{"id":5289,"date":"2024-08-04T18:15:20","date_gmt":"2024-08-04T18:15:20","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=5289"},"modified":"2024-08-04T18:15:20","modified_gmt":"2024-08-04T18:15:20","slug":"dihydromyricetin-2","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/dihidromiricetin-2\/","title":{"rendered":"A dihidromiricetin mechanizmus\u00e1nak felt\u00e1r\u00e1sa a vesefibr\u00f3zis jav\u00edt\u00e1s\u00e1ban db\/db egerekben a h\u00e1l\u00f3zati farmakol\u00f3gia \u00e9s a k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n"},"content":{"rendered":"

A dihidromiricetin mechanizmus\u00e1nak felt\u00e1r\u00e1sa a vesefibr\u00f3zis jav\u00edt\u00e1s\u00e1ban db\/db egerekben a h\u00e1l\u00f3zati farmakol\u00f3gia \u00e9s a k\u00eds\u00e9rleti ellen\u0151rz\u00e9s alapj\u00e1n
\nA diabetes nephropathia (DKD) a 2-es t\u00edpus\u00fa diabetes mellitus (T2DM) egyik legfontosabb mikrovaszkul\u00e1ris sz\u00f6v\u0151dm\u00e9nye \u00e9s a v\u00e9gst\u00e1dium\u00fa vesebetegs\u00e9g f\u0151 oka. F\u0151 jellemz\u0151i a glomerul\u00e1ris baz\u00e1lis membr\u00e1n megvastagod\u00e1sa, a mesenterium \u00e9s a tubulointerstitialis m\u00e1trix kit\u00e1gul\u00e1sa, valamint a podocit\u00e1k elveszt\u00e9se, ami mikroalbuminuria \u00e9s cs\u00f6kkent vesefunkci\u00f3 kialakul\u00e1s\u00e1hoz vezet. A diab\u00e9teszes vesebetegs\u00e9g (DKD) folyamatos fejl\u0151d\u00e9s\u00e9vel a vesesz\u00f6vet mikrostrukt\u00far\u00e1ja tart\u00f3s gyullad\u00e1son \u00e9s k\u00e1rosod\u00e1son megy kereszt\u00fcl, ami diff\u00faz interstici\u00e1lis fibr\u00f3zishoz vezet, amely elpuszt\u00edtja a norm\u00e1lis vese mikrostrukt\u00far\u00e1j\u00e1t, \u00e9s v\u00e9g\u00fcl vesefibr\u00f3ziss\u00e1 (RF) fejl\u0151dik. Jelenleg a DKD RF-hez val\u00f3 progresszi\u00f3j\u00e1nak enyh\u00edt\u00e9s\u00e9re szolg\u00e1l\u00f3 eszk\u00f6z\u00f6k els\u0151sorban a DKD jav\u00edt\u00e1s\u00e1ra \u00f6sszpontos\u00edtanak. A cukorbetegs\u00e9g legt\u00f6bb sz\u00f6v\u0151dm\u00e9ny\u00e9nek, k\u00f6zt\u00fck a DKD-nek a mechanizmusa azonban m\u00e9g nem tiszt\u00e1zott, \u00edgy a DKD RF-v\u00e9 alakul\u00e1s\u00e1nak komplex mechanizmusa nem vil\u00e1gos, ami a DKD \u00e9s az RF nem kiel\u00e9g\u00edt\u0151 ter\u00e1pi\u00e1s hat\u00e1saihoz vezet. Ez\u00e9rt s\u00fcrg\u0151s a DKD patogenezis\u00e9nek felt\u00e1r\u00e1sa \u00e9s \u00faj ter\u00e1pi\u00e1s c\u00e9lpontok felfedez\u00e9se a kialakul\u00e1s\u00e1nak g\u00e1tl\u00e1sa \u00e9rdek\u00e9ben.
\nA dihidromiricetin (DHM) egy term\u00e9szetes flavonoid vegy\u00fclet, amely k\u00fcl\u00f6nb\u00f6z\u0151 farmakol\u00f3giai hat\u00e1sokkal rendelkezik, bele\u00e9rtve a gyullad\u00e1scs\u00f6kkent\u0151, antioxid\u00e1ns, szabadgy\u00f6k-fog\u00f3, a mitokondri\u00e1lis diszfunkci\u00f3 jav\u00edt\u00e1s\u00e1t \u00e9s az autof\u00e1gia szab\u00e1lyoz\u00e1s\u00e1t. Jelenleg t\u00f6bb tanulm\u00e1ny is kimutatta, hogy a DHM nagy potenci\u00e1llal rendelkezik az anyagcsere-betegs\u00e9gek kezel\u00e9s\u00e9ben. Nemcsak az autof\u00e1gia induk\u00e1l\u00e1s\u00e1val, az oxidat\u00edv stressz jav\u00edt\u00e1s\u00e1val, a gyullad\u00e1s g\u00e1tl\u00e1s\u00e1val \u00e9s a mitokondri\u00e1lis aktivit\u00e1s n\u00f6vel\u00e9s\u00e9vel jav\u00edthatja az inzulinrezisztenci\u00e1t \u00e9s cs\u00f6kkentheti a v\u00e9rcukorszintet, hanem; Ugyanakkor jav\u00edthatja a cukorbetegs\u00e9g sz\u00e1mos sz\u00f6v\u0151dm\u00e9ny\u00e9t, p\u00e9ld\u00e1ul a cukorbetegs\u00e9g encephalopathi\u00e1j\u00e1t, a cukorbetegs\u00e9g kardiomiop\u00e1ti\u00e1j\u00e1t stb. A cukorbetegs\u00e9g sz\u00f6v\u0151dm\u00e9nyeit jav\u00edt\u00f3 DHM-re vonatkoz\u00f3 kutat\u00e1s azonban nem elegend\u0151, \u00e9s a kapcsol\u00f3d\u00f3 farmakol\u00f3giai mechanizmust m\u00e9g tov\u00e1bb kell vizsg\u00e1lni. Ezenk\u00edv\u00fcl korl\u00e1tozott a kutat\u00e1s arra vonatkoz\u00f3an, hogy a DHM tov\u00e1bb jav\u00edthatja-e a DHM \u00e1ltal okozott RF-t, \u00e9s a ter\u00e1pi\u00e1s hat\u00e1s m\u00e9g mindig nem vil\u00e1gos.
\nA h\u00e1l\u00f3zati farmakol\u00f3gia a hagyom\u00e1nyos k\u00ednai gy\u00f3gy\u00e1szat \u00f6sszetev\u0151inek szerkezete, biol\u00f3giai hat\u00e1sai \u00e9s a betegs\u00e9ggel kapcsolatos c\u00e9lpontok alapj\u00e1n a biol\u00f3giai folyamatok hatalmas h\u00e1l\u00f3zat\u00e1nak \u00f6sszef\u00fcgg\u00e9s\u00e9ben egy \"gy\u00f3gyszer\u00f6sszetev\u0151 c\u00e9lbetegs\u00e9g\" k\u00f6lcs\u00f6nhat\u00e1si h\u00e1l\u00f3zatot \u00e9p\u00edthet fel. Ez hat\u00e9kony eszk\u00f6z a hagyom\u00e1nyos k\u00ednai orvosl\u00e1s hat\u00e9kony \u00f6sszetev\u0151inek, molekul\u00e1ris mechanizmusainak \u00e9s potenci\u00e1lis c\u00e9lpontjainak felt\u00e1r\u00e1s\u00e1ra. A molekul\u00e1ris dokkol\u00e1s k\u00e9pes szimul\u00e1lni a molekul\u00e1k \u00e9s feh\u00e9rj\u00e9k k\u00f6z\u00f6tti k\u00f6lcs\u00f6nhat\u00e1st, megj\u00f3solni a ligandumok \u00e9s receptorok konform\u00e1ci\u00f3j\u00e1t, kisz\u00e1m\u00edtani \u00e9s megj\u00f3solni az affinit\u00e1st \u00e9s a k\u00f6t\u0151d\u00e9si m\u00f3dokat, hogy ellen\u0151rizni lehessen a gy\u00f3gyszerkomponensek f\u0151 c\u00e9lpontokra gyakorolt specifikus hat\u00e1sm\u00f3dj\u00e1t. Ez\u00e9rt ez a tanulm\u00e1ny h\u00e1l\u00f3zati farmakol\u00f3gi\u00e1t haszn\u00e1lt a DHM potenci\u00e1lis c\u00e9lpontjainak sz\u0171r\u00e9s\u00e9re \u00e9s el\u0151rejelz\u00e9s\u00e9re a DKD \u00e9s RF eset\u00e9ben, fel\u00e9p\u00edtett egy \"komponens-c\u00e9lbetegs\u00e9g\" k\u00f6lcs\u00f6nhat\u00e1si h\u00e1l\u00f3zatot, \u00e9s valid\u00e1lta a megj\u00f3solt f\u0151 c\u00e9lpontokat molekul\u00e1ris dokkol\u00e1ssal \u00e9s in vivo k\u00eds\u00e9rletekkel. Felt\u00e1rtuk a dihidromiricetin vesefibr\u00f3zist jav\u00edt\u00f3 molekul\u00e1ris mechanizmus\u00e1t a db\/db egerekben, elm\u00e9leti alapot szolg\u00e1ltatva a DHM klinikai alkalmaz\u00e1s\u00e1hoz.<\/p>\n

 <\/p>\n

\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"\"
\nJelenleg a cukorbetegs\u00e9g \u00e1ltal\u00e1nos kezel\u00e9se els\u0151sorban a v\u00e9rcukorszint szab\u00e1lyoz\u00e1s\u00e1n m\u00falik, m\u00edg a cukorbetegs\u00e9g egyik legs\u00falyosabb sz\u00f6v\u0151dm\u00e9ny\u00e9nek, a DKD-nek nincs hat\u00e9kony kezel\u00e9si strat\u00e9gi\u00e1ja. Ez\u00e9rt nagyon fontos a DKD patogenezis\u00e9nek m\u00e9lyrehat\u00f3 meg\u00e9rt\u00e9se \u00e9s hat\u00e9kony kezel\u00e9si strat\u00e9gi\u00e1k megtal\u00e1l\u00e1sa a DKD vesefibr\u00f3ziss\u00e1 alakul\u00e1s\u00e1nak elfojt\u00e1s\u00e1ra. A term\u00e9szetes gy\u00f3gyszerek bizony\u00edtottan egyed\u00fcl\u00e1ll\u00f3 el\u0151nyei k\u00f6z\u00e9 tartozik a kevesebb mell\u00e9khat\u00e1s \u00e9s a t\u00f6bb c\u00e9lpontot \u00e9rint\u0151 hat\u00e9konys\u00e1g, ami az ut\u00f3bbi \u00e9vekben a kr\u00f3nikus betegs\u00e9gek \u00faj gy\u00f3gyszereinek kifejleszt\u00e9s\u00e9ben fontos forr\u00e1ss\u00e1 tette \u0151ket. A DHM tov\u00e1bbi kutat\u00e1sa jelent\u0151s ter\u00e1pi\u00e1s potenci\u00e1lt t\u00e1rt fel az anyagcsere-betegs\u00e9gek jav\u00edt\u00e1s\u00e1ban. Ez\u00e9rt a DHM \u00e1ltal a vesefibr\u00f3zis javul\u00e1sa a db\/db egerekben, ez a tanulm\u00e1ny a h\u00e1l\u00f3zati farmakol\u00f3gi\u00e1t \u00e9s a molekul\u00e1ris dokkol\u00e1si technol\u00f3gi\u00e1t kombin\u00e1lja a DHM potenci\u00e1lis ter\u00e1pi\u00e1s c\u00e9lpontjainak \u00e9s molekul\u00e1ris mechanizmusainak felt\u00e1r\u00e1s\u00e1ra a vesefibr\u00f3zis jav\u00edt\u00e1s\u00e1ban a db\/db egerekben, \u00e9s \u00e1llatk\u00eds\u00e9rleteken kereszt\u00fcl ellen\u0151rzi \u0151ket.<\/p>\n

El\u0151sz\u00f6r is, megfigyelt\u00fck, hogy a 10 hetes DHM beavatkoz\u00e1s hat\u00e9konyan enyh\u00edti a v\u00e9rcukorszintet, a testt\u00f6meget, a kreatinint, a karbamid nitrog\u00e9nt, a vizeletfeh\u00e9rj\u00e9t \u00e9s a vese patol\u00f3giai megnyilv\u00e1nul\u00e1sait a db\/db egerekben, ami azt jelzi, hogy a DHM enyh\u00edtheti a vesefunkci\u00f3 k\u00e1rosod\u00e1s\u00e1t \u00e9s lass\u00edthatja a DKD kialakul\u00e1s\u00e1t a db\/db egerekben. A DHM, a DKD \u00e9s az RF 37 egym\u00e1st keresztez\u0151 c\u00e9lpontj\u00e1nak elemz\u00e9se \u00e9s sz\u0171r\u00e9se ut\u00e1n meg\u00e1llap\u00edtott\u00e1k, hogy 10 c\u00e9lpont, k\u00f6zt\u00fck az AKT1, ALB, CASP3, EGFR, MMP9, IGF1, PPARG, KDR, MMP2, ACE, kulcsfontoss\u00e1g\u00fa c\u00e9lpontjai lehetnek a DHM-nek a DKD jav\u00edt\u00e1s\u00e1ra. Az AKT1, CASP3, EGFR, MMP9, IGF1, MMP2, ACE bizony\u00edtottan aktiv\u00e1l\u00f3dnak a cukorbetegs\u00e9g k\u00f6rnyezet\u00e9ben, \u00e9s a specifikus g\u00e1tl\u00e1s jav\u00edthatja a DKD k\u00e1rosodott \u00e1llapot\u00e1t \u00e9s lass\u00edthatja a fibr\u00f3zis fejl\u0151d\u00e9si tendenci\u00e1j\u00e1t. A PPARG \u00e9s a KDR g\u00e1tolt a cukorbetegs\u00e9g fiziol\u00f3gi\u00e1s k\u00f6rnyezet\u00e9ben, \u00e9s szerepet j\u00e1tszik a vese v\u00e9delm\u00e9ben az aktiv\u00e1l\u00e1st k\u00f6vet\u0151en. Az ALB fontos biok\u00e9miai indik\u00e1tor a vesek\u00e1rosod\u00e1s m\u00e9rt\u00e9k\u00e9nek megfigyel\u00e9s\u00e9re a cukorbetegs\u00e9g kialakul\u00e1sa sor\u00e1n. A DKD kialakul\u00e1s\u00e1val \u00e1ltal\u00e1ban n\u00f6vekszik, \u00e9s a DKD javul\u00e1sa ut\u00e1n cs\u00f6kken. Ez azt jelenti, hogy az \u00e1ltalunk \u00e1tvizsg\u00e1lt 10 kulcsfontoss\u00e1g\u00fa g\u00e9n nemcsak a DKD potenci\u00e1lis biomarkerek\u00e9nt, hanem a DKD patogenezis\u00e9nek \u00e9s kezel\u00e9s\u00e9nek tov\u00e1bbi felt\u00e1r\u00e1s\u00e1hoz kulcsfontoss\u00e1g\u00fa c\u00e9lpontk\u00e9nt is szolg\u00e1lhat.<\/p>\n

A KEGG \u00fatvonalak gazdagod\u00e1si elemz\u00e9se azt mutatta, hogy a DHM javul\u00e1sa a DKD-n\u00e9l mag\u00e1ban foglalhatja az AGE-RAGE jel\u00e1tviteli \u00fatvonalat, a diab\u00e9teszes kardiomiop\u00e1ti\u00e1t \u00e9s a FoxO jel\u00e1tviteli \u00fatvonalat. Az AGE-RAGE jel\u00e1tviteli \u00fatvonal \u00e9s a FoxO jel\u00e1tviteli \u00fatvonal kulcsfontoss\u00e1g\u00fa szab\u00e1lyoz\u00f3 szerepet j\u00e1tszik a DKD kialakul\u00e1s\u00e1ban. A kutat\u00e1sok azt tal\u00e1lt\u00e1k, hogy az AGE-k specifikusan aktiv\u00e1l\u00f3dnak a DKD betegek endot\u00e9lsejtjeiben, vesetubulusaiban, mezangi\u00e1lis sejtjeiben \u00e9s podocit\u00e1iban, \u00e9s k\u00f6lcs\u00f6nhat\u00e1suk a RAGE-vel fokoz\u00f3dik, tov\u00e1bb s\u00falyosb\u00edtva az oxidat\u00edv stresszt \u00e9s a gyullad\u00e1st a ves\u00e9ben, ami a DKD roml\u00e1s\u00e1hoz vezet. Ezenk\u00edv\u00fcl az aktiv\u00e1lt FoxO3a g\u00e1tolhatja az oxidat\u00edv stressz szintj\u00e9t a cukorbeteg patk\u00e1nyok ves\u00e9j\u00e9ben, jav\u00edthatja a gyullad\u00e1st, majd g\u00e1tolhatja a DKD el\u0151fordul\u00e1s\u00e1t. Ez azt jelzi, hogy az AGE-RAGE jel\u00e1tviteli \u00fatvonal vagy a FoxO jel\u00e1tviteli \u00fatvonal specifikus szab\u00e1lyoz\u00e1sa nagy jelent\u0151s\u00e9ggel b\u00edrhat a DKD megel\u0151z\u00e9s\u00e9ben \u00e9s kezel\u00e9s\u00e9ben.<\/p>\n

A molekul\u00e1ris dokkol\u00e1si eredm\u00e9nyek azt mutatt\u00e1k, hogy a DHM j\u00f3 k\u00f6t\u0151d\u00e9si affinit\u00e1st mutatott a top 5 kiv\u00e1lasztott c\u00e9lponthoz, ami azt jelzi, hogy a DHM hat\u00e9konys\u00e1g\u00e1t a DKD kezel\u00e9s\u00e9ben molekul\u00e1ris szinten valid\u00e1lt\u00e1k. Ezenk\u00edv\u00fcl \u00e9szrevett\u00fck, hogy a kulcsfontoss\u00e1g\u00fa c\u00e9lg\u00e9n AKT1, amely a sz\u0171r\u00e9s sor\u00e1n az els\u0151 helyre ker\u00fclt, a KEGG-\u00fatvonal gazdagod\u00e1si elemz\u00e9s\u00e9n kereszt\u00fcl szorosan kapcsol\u00f3dik az AGE-RAGE jel\u00e1tviteli \u00fatvonalhoz \u00e9s a FoxO jel\u00e1tviteli \u00fatvonalhoz a DKD kialakul\u00e1s\u00e1ban. Az AGE-RAGE jel\u00e1tviteli \u00fatvonal a PI3K\/Akt jel\u00e1tviteli \u00fatvonallal szinergi\u00e1ba l\u00e9pve oxidat\u00edv stresszt \u00e9s kr\u00f3nikus gyullad\u00e1st id\u00e9zhet el\u0151 a ves\u00e9ben, ami vesebetegs\u00e9ghez vezet. A PI3K\/Akt\/FoxO3a \u00fatvonal aktiv\u00e1l\u00e1sa jav\u00edthatja a vese fiziol\u00f3giai funkci\u00f3j\u00e1t cukorbetegs\u00e9gben. Ez\u00e9rt tov\u00e1bbi k\u00eds\u00e9rletet tett\u00fcnk az AKT1 \u00e9s a DHM el\u0151tti Notch-\u00fatvonal k\u00f6z\u00f6tti k\u00f6lcs\u00f6nhat\u00e1s vizsg\u00e1lat\u00e1ra, \u00e9s molekul\u00e1ris dokkol\u00f3 valid\u00e1l\u00e1st v\u00e9gezt\u00fcnk. A molekul\u00e1ris dokkol\u00e1si eredm\u00e9nyek azt mutatt\u00e1k, hogy a DHM j\u00f3 k\u00f6t\u00e9si affinit\u00e1st mutatott a Notch1 \u00e9s a PTEN k\u00f6z\u00f6tt.<\/p>\n

Kor\u00e1bbi tanulm\u00e1nyok kimutatt\u00e1k, hogy a Notch-\u00fatvonal t\u00falm\u0171k\u00f6dik a DKD kialakul\u00e1sa sor\u00e1n, ami a Notch1, NICD, Hes1 \u00e9s Hey1 fokozott expresszi\u00f3j\u00e1ban nyilv\u00e1nul meg. A Notch1 g\u00e1tl\u00f3i a Hes1 aktiv\u00e1l\u00f3d\u00e1s\u00e1nak cs\u00f6kkent\u00e9s\u00e9vel aktiv\u00e1lhatj\u00e1k a PTEN-t, ez\u00e1ltal jav\u00edtva az autof\u00e1gia rendelleness\u00e9geit \u00e9s lass\u00edtva az RF kialakul\u00e1s\u00e1t. Ezenk\u00edv\u00fcl m\u00e1s vizsg\u00e1latok azt tal\u00e1lt\u00e1k, hogy a PTEN aktiv\u00e1l\u00e1sa a PI3K\/Akt \u00fatvonal g\u00e1tl\u00e1s\u00e1val a DKD progresszi\u00f3j\u00e1t is enyh\u00edtheti. A fenti eredm\u00e9nyek alapj\u00e1n felt\u00e9telezz\u00fck, hogy a DHM jav\u00edthatja a DKD-t a Notch\/PTEN\/AKT \u00fatvonal szab\u00e1lyoz\u00e1s\u00e1val. A Western blot eredm\u00e9nyek a Notch \u00fatvonal aktiv\u00e1l\u00f3d\u00e1s\u00e1nak k\u00f3ros n\u00f6veked\u00e9s\u00e9t, a PTEN expresszi\u00f3j\u00e1nak cs\u00f6kken\u00e9s\u00e9t \u00e9s az AKT foszforil\u00e1ci\u00f3 n\u00f6veked\u00e9s\u00e9t mutatt\u00e1k ki a db\/db egerek ves\u00e9iben. A DHM bevitele pedig g\u00e1tolhatja a Notch-\u00fatvonal aktiv\u00e1l\u00f3d\u00e1s\u00e1t, aktiv\u00e1lhatja a PTEN-t \u00e9s g\u00e1tolhatja az AKT foszforil\u00e1ci\u00f3j\u00e1t. B\u00e1r a Notch \/ PTEN \/ AKTT jeltengelyt mint teljes \u00fatvonalat ritk\u00e1n vizsg\u00e1lt\u00e1k a vesev\u00e9delemmel kapcsolatban a cukorbetegs\u00e9gben, kutat\u00e1sunk bizonyos m\u00e9rt\u00e9kig jav\u00edtotta a vonatkoz\u00f3 kutat\u00e1st, \u00e9s t\u00f6bb c\u00e9lponton kereszt\u00fcl gazdag\u00edtotta a DHM biol\u00f3giai v\u00e9delm\u00e9nek molekul\u00e1ris mechanizmus\u00e1t.<\/p>\n

\u00d6sszefoglalva, a DKD patol\u00f3giai megnyilv\u00e1nul\u00e1sait jav\u00edt\u00f3 DHM megfigyel\u00e9se alapj\u00e1n ez a tanulm\u00e1ny kombin\u00e1lta a h\u00e1l\u00f3zati farmakol\u00f3gi\u00e1t \u00e9s a molekul\u00e1ris dokkol\u00e1si technol\u00f3gi\u00e1t, hogy el\u0151zetesen kimutassa, hogy a DHM szerepe a DKD progresszi\u00f3j\u00e1nak jav\u00edt\u00e1s\u00e1ban olyan kulcsfontoss\u00e1g\u00fa c\u00e9lpontokon kereszt\u00fcl \u00e9rhet\u0151 el, mint az AKT1, ALB, CASP3, EGFR, MMP9, IGF1, PPARG, KDR, MMP2, ACE, \u00e9s elemezte a vonatkoz\u00f3 \u00fatvonalakat; V\u00e9g\u00fcl a DHM potenci\u00e1lis AKT c\u00e9lpontjainak el\u0151zetes valid\u00e1l\u00e1s\u00e1t \u00e9s elemz\u00e9s\u00e9t v\u00e9gezt\u00fck el \u00e1llatk\u00eds\u00e9rleteken kereszt\u00fcl, \u00e9s meg\u00e1llap\u00edtottuk, hogy a DHM szerepet j\u00e1tszhat a DKD megel\u0151z\u00e9s\u00e9ben \u00e9s kezel\u00e9s\u00e9ben a Notch\/PTEN\/AKT \u00fatvonal szab\u00e1lyoz\u00e1s\u00e1val (l\u00e1sd a 14. \u00e1br\u00e1t). Jelenleg azonban viszonylag kev\u00e9s kutat\u00e1s foglalkozik a DHM sz\u00f6v\u0151dm\u00e9nyeivel T2DM-ben, \u00e9s ter\u00e1pi\u00e1s potenci\u00e1lja m\u00e9g tov\u00e1bbi vizsg\u00e1latokat ig\u00e9nyel.<\/p>","protected":false},"excerpt":{"rendered":"

Exploring the mechanism of dihydromyricetin in improving renal fibrosis in db\/db mice based on network pharmacology and experimental verification Diabetes nephropathy (DKD) is one of the major microvascular complications of type 2 diabetes mellitus (T2DM) and the main cause of end-stage renal disease. Its main characteristics are thickening of the glomerular basement membrane, expansion of […]<\/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 dihydromyricetin in improving renal fibrosis in db\/db mice 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\/dihidromiricetin-2\/\" \/>\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 dihydromyricetin in improving renal fibrosis in db\/db mice based on network pharmacology and experimental verification - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Exploring the mechanism of dihydromyricetin in improving renal fibrosis in db\/db mice based on network pharmacology and experimental verification Diabetes nephropathy (DKD) is one of the major microvascular complications of type 2 diabetes mellitus (T2DM) and the main cause of end-stage renal disease. 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