{"id":7514,"date":"2024-08-06T20:17:59","date_gmt":"2024-08-06T20:17:59","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=7514"},"modified":"2024-08-06T20:17:59","modified_gmt":"2024-08-06T20:17:59","slug":"kaempferol","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/da\/kaempferol\/","title":{"rendered":"Mekanismen for kaempferol, der inducerer apoptose af tredobbelt negative brystkr\u00e6ftceller gennem mitokondriel apoptosevej"},"content":{"rendered":"

Mekanismen for kaempferol, der inducerer apoptose af tredobbelt negative brystkr\u00e6ftceller gennem mitokondriel apoptosevej
\nTriple negativ brystkr\u00e6ft (TNBC), som en s\u00e6rlig undertype af brystkr\u00e6ft, tegner sig for 15%~20% af det samlede antal brystkr\u00e6fttilf\u00e6lde. Det har de kliniske egenskaber ved kort samlet overlevelsesperiode, h\u00f8j malignitet, st\u00e6rk invasion, h\u00f8j tidlig tilbagefaldshastighed osv. N\u00e5r metastase opst\u00e5r, er patienternes medianoverlevelsesperiode kun 10 ~ 13 m\u00e5neder. P\u00e5 grund af TNBC's uf\u00f8lsomhed over for endokrin terapi og m\u00e5lrettet terapi er kemoterapi den vigtigste behandlingsmetode. L\u00e6gemiddelresistens og behandlingsrelaterede bivirkninger giver dog stadig anledning til bekymring. I de senere \u00e5r er den traditionelle kinesiske medicins rolle i forebyggelse og behandling af TNBC blevet mere og mere v\u00e6rdsat p\u00e5 grund af dens unikke teoretiske system og ekspertise inden for individualiserede behandlingsplaner. Vores forskningsgruppe fandt ud af, at tils\u00e6tning og reduktion af Chaihu Guizhi Decoction kombineret med capecitabin kan h\u00e6mme v\u00e6ksten af subkutan transplanteret tumor af tredobbelt negativ brystkr\u00e6ft i n\u00f8genmus gennem tidligere forskning. Yderligere analyse ved hj\u00e6lp af netv\u00e6rksfarmakologimetoden viste, at kaempferol (KA) er en vigtig effektiv komponent i tils\u00e6tning og reduktion af Chaihu Guizhi Decoction, hvilket giver os et eksperimentelt grundlag for at bruge kaempferol til behandling af tredobbelt negativ brystkr\u00e6ft.
\nKaempferol er en flavonoidforbindelse, der findes i gr\u00f8ntsager, frugt og traditionel kinesisk medicin. Det har forskellige virkninger som f.eks. anti-cancer, anti-inflammatorisk, antioxidant og antiviral. Det kan h\u00e6mme spredning og invasion af tumorceller ved at fremkalde celleapoptose, regulere cellecyklus, h\u00e6mme angiogenese og tumormetastase. Forskning har vist, at KA inducerer v\u00e6ksth\u00e6mning og apoptose i lungekr\u00e6ftceller ved at aktivere MEK-MAPK. In vitro og in vivo h\u00e6mmer KA AKT\/PI3K- og ERK-vejene, aktiverer den mitokondrielle apoptosevej og \u00f8ger str\u00e5lingsdr\u00e6bning af lungekr\u00e6ftceller. I tyktarmskr\u00e6ft rekonstruerer KA intercellul\u00e6r kommunikation af gap junctions ved at \u00f8ge ekspressionen og fosforyleringen af junction protein 43 i tyktarmskr\u00e6ftceller og derved inducere celleapoptose. KA kan ogs\u00e5 fremkalde apoptose og aldring i humane livmoderhalskr\u00e6ftceller ved at nedregulere PI3K\/AKT- og hTERT-vejene. Ved brystkr\u00e6ft er det blevet rapporteret, at KA spiller en antitumorrolle gennem forskellige mekanismer. KA kan h\u00e6mme invasionen af brystkr\u00e6ftceller ved at blokere ekspressionen og aktiviteten af PKC \u03b4\/MAPK\/AP-1-kaskaden og efterf\u00f8lgende matrixmetalloproteinase-9 (MMP-9). Li et al fandt ud af, at KA kan h\u00e6mme spredningen af brystkr\u00e6ft SK-BR-3-celler ved at regulere Notch1-proteinet. Derudover kan KA ogs\u00e5 h\u00e6mme den epitheliale mesenkymale transformation (EMT) og metastaserelaterede adf\u00e6rd hos MCF-7 brystkr\u00e6ftceller induceret af triclosan. Selvom KA's anticancereffekt i en r\u00e6kke forskellige tumorer er blevet bekr\u00e6ftet, er der ingen rapport om, hvorvidt KA kan inducere apoptose af tredobbelt negative brystkr\u00e6ftceller og dens molekyl\u00e6re mekanisme. Denne unders\u00f8gelse vil tage den humane TNBC-celle MDA-MB-231 som forskningsobjekt for at observere effekten af kaempferol p\u00e5 MDA-MB-231-celleapoptose, og om den mulige mekanisme er relateret til den mitokondrielle apoptosevej, for at give teoretisk grundlag og eksperimentelt grundlag for klinisk brug af kaempferol til behandling af tredobbelt negativ brystkr\u00e6ft.<\/p>\n

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\nKaempferol, som er en udbredt polyolhydroxyflavonoidforbindelse i forskellige planter, kan ikke kun effektivt h\u00e6mme tumorcellev\u00e6kst og fremkalde apoptose, men ogs\u00e5 opretholde normale cellers v\u00e6kstvitalitet. Chen et al. fandt, at KA kan inducere prostatacancercellecyklusstop, h\u00e6mme celleproliferation og ikke have nogen effekt p\u00e5 levedygtigheden af normale humane forhudsfibroblaster (HFF), hvilket indikerer, at KA har god antitumoreffektivitet og lav toksicitet. Tu et al. fandt, at KA effektivt kan h\u00e6mme spredning og metastase af humane livmoderhalskr\u00e6ftceller, mens dens cytotoksiske virkning p\u00e5 carcinoembryonale nyreceller og normale leverceller er relativt lille, hvilket indikerer, at KA har en h\u00f8j kr\u00e6ftcellem\u00e5lretningsevne. Der er kun f\u00e5 unders\u00f8gelser af KA i tredobbelt negative brystkr\u00e6ftceller. Derfor bekr\u00e6ftede denne unders\u00f8gelse, at KA kan h\u00e6mme spredningen af TNBC-celler betydeligt og fremme celleapoptose gennem in vitro-unders\u00f8gelser af MDA-MB-231- og MCF-10A-celler, men ikke har nogen effekt p\u00e5 spredningen af normale brystepitelceller MCF-10A.
\nP\u00e5 dette grundlag unders\u00f8ger dette eksperiment yderligere apoptose-induktionsmekanismen for KA p\u00e5 MDA-MB-231-celler. P\u00e5 nuv\u00e6rende tidspunkt har forskning fundet, at celleapoptose hovedsageligt involverer tre veje baseret p\u00e5 initieringsprocessen: mitokondrievej, d\u00f8dsreceptorvej og endoplasmatisk retikulumvej, og mitokondrievejen spiller en vigtig rolle i formidlingen af celleapoptose. Mitokondrielt membranpotentiale er en af de bedste indikatorer, der afspejler permeabiliteten af den mitokondrielle indre membran. Faldet i mitokondriemembranpotentialet anses for at v\u00e6re den tidligste begivenhed i kaskaden af celleapoptose. N\u00e5r mitokondriernes membranpotentiale kollapser, bliver celleapoptose irreversibel. Feng et al. isolerede en arabinogalactan fra Artemisia scoparia, som kan dr\u00e6be humane nasofaryngeale karcinom CNE-2-celler ved at for\u00e5rsage tab af mitokondriemembranpotentiale. Denne unders\u00f8gelse viste, at KA reducerer mitokondriemembranpotentialet i MDA-MB-231-celler, hvilket tyder p\u00e5, at en af de mekanismer, hvormed kaempferol h\u00e6mmer celleproliferation og fremmer apoptose, kan opn\u00e5s gennem den mitokondriemedierede apoptosevej. For yderligere at unders\u00f8ge forholdet mellem KA-induceret apoptose af MDA-MB-231-celler og mitokondriel apoptosesignalvej, p\u00e5viste denne unders\u00f8gelse udtrykket af Bcl-2, Bax, CytC, Cyclin D1 samt aktiviteten af Caspase-3 og Caspase-9.<\/p>\n

Bcl-2-familien af proteiner omfatter det anti-apoptotiske protein Bcl-2 og det pro-apoptotiske protein Bax. Som regulatorer af den mitokondrielle ydre membrans integritet spiller de en vigtig rolle i reguleringen af den mitokondrielle apoptosevej. Efter at have modtaget det apoptotiske signal translokeres Bax i cytoplasmaet til mitokondrierne, og det antiapoptotiske protein Bcl-2 styrer frigivelsen af cytokrom C fra mitokondrierne, hvilket fremmer selvaktiveringen af Caspase-9-forstadiet. Aktiveret Caspase-9 aktiverer Caspase-3, hvilket i sidste ende f\u00f8rer til celleapoptose. Liu et al. fandt, at KA h\u00e6mmer spredningen af humane galdebl\u00e6recancerceller og inducerer deres apoptose gennem den mitokondrielle apoptosevej. I denne unders\u00f8gelse observerede vi, at KA \u00f8gede ekspressionen af Bax og reducerede ekspressionen af Bcl-2 i MDA-MB-231-celler, hvilket fremmede frigivelsen af CytC i cytoplasmaet gennem den mitokondrielle apoptosevej, hvilket resulterede i \u00f8get ekspression. Samtidig \u00f8ges mitokondriemembranens permeabilitet, membranpotentialet falder, pr\u00e6apoptotiske faktorer frigives, hvilket udl\u00f8ser downstream-aktivering af Caspase-3 og Caspase-9, hvilket i sidste ende f\u00f8rer til celleapoptose. Derudover er apoptose t\u00e6t forbundet med unormal celleproliferation, og hoved\u00e5rsagen til celleproliferation er unormal cellecyklus. Cyclin D1, som et vigtigt reguleringsprotein i cellecyklussen, kan fremme overgangen af celler fra G1-fase til S-fase, fremskynde cellecyklusprocessen, og dens opregulering kan for\u00e5rsage unormal celleproliferation, fremkalde \u00e6ndringer i mitokondriemembranpotentialet og f\u00f8re til tumorudvikling. Resultaterne af dette eksperiment indikerer, at KA kan nedregulere ekspressionen af apoptoserelaterede proteiner Cyclin D1 og Bcl-2 i MDA-MB-231-celler, reducere mitokondriemembranpotentialet, h\u00e6mme celleproliferation og fremme celleapoptose.<\/p>\n

For at opsummere har denne unders\u00f8gelse afklaret kaempferols anticancereffekt p\u00e5 triple negative brystkr\u00e6ftceller in vitro og har en vis sikkerhed og afklaret mekanismen for KA, der inducerer apoptose af MDA-MB-231-celler gennem mitokondriel apoptosesignalvej. Senere kan den h\u00e6mmende effekt af KA p\u00e5 TNBC unders\u00f8ges yderligere gennem in vivo-eksperimenter, hvilket giver eksperimentelt grundlag for udvikling og klinisk anvendelse af KA.<\/p>","protected":false},"excerpt":{"rendered":"

The mechanism of kaempferol inducing apoptosis of triple negative breast cancer cells through mitochondrial apoptosis pathway Triple negative breast cancer (TNBC), as a special subtype of breast cancer, accounts for 15%~20% of the total number of breast cancer. It has the clinical characteristics of short overall survival period, high malignancy, strong invasion, high early recurrence […]<\/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":"\nThe mechanism of kaempferol inducing apoptosis of triple negative breast cancer cells through mitochondrial apoptosis pathway - 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\/da\/kaempferol\/\" \/>\n<meta property=\"og:locale\" content=\"da_DK\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The mechanism of kaempferol inducing apoptosis of triple negative breast cancer cells through mitochondrial apoptosis pathway - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"The mechanism of kaempferol inducing apoptosis of triple negative breast cancer cells through mitochondrial apoptosis pathway Triple negative breast cancer (TNBC), as a special subtype of breast cancer, accounts for 15%~20% of the total number of breast cancer. 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