{"id":7321,"date":"2024-08-06T19:26:38","date_gmt":"2024-08-06T19:26:38","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=7321"},"modified":"2024-08-06T19:26:38","modified_gmt":"2024-08-06T19:26:38","slug":"three-hundred-rods","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/da\/three-hundred-rods\/","title":{"rendered":"Tre hundrede stave baseret p\u00e5 PI3K\/AKT\/mTOR-stien fremmer lipopolysakkarid-induceret autofagi og h\u00e6mmer inflammation i RAW264.7-celler"},"content":{"rendered":"

Tre hundrede stave baseret p\u00e5 PI3K\/AKT\/mTOR-stien fremmer lipopolysakkarid-induceret autofagi og h\u00e6mmer inflammation i RAW264.7-celler
\nLipopolysaccharid (LPS) er et endotoksin, der frigives af gramnegative bakterier, og som kan stimulere inflammatoriske immunresponser ved bakterietoksicitet for\u00e5rsaget af gramnegative bakterieinfektioner i menneskekroppen. Makrofager deltager ofte i inflammatoriske reaktioner og fagocytose, og den LPS-behandlede makrofaglinje RAW 264.7 er en almindeligt anvendt cellemodel for inflammatoriske reaktioner i immunceller. Autofagi er en katabolsk proces, hvor cytoplasmatisk indhold transporteres af autofagosomer til lysosomer til omfattende nedbrydning for at opretholde cellul\u00e6r homeostase. Autofagi, som er en vigtig cellul\u00e6r mekanisme, er involveret i forekomsten og udviklingen af forskellige sygdomme som autoimmune sygdomme, inflammatoriske sygdomme og tumorer. Inflammatorisk respons er en type immunforsvarsfunktion i kroppens v\u00e6v. Moderat inflammatorisk respons hj\u00e6lper med at reparere skader p\u00e5 kroppen, men overdreven inflammatorisk respons kan f\u00f8re til u\u00f8nskede reaktioner i kroppen og for\u00e5rsage degeneration og nekrose af organer, v\u00e6v og celler og endda bringe livet i fare. Mange studier har fundet en tovejskommunikation mellem autofagi og inflammation. Moderat autofagi kan sv\u00e6kke den inflammatoriske reaktion, men overdreven autofagi kan forv\u00e6rre den inflammatoriske reaktion. Flere immunmediatorer kan inducere eller h\u00e6mme autofagi, men genoprettelsen af dens homeostase er st\u00e6rkt afh\u00e6ngig af autofagi. Derfor kan en fuld forst\u00e5else af den regulerende mekanisme for autofagi p\u00e5 inflammation effektivt behandle inflammatoriske og autoimmune sygdomme.
\nTre hundrede pinde stammer fra roden af Toddalia asiatica (L.) Lam, en plante i Rutaceae-familien. I \"Tujia Medicinal Records\" st\u00e5r der tydeligt, at den virker ved at \"fordrive vind og fugt, fremme blodcirkulationen og afslappe sener, reducere h\u00e6velser og lindre smerter\". Unders\u00f8gelser af den kemiske sammens\u00e6tning har vist, at de vigtigste kemiske komponenter i Sanbai-staven er alkaloider og coumariner. Moderne farmakologisk forskning har bekr\u00e6ftet, at ekstraktet af Sanbai-staven har antireumatiske, antiinflammatoriske, antitumor- og andre virkninger. Vores forel\u00f8bige eksperimentelle forskning har vist, at Sanbai stick kan blokere autofagi flow gennem phosphatidylinositol 3-kinase \/ proteinkinase B \/ mammalian rapamycin target protein (PI3K \/ AKT \/ MTOR) signalvej og derved h\u00e6mme spredningen og inducere apoptose af fibroblastcellelinjen MH7A. Toddalia asiatica alkoholekstrakts (TAAE) rolle i autofagi er dog stadig umoden. Resultaterne af denne unders\u00f8gelse viste, at TAAE udl\u00f8ser autofagi p\u00e5 en koncentrationsafh\u00e6ngig m\u00e5de. For yderligere at verificere, om TAAE spiller en vigtig rolle i autofagi af RAW 264.7-makrofager gennem PI3K\/AKT\/mTOR-vejen, brugte dette eksperiment LPS-stimulerede RAW 264.7-celler som en model til at unders\u00f8ge virkningerne af TAAE p\u00e5 autofagi og immunfunktion af RAW 264.7-celler og udforske den molekyl\u00e6re mekanisme for TAAE-regulering af medf\u00f8dt immunrespons.<\/p>\n

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\nMakrofager er en af de vigtigste immunceller i menneskekroppen. De kan hurtigt aktivere stresstilstande mod patogener, der invaderer menneskets v\u00e6v og blod, hvilket f\u00f8rer til en r\u00e6kke inflammatoriske reaktioner. De er vigtige medf\u00f8dte immunceller, der er t\u00e6t forbundet med forekomsten og udviklingen af inflammation. Inflammation er en kompleks patologisk reaktion, som er for\u00e5rsaget af en r\u00e6kke fysiske reaktioner i immunsystemet, n\u00e5r det uds\u00e6ttes for ekstern skade eller infektion. Det er en vigtig del af patofysiologien ved mange kroniske sygdomme, f.eks. neurodegenerative sygdomme, leddegigt, arteriosklerose osv. En unders\u00f8gelse har vist, at TAAE kan h\u00e6mme Toll like receptor 4\/nuclear factor - \u03ba B (TLR4\/NF - \u03ba B) og derved reducere udtrykket af kollageninducerede inflammatoriske cytokiner interleukin-1 \u03b2 (IL-1 \u03b2) og tumornekrosefaktor - \u03b1 (TNF - \u03b1) i synovium hos rotter (CIA), h\u00e6mme rheumatoid arthritis synovitis og undertrykke udviklingen af rheumatoid arthritis. TAAE kan ogs\u00e5 h\u00e6mme den nukleare indtr\u00e6ngen af NF - \u03ba B og derved undertrykke frigivelsen af inflammatoriske faktorer og h\u00e6mme synovialproliferation. Yang et al. fandt, at ethanolekstraktet og ethylacetatekstraktet af 300 pinde kan h\u00e6mme ledh\u00e6velse i CIA-rotte-modeller, reducere proinflammatoriske faktorer som TNF - \u03b1, IL-1 \u03b2 og interleukin-6 (IL-6) og \u00f8ge udtrykket af den immunosuppressive faktor interleukin-10 (IL-10) i serum. Alt det ovenst\u00e5ende viser de fremragende antiinflammatoriske og antireumatiske virkninger af de tre hundrede pinde.<\/p>\n

Autofagi er den proces, hvor eukaryote celler bruger lysosomer til at nedbryde deres egne cytoplasmatiske proteiner og beskadigede organeller under regulering af autofagirelaterede gener. Denne proces kan nedbryde invaderende patogene mikroorganismer, beskadigede organeller og unormalt ophobede proteiner og spiller en vigtig rolle i biologiske processer som cellekvalitetskontrol, metabolisme og medf\u00f8dt og adaptiv immunitet. Mange unders\u00f8gelser har bekr\u00e6ftet, at autofagi har en dobbeltrettet effekt p\u00e5 inflammation: P\u00e5 den ene side kan autofagi modvirke inflammatoriske reaktioner ved at fjerne inflammatoriske proteinaggregater og nedregulere proinflammatoriske cytokiner, der for\u00e5rsager v\u00e6vsskade; P\u00e5 den anden side aktiverer autofagi inflammasomer, der producerer en stor m\u00e6ngde inflammatoriske faktorer og derved fremskynder den inflammatoriske proces. Efter at have afbalanceret de positive og negative aspekter af immunitet og inflammation kan autofagi ses som en beskytter mod infektion, autoimmunitet og inflammation. Det mikrotubuli-associerede protein light chain 3-II (LC3-II) er et kendetegnende protein for autofagi. Under autofagi forbindes LC3-I til et fosfatidylethanolmolekyle ved hj\u00e6lp af Atg5-Atg12-Atg16-komplekset for at danne LC3-II. P62 er et substrat for autofagisk nedbrydning og spiller en afg\u00f8rende rolle i genkendelsen og indkapslingen af nedbrudte substrater. N\u00e5r Beclin1 er overudtrykt i pattedyrceller, fremmer det cellul\u00e6r autofagi. Derfor kan LC3, Beclin1, P62 og Atg5 fungere som mark\u00f8rproteiner for autofagi. For at unders\u00f8ge, om den antiinflammatoriske effekt af TAAE er relateret til autofagi, brugte denne unders\u00f8gelse Western blot til at p\u00e5vise proteinudtrykket af autofagirelaterede proteiner P62, Beclin1, Atg5 og LC3 samt proteinudtrykket af inflammationsrelaterede proteiner TNF - \u03b1, IL-6 og cyclooxygenase-2 (COX-2). De eksperimentelle resultater viste, at efter TAAE-intervention steg proteinekspressionsniveauerne af Beclin1, Atg5 og LC3-II\/LC3- gradvist, mens ekspressionsniveauet af substrat P62-protein gradvist faldt, og ekspressionen af inflammationsrelaterede proteiner faldt ogs\u00e5. De eksperimentelle resultater ved hj\u00e6lp af MDC-metoden til m\u00e6rkning af autofagosomer og transmissionselektronmikroskopi til observation af autofagosomer viste ogs\u00e5, at TAAE fremmede autofagi i RAW 264.7-celler. For yderligere at demonstrere effekten af autofagi p\u00e5 inflammation blev autofagi-inhibitoren 3-MA, som ogs\u00e5 er en specifik inhibitor af PI3K-signalvejen, brugt til at kontrollere makrofag-autofagi, blokere autofagisk chelering og proteinnedbrydning. Resultaterne viste, at autofagi-inhibitoren 3-MA sv\u00e6kkede den h\u00e6mmende effekt af TAAE p\u00e5 inflammatoriske cytokiner, mens TAAE-intervention effektivt kunne reducere udskillelsen af cytokiner TNF - \u03b1 og IL-6 i den inflammatoriske model, hvilket igen viser, at TAAE ud\u00f8ver antiinflammatoriske virkninger ved at fremme autofagi i RAW 264.7-celler.<\/p>\n

PI3K\/AKT\/mTOR-signalvejen spiller en vigtig rolle i reguleringen af autofagi, og autofagi-niveauerne \u00f8ges, n\u00e5r PI3K\/AKT\/mTOR-vejen h\u00e6mmes. MTOR er et pattedyrsm\u00e5l for rapamycin og spiller en vigtig regulerende rolle i autofagi-responsen, idet det fungerer som en vigtig negativ regulerende akse for autofagi. Mange naturprodukter har vist sig at h\u00e6mme inflammation og autoimmune sygdomme ved at m\u00e5lrette PI3K\/AKT\/mTOR-medieret autofagi. Tidligere eksperimenter har bekr\u00e6ftet, at TAAE kan blokere autofagisk flow og fremme apoptose af MH7A-celler gennem PI3K\/AKT\/mTOR-signalvejen. PI3K\/AKT\/mTOR-signalvejen blev valideret ved Western blotting, og eksperimentelle data viste, at TAAE signifikant reducerede ekspressionsniveauerne af phosphoryleret PI3K, AKT og mTOR, hvilket indikerer, at TAAE udl\u00f8ser autofagi ved at h\u00e6mme PI3K\/AKT\/mTOR-vejen. Den samtidige brug af PI3K-agonist (740Y-P) viste yderligere, at TAAE inducerer autofagi ved at h\u00e6mme PI3K\/AKT\/mTOR-signalvejen. Desuden er PI3K\/AKT\/mTOR-signalvejen direkte relateret til inflammation og immunitet. Denne unders\u00f8gelse viste, at TAAE-behandling reducerede niveauerne af pro-inflammatoriske cytokiner i LPS-inducerede RAW 264.7-celler. Denne unders\u00f8gelse viser, at i det LPS-inducerede inflammatoriske milj\u00f8 i RAW 264.7-celler h\u00e6mmer TAAE den autofagirelaterede vej PI3K\/AKT\/mTOR, regulerer autofagirelaterede proteiner og inflammatoriske faktorer, fremmer autofagosomlysosomfusion og nedbrydning, p\u00e5virker homeostasen i inflammatoriske celler, h\u00e6mmer inflammatoriske reaktioner og ud\u00f8ver s\u00e5ledes antiinflammatoriske virkninger. Resultaterne af denne unders\u00f8gelse tyder p\u00e5, at PI3K\/AKT\/mTOR er en effektiv vej for TAAE til at ud\u00f8ve antiinflammatoriske virkninger og \u00f8ge autofagisk aktivitet, hvilket kan give nye ideer til klinisk behandling af autoimmune og metaboliske sygdomme relateret til bet\u00e6ndelse og er v\u00e6rd at yderligere dybtg\u00e5ende forskning.<\/p>","protected":false},"excerpt":{"rendered":"

Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells Lipopolysaccharide (LPS) is an endotoxin released by Gram negative bacteria, which can stimulate immune inflammatory responses in bacterial toxicity caused by Gram negative bacterial infections in the human body. Macrophages often participate in inflammatory responses and phagocytosis, and […]<\/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":"\nThree hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells - 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\/three-hundred-rods\/\" \/>\n<meta property=\"og:locale\" content=\"da_DK\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells Lipopolysaccharide (LPS) is an endotoxin released by Gram negative bacteria, which can stimulate immune inflammatory responses in bacterial toxicity caused by Gram negative bacterial infections in the human body. 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