan, insan v\u00fccudu i\u00e7in gerekli bir amino asittir. K\u00f6pek idrar amino asit yolundaki dengesizlik AD ile ili\u015fkilidir. Kin\u00fcrenin yolu, ksantin ve kin\u00fcrenin olu\u015fumuna veya 3-hidroksiantranilat ve 3-metoksiantranilat \u00fcretimine yol a\u00e7an iki koldan olu\u015fur. Bir N-metil-D-aspartat resept\u00f6r antagonisti olarak k\u00f6pek \u00fcrik asidinin n\u00f6roprotektif etkileri oldu\u011fu d\u00fc\u015f\u00fcn\u00fcl\u00fcrken, 3-hidroksiantranilik asit ve 3-metoksiantranilik asit tuzlar\u0131 dahil olmak \u00fczere di\u011fer dallardan gelen metabolitlerin n\u00f6rotoksisiteye sahip oldu\u011funa inan\u0131lmaktad\u0131r. 3-hidroksiantranilik asit ve 3-metoksiantranilik asit tuzlar\u0131n\u0131n birikimi astrositlerin ve baz\u0131 sinir h\u00fccrelerinin apoptozisine yol a\u00e7abilir, b\u00f6ylece mikroglial sinir a\u011f\u0131n\u0131n \u00e7al\u0131\u015fmas\u0131n\u0131 zay\u0131flat\u0131r, n\u00f6rotrofik fakt\u00f6rlerin sentezini azalt\u0131r ve t\u00fcm sinir sistemine zarar verebilir. Er Zhi Wan, AD s\u0131\u00e7anlar\u0131n\u0131n idrar\u0131ndaki 3-hidroksiantranilat i\u00e7eri\u011fini azaltarak Er Zhi Wan'\u0131n n\u00f6rotoksik maddeleri azaltarak sinir h\u00fccrelerini koruyabilece\u011fini g\u00f6sterir.<\/p>\n

Ayr\u0131ca, \u00e7al\u0131\u015fmalar doku proteaz D'nin AD i\u00e7in \u00f6nemli bir tan\u0131sal fakt\u00f6r olabilece\u011fini g\u00f6stermi\u015ftir. \u00c7al\u0131\u015fma, kontrol deneklerinden ve bili\u015fsel bozuklu\u011fu olan hastalardan al\u0131nan plazma \u00f6rneklerinde Alzheimer hastal\u0131\u011f\u0131n\u0131n patogenezi ile ili\u015fkili se\u00e7ilmi\u015f protein seviyelerindeki de\u011fi\u015fiklikleri incelemi\u015ftir. Hastal\u0131\u011f\u0131 do\u011fru bir \u015fekilde s\u0131n\u0131fland\u0131rmak i\u00e7in 56 kat\u0131l\u0131mc\u0131ya klinik bili\u015fsel testler, amiloid pozitron emisyon tomografisi ve manyetik rezonans g\u00f6r\u00fcnt\u00fcleme skorlar\u0131 kullan\u0131larak beyaz madde hiperintensiteleri uyguland\u0131. Deneklerin plazma katepsin D d\u00fczeyleri imm\u00fcnoblotlama ve enzime ba\u011fl\u0131 imm\u00fcnosorbent deneyi (ELISA) ile incelenmi\u015ftir. Plazma doku proteaz D d\u00fczeyleri ile AD ile ili\u015fkili fakt\u00f6rler ve klinik \u00f6zellikler aras\u0131ndaki korelasyonu istatistiksel analiz yoluyla incelemek. Kantitatif imm\u00fcnoblotlama ve ELISA analizi ile, kontrol grubu ile kar\u015f\u0131la\u015ft\u0131r\u0131ld\u0131\u011f\u0131nda, beyindeki amiloid plaklarda biriken katepsin D'nin (maj\u00f6r bir lizozomal proteaz) plazma seviyelerinin azald\u0131\u011f\u0131n\u0131 bulduk. Plazma katepsin D d\u00fczeyi, Klinik Demans Derecelendirme \u00d6l\u00e7e\u011fi toplam puan\u0131 ile negatif korelasyon g\u00f6stermektedir. Kapsaml\u0131 \u00e7ok de\u011fi\u015fkenli lojistik regresyon modeli, plazma doku proteaz D d\u00fczeylerinin AH hastalar\u0131n\u0131 AH olmayan hastalardan ay\u0131rt etmede y\u00fcksek performansa sahip oldu\u011funu g\u00f6stermektedir. Bu sonu\u00e7lar, plazma doku proteaz D d\u00fczeylerinin AH ile yak\u0131ndan ili\u015fkili oldu\u011funu ve AH i\u00e7in tan\u0131sal bir biyobelirte\u00e7 fenolojik se\u00e7ici olarak geli\u015ftirilebilece\u011fini g\u00f6stermektedir.<\/p>\n

AD s\u0131\u00e7anlar\u0131nda Er Zhi Wan ile m\u00fcdahaleden sonra, \u00fcridin, 3-hidroksiantranilik asit, p-kresol s\u00fclfat, p-kresol, N-asetilserotonin, 3-metoksi-4-hidroksifenilen glikol s\u00fclfat seviyeleri, 4-guanidinob\u00fctirik asit, adenozin, kreatinin, vanilik asit, taurin, indoliloksi s\u00fclfat, hipervanadat, sitrik asit ve fenilasetilglisin normale d\u00f6nm\u00fc\u015ft\u00fcr. Yol zenginle\u015ftirme analizinin sonu\u00e7lar\u0131, Er Zhi Wan'\u0131n triptofan metabolizmas\u0131, taurin ve d\u00fc\u015f\u00fck taurin metabolizmas\u0131, sitrik asit d\u00f6ng\u00fcs\u00fc (TCA d\u00f6ng\u00fcs\u00fc), glioksilat ve dikarboksilik asit metabolizmas\u0131 gibi s\u00fcre\u00e7leri d\u00fczenleyerek AD'de sinerjik m\u00fcdahale sa\u011flayabilece\u011fini g\u00f6stermektedir. A\u011f farmakolojisinin sonu\u00e7lar\u0131, form\u00fcldeki birden fazla bile\u015fenin birlikte \u00e7al\u0131\u015ft\u0131\u011f\u0131n\u0131, AD ile ilgili birden fazla hedefi i\u00e7erdi\u011fini ve geleneksel \u00c7in t\u0131bb\u0131 re\u00e7etelerindeki birden fazla bile\u015fen ve hedefin sinerjik etkisini yans\u0131tt\u0131\u011f\u0131n\u0131 g\u00f6stermektedir. En \u00f6nemli ke\u015fif, metabolomik ve a\u011f farmakolojisinin kesi\u015fimi, yani Er Zhi Wan'\u0131n AD tedavisindeki etkinli\u011finin temel hedefi ve anahtar\u0131 olabilecek katepsin D'dir. Bununla ilgili do\u011frudan etkili bile\u015fen, hem Ligustrum lucidum hem de Alternanthera philoxeroides'de bulunan ve bu form\u00fcl\u00fcn etkili bile\u015fenlerinden biri oldu\u011fu teyit edilen kuersetindir. Yukar\u0131daki sonu\u00e7lara dayanarak, bu \u00e7al\u0131\u015fma AD tedavisinde \u00f6nemli bir ara\u015ft\u0131rma \u00f6nemine sahip oldu\u011funa inanmaktad\u0131r ve daha fazla do\u011frulama ara\u015ft\u0131rmas\u0131 kademeli olarak quercetin'in doku proteaz D \u00fczerindeki ilgili \u00e7al\u0131\u015fmalar\u0131na odaklanacakt\u0131r. Bu \u00e7al\u0131\u015fman\u0131n sonucu, Er Zhi Wan'\u0131n anti AD mekanizmas\u0131n\u0131n incelenmesi i\u00e7in teorik bir temel sa\u011flar ve daha fazla ara\u015ft\u0131rmaya hala ihtiya\u00e7 vard\u0131r.<\/p>","protected":false},"excerpt":{"rendered":"

Study on the mechanism of action of Er Zhi Wan in combating Alzheimer’s disease based on serum metabolomics and network pharmacology Er Zhi Wan comes from the classic Ming Dynasty prescription “Yi Bian” Volume 1, and has the effects of nourishing kidney essence, stopping bleeding, and strengthening the body and bones. 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