{"id":3648,"date":"2024-08-02T15:59:52","date_gmt":"2024-08-02T15:59:52","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=3648"},"modified":"2024-08-02T15:59:52","modified_gmt":"2024-08-02T15:59:52","slug":"seabuckthorn-flavone","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/da\/havtorn-flavon\/","title":{"rendered":"Mekanismeunders\u00f8gelse af den hjertebeskyttende effekt af havtornflavonoider p\u00e5 rotter med langvarig udmattelsestr\u00e6ning"},"content":{"rendered":"

Mekanismeunders\u00f8gelse af den hjertebeskyttende effekt af havtornflavonoider p\u00e5 rotter med langvarig udmattelsestr\u00e6ning
\nForskning har bekr\u00e6ftet, at moderat fysisk tr\u00e6ning kan fremkalde godartede \u00e6ndringer i hjertets form, struktur og funktion, men langvarig udmattende tr\u00e6ning kan have negative virkninger p\u00e5 det kardiovaskul\u00e6re system og endda f\u00f8re til tr\u00e6ningsinduceret myokardieskade. Under kontinuerlig udmattende tr\u00e6ning sker der en stigning i dannelsen af endogene reaktive iltarter (ROS), hvilket begr\u00e6nser evnen til at fjerne ROS. Overdreven ROS inducerer dysfunktion af myokardieceller, protein- og lipidperoxidation og DNA-skader. Derudover kan langvarig udmattende tr\u00e6ning fremkalde en udbredt inflammatorisk reaktion i kroppen, og infiltrationen af inflammatoriske celler kan for\u00e5rsage strukturel og funktionel sv\u00e6kkelse af myokardiecellerne. Den oxidative stress og det inflammatoriske respons, der fremkaldes af udmattende tr\u00e6ning, aktiverer forskellige hjertemuskelhypertrofi-signalkinaser og transkriptionsfaktorer og fremkalder celleapoptose gennem DNA- og mitokondrieskader samt aktivering af pro-apoptotiske signaler. En unders\u00f8gelse viste, at 6-ugers udmattelsestr\u00e6ning kan aktivere apoptoseprogrammet for myokardieceller og fremskynde den funktionelle \"ombygningsproces\" af hjertestrukturen ved at opregulere ekspressionsforholdet mellem Bcl-2-associeret X-protein (Bax)\/B-celle-lymfom-2-gen (Bcl-2) i myokardieceller fra rotter. Desuden har unders\u00f8gelser bekr\u00e6ftet, at aflejring og fibrose af ekstracellul\u00e6re matrixkomponenter, der fremkaldes af langvarig udmattende tr\u00e6ning, kan v\u00e6re t\u00e6t forbundet med celleapoptose.<\/p>\n

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\nHavtorn tilh\u00f8rer familien Elapidae og er en traditionel medicinsk og spiselig plante i Kina. Dens antioxidant-, antitumor- og antiapoptotiske virkninger er blevet bredt bekr\u00e6ftet. Havtornflavonoider (SF) er den vigtigste aktive komponent i havtorn. 50-250 \u03bc g\/mL SF kan forbedre den fagocytiske evne hos museceller og effektivt h\u00e6mme dannelsen af oxidativt stress og inflammatoriske mark\u00f8rer i Raw 264.7-celler; 4 g\/kg SF-sonde kombineret med aerob tr\u00e6ning kan h\u00e6mme apoptoseresponsen i rottehippocampusv\u00e6v. Der mangler dog i \u00f8jeblikket forskning i de kardiobeskyttende virkninger af SF p\u00e5 langtidsudmattede tr\u00e6ningsrotter. Baseret p\u00e5 dette har denne unders\u00f8gelse til form\u00e5l at etablere en rottemodel for tr\u00e6ningsinduceret myokardieskade gennem langvarig udmattende tr\u00e6ning og unders\u00f8ge SF's interventionseffekt p\u00e5 myokardieskade hos rotter med langvarig udmattende tr\u00e6ning for at tilvejebringe eksperimentelle beviser for forebyggelse og rehabilitering af tr\u00e6ningsinduceret myokardieskade.<\/p>\n

Systematisk og videnskabelig tr\u00e6ning kan fremkalde gavnlige adaptive \u00e6ndringer i hjertet, men langvarig udmattende tr\u00e6ning kan have negative virkninger p\u00e5 myokardiev\u00e6v gennem inflammatoriske reaktioner, oxidative stressreaktioner, aktivering af celleapoptose og fibrose. Der er forskning, der bekr\u00e6fter, at langvarig udmattende tr\u00e6ning kan aktivere myokardiecellernes oxidative stressrespons og formidle apoptoseprogrammet. Aktiveringsprocessen af ROS og Caspase-3-veje er t\u00e6t forbundet, hvilket kan fremkalde mitokondriel skade og f\u00f8re til mekanisk dysfunktion i myokardiet. I mellemtiden kan cytokinfrigivelse og neutrofil infiltration induceret inflammatorisk respons v\u00e6re de igangs\u00e6ttende faktorer for celleapoptose, og forekomsten af apoptose giver ogs\u00e5 betingelser for forv\u00e6rring af v\u00e6vsinflammatorisk respons. Forskning har vist, at ekspressionsprofilen af myokardieapoptosegener \u00e6ndres efter udmattende tr\u00e6ning, med signifikant opregulering af myokardieproapoptotisk genekspression og Bax\/Bcl-2 ratio. Lignende resultater blev observeret i dette eksperiment, hvor langvarig udmattende tr\u00e6ning f\u00f8rte til signifikante stigninger i MDA, IL-1 \u03b2, IL-6, TNF - \u03b1-niveauer, Caspase-3, Bax-proteinekspression og Bcl-2\/Bax-forhold i rotte-myokardiet. SOD, GSH Px-niveauer og Bcl-2-proteinekspression blev signifikant reduceret, hvilket indikerer, at langvarig udmattende tr\u00e6ning forv\u00e6rrede oxidativ stress og inflammatoriske reaktioner og inducerede aktivering af rotte-myokardiev\u00e6vets apoptoseprogram.<\/p>\n

Forskning har vist, at overdreven tr\u00e6ningsstimulering kan fremkalde myokardiev\u00e6vsfibrose gennem forskellige veje, og aktivering af myokardiev\u00e6vsapoptose kan fremskynde kollagensyntese og processen med myokardiefibrose. Langvarig udmattende tr\u00e6ning fremmer myokardieinfarkt og fibrose ved at fremkalde mikromilj\u00f8skader (inflammation, celleapoptose osv.) i kroppen. Langvarig udmattelsestr\u00e6ning kan fremkalde myokardiev\u00e6vsinflammation gennem ekspression af pro-inflammatoriske cytokiner som TNF-\u03b1 og intercellul\u00e6rt adh\u00e6sionsmolekyle-1 hos rotter, hvilket f\u00f8rer til tr\u00e6ningsinduceret myokardiev\u00e6vsstrukturel mikroskade og atriefibrose. Udmattende tr\u00e6ning induceret af myokardialt oxidativt stressrespons kan yderligere inducere myokardiefibrose, men der mangler i \u00f8jeblikket direkte beviser. Desuden har unders\u00f8gelser vist, at 6 ugers udmattende tr\u00e6ning kan fremkalde myokardiefibrose og fibroblastproliferation ved at opregulere Bax\/Bcl-2-forholdet i myokardiev\u00e6v fra rotter og aktivere p38 MAPK\/Smad2\/3-signalvejen. Dette eksperiment er i overensstemmelse med tidligere unders\u00f8gelser. En langvarig udmattelses\u00f8velse p\u00e5 l\u00f8beb\u00e5nd blev brugt til at etablere en dyremodel for tr\u00e6ningsinduceret myokardieskade. Resultaterne viste, at rotter udsat for langvarig udmattelsestr\u00e6ning udviste opregulering af myokardieskademark\u00f8rer i serum, \u00f8get oxidativ stress, inflammatorisk respons og celleapoptose i myokardiev\u00e6v samt \u00e6ndringer i v\u00e6vsmorfologi og fibrose.<\/p>\n

P\u00e5 nuv\u00e6rende tidspunkt er der mangel p\u00e5 forskning i SF's effekt p\u00e5 tr\u00e6ningsinduceret myokardieskade. Imidlertid viser nogle beviser for sideintervention af planteafledte flavonoidekstrakter, at forskellige planteafledte flavonoidekstrakter har forebyggende og terapeutiske virkninger p\u00e5 tr\u00e6ningsinduceret myokardieskade. I dette eksperiment reducerede mellemstore og h\u00f8je doser af SF (200, 400 mg\/kg) sammenlignet med modelgruppen effektivt serummark\u00f8rer for myokardieskade hos rotter. Samtidig viste HE-farvning af myokardiet, at mellemstore og h\u00f8je doser af SF (200, 400 mg\/kg) effektivt afhjalp den morfologiske skade p\u00e5 myokardiev\u00e6v for\u00e5rsaget af langvarig udmattelsestr\u00e6ning. P\u00e5 nuv\u00e6rende tidspunkt er SF's antioxidante og antiinflammatoriske aktiviteter blevet bredt anerkendt, og denne unders\u00f8gelse underst\u00f8tter ogs\u00e5 tidligere forskningskonklusioner. I denne unders\u00f8gelse blev det ogs\u00e5 bekr\u00e6ftet, at tilskud med 200 og 400 mg\/(kg - d) SF effektivt kan h\u00e6mme oxidativ stress, inflammatorisk respons og ekspression af serummark\u00f8rer for myokardieskade i myokardiev\u00e6v. Sammenlignet med modelgruppen kan indgift af 100 mg\/kg SF ogs\u00e5 reducere niveauerne af inflammatoriske faktorer og oxidativ stress i myokardiev\u00e6v hos rotter, der har v\u00e6ret udmattede i l\u00e6ngere tid, men effekten er ikke signifikant. Forskning har vist, at havtornvandsekstrakt kan h\u00e6mme apoptose og fremme spredning af humane ud\u00f8delige keratinocytter, samtidig med at det deltager i multi-target downstream apoptose signalvej regulering. Derudover kan oral administration af havtornpolysaccharider (200 mg \/ kg) h\u00e6mme apoptose af leverceller i septisk induceret leverskade mus, opregulere udtrykket af peroxisom proliferatoraktiveret receptor gamma og Bcl-2 i septisk muselever og nedregulere udtrykket af NF - \u03ba B, Bax og Caspase-3.
\nDenne unders\u00f8gelse viste, at efter SF-intervention steg udtrykket af Caspase-3- og Bax-proteiner og Bcl-2\/Bax-forholdet i myokardiet hos udmattede tr\u00e6ningsrotter betydeligt, mens udtrykket af Bcl-2-protein faldt betydeligt. Dette beviser, at SF (100, 200, 400 mg\/(kg - d)) kan h\u00e6mme kardiomyocyt-apoptose-responsen induceret af langvarig udmattende tr\u00e6ning. Forskning har vist, at totale flavonoider fra havtorn kan reducere udtrykket af fibrose-relaterede proteiner ved at h\u00e6mme de inflammatoriske og oxidative stressresponser i hypertrofisk arv\u00e6v i kanin\u00f8rer, hvorved effektiviteten af fibroblasttransformation i fibrotisk v\u00e6v reduceres og progressionen af hypertrofiske ar h\u00e6mmes. Flavonoide aktive stoffer opregulerer ekspressionen af fibroblastv\u00e6kstfaktor 21-protein, h\u00e6mmer transformationsv\u00e6kstfaktoren - \u03b2 1-signalvejen, inducerer nedregulering af myokardiefibrosemark\u00f8rer CTGF, kollagen-I og kollagen-III-ekspression og reducerer derved myokardiefibrose, oxidativ stress og celleapoptose og forbedrer i sidste ende hjertefunktionen hos mus med myokardiefibrose. Lignende resultater blev opn\u00e5et i dette eksperiment, hvor langvarig udmattende tr\u00e6ning signifikant opregulerede udtrykket af CTGF- og kollagen-I-proteiner i myokardiev\u00e6v fra rotter samt CVF i myokardiev\u00e6v. SF (100, 200, 400 mg\/(kg - d)) kunne effektivt h\u00e6mme fibrose i myokardiev\u00e6v.
\nSammenfattende indikerer denne unders\u00f8gelse, at 6-ugers kontinuerlig udmattende tr\u00e6ning inducerer oxidativ stress og \u00f8get inflammatorisk respons i rotte-myokardiev\u00e6v, hvilket f\u00f8rer til myokardiecelle-apoptose og fibrose, hvilket resulterer i myokardiev\u00e6vsskade. SF kan effektivt lindre oxidativ stress og inflammatorisk respons i myokardiev\u00e6v hos langtidsudmattede tr\u00e6ningsrotter, h\u00e6mme myokardiecelleapoptose og fibrose og dermed ud\u00f8ve myokardiebeskyttende effekter.<\/p>","protected":false},"excerpt":{"rendered":"

Mechanism study on the cardioprotective effect of seabuckthorn flavonoids on long-term exhaustion exercise rats Research has confirmed that moderate physical exercise can induce benign changes in the shape, structure, and function of the heart, but long-term exhaustive exercise may have negative effects on the cardiovascular system and even lead to exercise-induced myocardial injury. During continuous […]<\/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":"\nMechanism study on the cardioprotective effect of seabuckthorn flavonoids on long-term exhaustion exercise rats - 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\/havtorn-flavon\/\" \/>\n<meta property=\"og:locale\" content=\"da_DK\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Mechanism study on the cardioprotective effect of seabuckthorn flavonoids on long-term exhaustion exercise rats - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Mechanism study on the cardioprotective effect of seabuckthorn flavonoids on long-term exhaustion exercise rats Research has confirmed that moderate physical exercise can induce benign changes in the shape, structure, and function of the heart, but long-term exhaustive exercise may have negative effects on the cardiovascular system and even lead to exercise-induced myocardial injury. 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