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ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.
Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto mɛrɛsin, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.
Ovaviu fɔ di tin dɛn we dɛn dɔn lan
di liva, as imכtant mεtabolik כgan na di mכtalman bכdi, kin pwεl frכm difrεn tin dεm, lεk dכg, rכkכl, vayral infεkshכn, εn di tכxin dεm we de na di envayroment. If dɛn nɔ kɔntrol di liva we de pwɛl fayn fayn wan, i kin go bifo to liva fibrosis, sirosis, ɔ ivin liva kansa, we kin rili ambɔg mɔtalman wɛlbɔdi. כksidεtiv strεs de ple imכtant rol fכ divεlכpmεnt fכ di liva dεm we de pwεl. we di liva de pan tin dεm we de damej, di bεlε bitwin di bכdi in כksidεtiv εn antioksidant sistεm dεm de disrupt, we de mek di riaktiv כksijεn spεshal (ROS) εn כda fri radikal dεm de prodyuz pasmak. dis fri radikal dεm pas di bכdi in antioksidant difεns sistεm in kapasiti fכ nyutralayz dεm, we de trigεr כksidεtiv strεs riakshכn dεm. dis fri radikal dεm we pasmak de atak di bayolojikal makromכlikul dεm na di liva sεl dεm, lεk di sεl mεmbran, protin, εn nyukliyk asid, we de mek di liva sεl dεm dεm, apoptosis, כ nεkrכsis.
Figure 1 di jεnarכl mεkanism skim fכ כksidεtiv strεs we difrεn fכs tin dεm de indyuz pan liva sik.
Livagen, as sכbstans we gεt pכtεnshal antioksidant prכpati dεm, kin mitigate di כksidεtiv strεs-indyus liva dεm bay we i de rεgεl di bכdi in antioksidant difεns sistεm, we de gi nyu we fכ di prεvεnshכn εn tritmεnt fכ di liva injuri.
Di Rol we Livagen de ple pan Antiɔksidant Strɛs ɛn Liva Injuri
Rigulεt di Antioksidant εnzym Aktiviti
livagen de inkrεs di aktiviti fכ di antioksidant εnzym dεm na di liva, lεk supεrכksayd dismutase (SOD) εn glutathione pεrכksidayz (GSH-Px). SOD na di fכs layn fכ difεns insay di bכdi in antioksidant difεns sistεm, we de katalayz di dismutεshכn riakshכn fכ supεrכksayd aniכn fri radikal dεm fכ prodyuz haydrojεn pεrכksayd εn כksijεn, we de ridyus di dεm we supεrכksayd aniכn fri radikal dεm de kכz to di liva sεl dεm. GSH-Px de yuz ridyus glutathione (GSH) fכ ridyus haydrojεn pεrכksayd to wata εn lipid pεrכksayd to dεn kכrεspכndεnt alkכhol dεm, we de inhεbit di prכgreshכn fכ lipid pεrכksidεshכn chen riakshכn dεm εn protεkt di integriti fכ di liva sεl mεmbran dεm.
Mentεn di Glutathione (GSH) Lεvεl
GSH na imכtant nכn-εnzym antioksidant na di liva, we de ple wan kכl rol fכ mεnten intasεlulyar rεdכks homכstasis. livagen kin mεnten di GSH lεvεl dεm na di liva bay we i de protεkt GSH sεntesis כ inhεbit in kכnsכmshכn. GSH nכ de כnli dayrekt patisipeyt insay fri radikal skavεnj riakshכn dεm bכt i de sכv lεk sabstεrayt fכ GSH-Px, we de εnhans in antioksidant aktiviti. we di liva de sכbjεkt כksidεtiv strεs, dεn de it GSH bכku bכku wan, we de mek in lεvεl dεm dכn. di intavεnshכn we livagen de du kin mek di GSH lεvεl dεm kam bak, we de mek di liva in antioksidant difεns kεpasiti εn ridyus di damej we di כksidεtiv strεs indyuz to di εpatosayt dεm.
Inhibiting di εksprεshכn כf inflammatory fכktכr dεm
כksidεtiv strεs εn inflammatory rεspכns dεm de intarakt εn rεinfכs dεn wan dεm we di liva de dεm. Livagen kin ridyus di liva inflameshn bay we i de inhibit di εksprεshכn fכ inflammatory fכktכ dεm, we de indaykt wan εksyεrt wan antioksidant ifekt. nyuklia fכktכ-κB (NF-κB) na di kכl transkripshכn fכktכ we de ple sεntri rol fכ rεgεl inflammatory rεspכns dεm. we di liva de εkspos to injuri stimuli, NF-κB de aktibכt, we de mek di εksprεshכn fכ difrεn inflammatory fכktכ dεm lεk tכmכro nεkrכsis fכktכ-α (TNF-α) εn intalyukin-1β (IL-1β). dis inflammatory fכktכ dεm de mek כksidεtiv strεs mכr, we de mek wan bad bad saykl. livagen kin inhεbit NF-κB aktibכshכn, ridyus di εksprεshכn fכ inflammatory fכktכ dεm, we de mek di liva inflammatory damej εn rεliv כksidεtiv strεs.
Figure 2 Di rεdכks homכstasis na di liva.
Fɔ mek di lipid pεrכksidεshכn dεm dεm dεm
lipid pεrכksidεshכn na wan pan di kכl mεkanism dεm we כksidεtiv strεs de mek di liva sεl dεm dεm. ROS de atak polyunsaturated fεt asid dεm na di sεl mεmbran, we de trigεr lipid pεrכksidεshכn riakshכn dεm εn jεnarεt lipid pεrכksidεshכn prodakt dεm lεk malondialdehyde (MDA). dis prodakt dεm na saytotoksik, we de disrupt di strכkchכ εn wok we di sεl mεmbran dεm de du εn mek di liva sεl dεm de damej. livagen, tru in antioksidant ifekt dεm, kin ebul fכ inhεbit di lipid pεrכksidεshכn riakshכn dεm fayn fayn wan, ridyus di MDA lεvεl dεm na di liva tisu, mitigate di sεl mεmbran dεm we dεn dכn pwεl, εn protεkt di nכmal fכnshכn fכ di liva sεl dεm.
Aplikeshɔn fɔ Livagen insay Liva Injuri Protɛkshɔn
Drug-Induse Liva Injuri
Drug-induced liver injury na wan pan di liva sik dɛm we kin kam pan klinik prɛktis. Bɔrku mɛrɛsin, lɛk asetaminofɛn ɛn antituberculosis drɔgs kin mek yu liva pwɛl we dɛn de trit sik dɛm. Livagen de sho fayn fayn protεktiv ifekt dεm na animal mכdel dεm fכ drog-induse liva injuri. Insay wan asetaminofɛn-indyuz liva injuri mɔdel, prɛ-tritmɛnt wit Livagen bin rili ridyus di sɛrum alanine transaminase (ALT) ɛn aspartate transaminase (AST) lɛvɛl, we sho se di ridɔkshɔn pan di siriɔs liva injuri. apat frכm dat, histopathכlכjik egzamεn fכ di liva tisu sho se Livagen impruv mכfכlכjik chenj dεm na di εpatosayt dεm, rεdכks hεpatosayt nεkrכsis, εn dεkrεs inflammatory sεl infiltεshכn. Dis sho se Livagen gɛt pɔtɛnɛshɛl aplikeshɔn valyu fɔ prɛvɛnshɔn ɛn tritmɛnt fɔ drɔg-indyuz liva injuri ɛn i kin sav as nyu opshɔn fɔ adjɔnt tɛrapi insay drɔg-indyuz liva injuri.
Alkohol liva injuri
If yu drink pasmak fɔ lɔng tɛm, dat kin mek yu gɛt injury na yu liva we yu de drink rɔm, ɛn dis kin mek di sikman dɛn kwaliti layf ɛn wɛlbɔdi prɔblɛm bad bad wan. Livagen de sho bak se i de protɛkt pɔsin frɔm di injuri we pɔsin kin gɛt we i de drink rɔm. insay animal εkspεriεns dεm fכ alkol liva injuri, afta dεn administret Livagen, כksidεtiv strεs mak dεm na di liva bin impruv, lεk inkrεs SOD aktiviti εn rεdכks MDA lεvεl. livagen kin rεgεl bak di aktiviti fכ di εnzym dεm we riliyt to alkכhol mεtabolism, we de ridyus di prodakshכn fכ fri radikal dεm we di alkol mεtabolism de du, we de mek i sכmtεm di damej we di alkol de mek. Livagen kin mek di liva inflammatory responses we alcohol-induced liva, lכs di inflammatory factor lεvεl, εn i kin protεkt di liva mכr frכm damej. Livagen gɛt di potenshal fɔ bi wan fayn drɔg fɔ di prɛvɛnshɔn ɛn tritmɛnt fɔ alkol liva injuri.
Dɔn
livagen de du antioksidant strεs ifekt tru mכltipכl mεkanism dεm, we inklud fכ rεgεl antioksidant εnzym aktiviti, mεnten GSH lεvεl, inhεbit inflammatory fכktכ εksprεshכn, εn ridyus lipid pεrכksidεshכn dεmεj, we de gi protεktiv ifekt εgεst di liva dεm we difrεn fכktכ dεm kכz. I de sho di pɔtɛnɛshɛl aplikeshɔn valyu na fil dɛm lɛk drɔg-indyuz liva damej ɛn alkol liva damej.
Sos dɛn we dɛn pul
[1] Liu Y, Liu Y, Dou B, ɛn ɔda pipul dɛn. Protektiv Efεkt כf Resveratrol pan Hεpatosayt Apoptosis in Alkohol Liva[J]. J ɔ rnal ɔ f Bayobased Matirial ɛn Bayoɛnaji, 2021. https://api.semanticscholar.org/KɔpɔsID:241263658. Di wan dɛn we de stɔdi bɔt di Baybul
[2] Li S, Tan H, Wang N, ɛn ɔda pipul dɛn. Di Rol we Oksidativ Strɛs ɛn Antiɔksidant dɛn de ple pan Liva sik dɛn[J]. Int ɛ rnash ɔ nal J ɔ rnal ɔ f Mɔlikul Sayns, 2015,16(11):26087-26124.DOI:10.3390/ijms161125942.
[3] Zhang Z, Gao L, Cheng Y, ɛn ɔda pipul dɛn. rεsvεratrol, we na nεchכral antioksidant, gεt prכtektiv ifekt pan di liva injuri we inכgεnik asεnik εkspכzכn de mek[J]. Bayomed Risach Int ɛ rnash ɔ nal, 2014,2014:617202.DOI:10.1155/2014/617202.
Prodak we de fɔ yuz fɔ risach nɔmɔ:
