Los ntawm Cocer Peptides 
26 hnub dhau los.
Lub siab, ua lub hauv paus hauv nruab nrab rau cov metabolism thiab detoxification hauv tib neeg lub cev, ua haujlwm tseem ceeb xws li biosynthesis, lub zog cia, thiab tshem tawm cov teeb meem tshuaj. Oxidative stress, toxin accumulation, thiab metabolic disorders yog thawj qhov ua rau lub siab raug mob, fatty siab, thiab hepatic fibrosis. Lub hauv paus tseem ceeb ntawm kev tiv thaiv daim siab, detoxification, thiab antioxidative kev nyuaj siab yog nyob rau hauv kev tswj hwm hepatocyte kev ua haujlwm zoo, txhim kho detoxifying enzyme kev ua, thiab tshem tawm cov dawb radicals ntau dhau. Cov tshuaj Peptide, nrog rau lawv cov kev ua haujlwm lom neeg siab thiab lub hom phiaj tshwj xeeb, tuaj yeem tswj cov kab mob siab metabolic, tiv thaiv hepatocytes los ntawm kev puas tsuaj oxidative, thiab txhawb nqa biotransformation thiab excretion ntawm co toxins, tawm los ua cov cuab yeej tshiab los tiv thaiv thiab cuam tshuam rau daim siab kab mob - ua rau pom muaj peev xwm tseem ceeb hauv cov kab mob siab cawv, tsis haus dej cawv (nrog rau daim siab mob plab).
Daim duab 1 Risk factor of non-alcoholic fatty liver disease (NAFLD). Tau qhov twg los: Kev Tshawb Fawb Txog Kev Tiv Thaiv Cov Teeb Meem thiab Molecular Mechanisms ntawm Berries Tawm Tsam Kev Nyuaj Siab Kev Noj Qab Haus Huv Kev Noj Qab Haus Huv: Tsis-Alcoholic Fatty Liver Disease (2024).
Core Application Areas
1. Kev Tiv Thaiv Kab Mob Siab: Ua kom muaj kab mob siab hepatocyte thiab kev ua haujlwm zoo
Cov tshuaj Peptide tsim kev tiv thaiv kab mob rau lub siab los ntawm kev tiv thaiv apoptosis, kev kho, thiab kev tswj hwm ntawm hepatocyte metabolism.
Inhibition ntawm hepatocyte apoptosis
Mitochondria-targeted peptides (xws li, SS-31) embed nyob rau hauv daim siab thiab mitochondrial daim nyias nyias, stabilizing mitochondrial membrane muaj peev xwm thiab inhibiting tso tawm ntawm cytochrome C thiab ua kom cov caspase-3. Qhov no txo oxidative kev nyuaj siab- los yog tshuaj-induced hepatocyte apoptosis. Lawv tiv thaiv cov nyhuv ntawm mitochondrial complexes tswj hepatocyte zog metabolism, tshwj xeeb tshaj yog mitigating hepatic lobular necrosis nyob rau hauv ischemia-reperfusion raug mob.
Copper peptides (piv txwv li, GHK-Cu) txhawb nqa phosphorylation ntawm hepatocyte txoj kev loj hlob zoo receptors, ua kom cov kab hauv qab kom nrawm DNA kho thiab organelle regeneration nyob rau hauv puas hepatocytes. Lawv kuj inhibit transforming loj hlob factor-β (TGF-β)-mediated fibrogenic signaling, ncua kev loj hlob ntawm hepatic fibrosis.
Kev tiv thaiv kab mob siab
Lub siab tiv thaiv peptides txo qis kev nkag mus ntawm cov hlab ntsha ntawm endotoxins thiab cov tshuaj lom metabolites los ntawm kev txhim kho cov lus qhia ntawm cov proteins nruj nreem nyob rau hauv daim nyias nyias, txo qis kev puas tsuaj rau hepatocytes los ntawm cov kab mob inflammatory. Qhov no ua rau lawv tsim nyog rau kev cuam tshuam thaum ntxov hauv kab mob siab cawv.
Daim duab 2 Nuclear factor erythroid 2-related factor 2 (NRF2) regulation and NRF2-mitochondrial interplay in chronic liver disease. Tau qhov twg los: Lub luag hauj lwm ntawm NFR2-Regulated Oxidative Stress thiab Mitochondrial Quality Control nyob rau hauv Chronic Liver Diseases (2023).
2. Detoxification: Txhim kho Hepatic Biotransformation thiab Excretion Functions
Lub siab ua haujlwm raws li lub cev lub cev detoxification, lub luag haujlwm rau metabolizing thiab tshem tawm cov tshuaj exogenous xws li co toxins thiab tshuaj. Lub siab tiv thaiv peptides koom nrog cov txheej txheem hepatic detoxification, txhawb cov metabolism thiab tshem tawm cov tshuaj lom kom txo tau lawv cov teebmeem hepatotoxic.
Ua kom cov theem I/II metabolic txoj kev
Glutathione (GSH, xws li GSH precursor peptides), uas yog ib qho tseem ceeb antioxidant thiab conjugation substrate nyob rau hauv hepatocytes, ncaj qha koom nyob rau hauv Phase II detoxification cov tshuaj tiv thaiv los ntawm khi rau electrophilic toxins los tsim cov dej-soluble complexes excreted los ntawm cov kua tsib. Qee cov peptides nce intracellular GSH reserves thiab txhim khu kev ua haujlwm ntawm glutathione S-transferase (GST), ua kom detoxification ntawm acetaminophen thiab cawv metabolites (xws li acetaldehyde).
Nicotinamide adenine dinucleotide (NAD, xws li NAD-txog peptides), ua ib coenzyme rau redox cov tshuaj tiv thaiv, koom nrog catalytic cov tshuaj tiv thaiv ntawm Phase I enzymes xws li cawv dehydrogenase thiab cytochrome P450, txhawb kev hloov pauv ntawm lipophilic co toxins rau hauv polar metabolites. Cov qib NAD nce ntxiv txhim kho lub siab lub siab ua haujlwm rau cov tshuaj thiab cov co toxins.
Kev tswj cov kua tsib acid metabolism
Lub siab tiv thaiv peptides (piv txwv li, Pnc 27) yog qhov xav tias yuav ua rau farnesoid X receptor (FXR) lossis cev xeeb tub X receptor (PXR), tswj kev qhia ntawm cov enzymes tseem ceeb thiab cov thauj khoom koom nrog hauv cov kua tsib acid synthesis. Qhov no txhawb cov kua tsib kua qaub excretion, txo intrahepatic tsub zuj zuj ntawm lom bile acids, thiab txhim kho lub pathological lub xeev ntawm cholestatic daim siab kab mob.
3. Antioxidative Stress: Tshem tawm cov dawb radicals thiab kho Oxidative puas
Hepatocyte raug mob los ntawm oxidative kev nyuaj siab yog ib kauj ruam tseem ceeb hauv kev mob siab rau daim siab. Peptide tshuaj tiv thaiv los ntawm ntau lub hom phiaj antioxidation.
Dawb radical scavenging thiab enzyme kev tswj hwm
Glutathione ncaj qha neutralizes dawb radicals xws li superoxide anions thiab hydrogen peroxide. Raws li lub substrate rau glutathione peroxidase, nws catalyzes txo cov lipid peroxides, txo cov membrane lipid peroxidation puas.
Antimicrobial peptides (piv txwv li, LL37), dhau ntawm lawv cov tshuaj tiv thaiv kab mob, inhibit NADPH oxidase kom txo qis intracellular reactive oxygen hom (ROS) ntau lawm hauv hepatocytes, thaiv oxidative stress-induced pathway activation thiab yog li inhibiting hepatocyte apoptosis thiab inflammatory factor secretion.
Mitochondrial muaj nuj nqi tiv thaiv
Mitochondria-targeted peptides (xws li, SS-31) tswj mitochondrial dynamic tshuav, txo mitochondrial fragmentation thiab ua tsis taus pa. Qhov no ua kom lub zog ruaj khov hauv hepatocytes thiab ua rau txo qis kev pheej hmoo ntawm oxidative puas tsuaj rau DNA thiab cov proteins.
Xaus
Kev siv cov tshuaj peptide hauv kev tiv thaiv oxidation thiab daim siab kev noj qab haus huv tsom rau cov txheej txheem tseem ceeb ntawm kev tiv thaiv hepatocyte, detoxification txoj kev txhim kho, thiab oxidative kev nyuaj siab, muab ntau yam kev daws teeb meem rau kev tiv thaiv thiab kho kab mob siab. Los ntawm kev tsom mus rau mitochondrial muaj nuj nqi, detoxifying enzyme systems, thiab redox tshuav nyiaj li cas, cov tshuaj no tsis tsuas yog ncaj qha scavenge dawb radicals thiab inhibit hepatocyte apoptosis tab sis kuj reshape hepatic metabolic phenotypes los ntawm nuclear receptor regulation-pom zoo mechanism nyob rau hauv cov kev tswj ntawm fatty siab, mob siab, thiab mob siab.
Tag nrho cov kab lus thiab cov ntaub ntawv ntawm cov khoom lag luam muab rau ntawm lub vev xaib no tsuas yog rau cov ntaub ntawv tshaj tawm kev tshaj tawm thiab cov hom phiaj kev kawm.
Cov khoom muab rau hauv lub vev xaib no yog npaj tshwj xeeb rau kev tshawb fawb hauv vitro. Kev tshawb fawb hauv vitro (Latin: * hauv iav *, lub ntsiab lus hauv iav) yog ua los ntawm tib neeg lub cev. Cov khoom no tsis yog tshuaj, tsis tau txais kev pom zoo los ntawm US Food and Drug Administration (FDA), thiab yuav tsum tsis txhob siv los tiv thaiv, kho, lossis kho txhua yam mob, kab mob, lossis mob. Nws raug txwv nruj raws li txoj cai los qhia cov khoom no rau hauv tib neeg lossis tsiaj lub cev hauv txhua daim ntawv.
