Na Cocer Peptides bin rayt am 
1 mɔnt dɔn pas
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 Sɛribrolaysin
Sεribrolaysin gεt nyuroprotεktiv εn nyurotrofik prכpati dεm. Frɔm we dɛn fɛn am, pipul dɛn dɔn pe atɛnshɔn to am bɔku pan di we aw dɛn de mɛn nyurolɔjik sik dɛn. Insay 1949, wan sayɛnsman we kɔmɔt Ɔstria we nem Gɛhart Hara we kɔmɔt na di Yunivasiti na Innsbruk bin ripɔt se Sɛribrolaysin, we na wan wata we gɛt prɔtin we dɛn kin mek tru ɛnzaym haydrolisis pan di bren tisu, kin mek di nɛv sɛl dɛn wok. na protin-bεys likwid miksכp we gεt 85% fri amino asid dεm εn 15% bayoaktiv lכw mכlikul-weyt amino asid sikεns dεm, we inklud lכw mכlikul-weyt nyuropεptida dεm lεk bren-dεriv nyurotrofik fכktכ (BDNF), glial sεl-dεriv nyurotrofik fכktכ (GDNF), nεv gכt fכktכ (NGF), εn ciliary nyurotrofik fכktכ (CNTF).
Mekanism fכ Akshɔn fכ Sεribrolaysin
fכ lεk di fכnshכn we di nyurotrofik fכktכ dεm de du: di aktv bren nyuropεptida dεm we de insay Sεribrolaysin kin kכmכt na di bכdi-bren barεri εn fכ lεk di fכnshכn we nεchכral nyurotrofik fכktכ dεm de du. nyurotrofik fכktכ dεm na implεnt fכ nyuronal sכvayvεns, gro, difrεns, εn sinaptik plastisiti. di bren-dεriv nyurotrofik fכktכ (BDNF) de ple wan kכl rol fכ mεnten nכmal nyuronal fכnshכn εn fכ mek nyural rigεnεreshכn. di sεm kayn kכmכpכnεnt dεm na Sεribrolysin kin biεn to kכrεspכndεnt rεsεpכta dεm na di nyuronal sεf, we de aktibכt dכwnstrim signal path dεm lεk di PI3K-Akt εn MAPK signal path dεm, we de protεkt nyuronal sכvayvεns εn growth we de ridyus nyuronal apoptosis.
rεgulεshכn fכ di nyurotransmit sistεm: I kin εksyεrt rεgεlεshכn ifekt pan di nyurotransmit sistεm. di nyurotransmitta dεm de ple wan sεntri rol fכ signal transmishכn bitwin nyuron dεm, εn dεn imbalans de kכl difrεn nyurolכjik dizכrd dεm. sεribralaysin kin mεnten di bεlε fכ di nyurotransmitta sistεm bay we i de rεgεl di rilis εn mεtabolism fכ nyurotransmit dεm lεk glutamεyt εn gama-aminobutyric acid (GABA). di tεm we di sεribra ischemia injuri, we di glutamεyt rilis pasmak kin mek i gεt εksitotoksisiti, we de pwεl di nyuron dεm. sεribrolaysin kin ridyus di nyuron dεm we di εksitotoksisiti de mek bay we i de rεgεl di glutamεyt transpכrta dεm εn i de dכn di εkstrasεlula glutamεyt akyumyuleshכn.
di antioksidant strεs ifekt dεm: Nyurolכjik sik dεm kin kam wit εnhans כksidεtiv strεs riakshכn dεm, usay di εksyכs riaktiv כksijεn spεshal (ROS) dεm de pwεl nyuronal sεl mεmbran dεm, protin dεm, εn DNA. sεribrolaysin gεt antioksidant strεs kεpabiliti dεm, we de ridyus di intasεlulyar ROS lεvεl dεm εn minimiz כksidεtiv dεmεj. insay wan in vitro haypoksia-induse nyuronal saytotoksisiti mכdel, Sεribrolysin kin ridyus di supεrכksayd lεvεl dεm, mεnten sεlyul mεtabolik aktiviti, εn ridyus apoptosis. in spεsifi k mεkanism kin riliyt to di aktibכshכn fכ di intasεlulyar antioksidant εnzym sistεm dεm, lεk supεrכksayd dismutase (SOD) εn glutathione pεrכksidεz (GPx), we kin skavεnj ROS εn protεkt nyuron dεm frכm כksidεtiv damej.
inhibishכn fכ inflammatory rεspכns dεm: inflammatory rεspכns dεm de ple imכtant rol bak fכ divεlכpmεnt fכ nyurolכjik sik dεm. sεribrolaysin kin εliviet inflammatory rispכns bay we i de inhibit di rilis fכ inflammatory fכktכ dεm εn rεgεl inflammatory signal pathways. insay wan sεribra ischemia-rεpεrfyushכn injuri mכdel, Sεribrolaysin kin ridyus di εksprεshכn fכ pro-inflammatory saytokεn dεm lεk tכmכr nεkrכsis fכktכ-α (TNF-α) εn intalyukin-1β (IL-1β), we i de inkrεs di lεvεl dεm fכ anti-inflammatory saytokεn dεm lεk intalyukin-10 (IL-10), we de mek di inflammatory dεmεj to nyuron dεm εn fכ protεkt di rεkכvri fכ di nyural fכnshכn.
fכ mek nyural plastisiti: Nyural plastisiti de tכk bכt di nεv sεstem in ebul fכ ripa insεf εn כganayz bak afta injuri. sεribrolaysin de εnhans nyural plastisiti bay we i de protεkt aksכnal rigεnεreshכn, dεndritik spayna fכmeshכn, εn sinaptik rεkכnstrכkshכn. i kin achy dis bay we i de aktibכt di rilevεnt signal path dεm, lεk di RhoA/ROCK signal path, fכ rεgεl chenj dεm na di saytoskεlet, we de mek di aksכnal gכd εn εkstenshכn. sεribrolaysin kin inkrεs bak di εksprεshכn fכ di sinaps-rεlatεd protin dεm, lεk sinapsin, fכ protεkt di sinaps fכmeshכn εn fכnshכnal rεkכvεshכn, we de gi strכkchכral fawndeshכn fכ di rεstכreshכn fכ nyural fכnshכn.
Di Ifɛkt dɛn we Sɛribrolaysin Gɛt
Ifekt pan akyu ischemic strok: Insay di tritmɛnt fɔ akyu ischemic strok, Cerebrolysin dɔn sho sɔm fayn fayn ifɛkt dɛn. Pan ɔl we di fɔs klinik trayal dɛm, we bin fɔs inrɔl pasɛnt dɛm we gɛt mild strok, bin sho ifekt dɛm na di flɔ ɔ siling ɛn dɛn nɔ bin ebul fɔ sho klia wan se difrɛns de bitwin di tritmɛnt grup dɛm, di sabgrup analisis dɛm fɔ di pasɛnt dɛm we gɛt mɔ siriɔs strok bin sho se i gɛt impɔtant pɔsitiv ifɛkt fɔ ɛp fɔ mek dɛn wɛl. di efficacy fכ Cerebrolysin de inkrεs wit di siriכs fכ di strכk. Sɔm stεdi dεm we dεn kכntrol dεn sho se dεn kin kכmbayn Cerebrolysin sef wan wit trombolytic tεrapi, εn pan pasεn dεm we gεt mכdarεt to siriכs strכk, i de sho se i efyushכn nכto כnli insay nyuroprotεkshכn bכt bak insay nyuro-rεkכvri pכtεnshal. we yu kכmpεr wit nyuro-rihabiliteshכn nכmכ, di kכmbaynshכn fכ Sεribrolysin εn nyuro-rihabiliteshכn de gi mכr signifyant ifekt pan fכnshכnal rεkכvεshכn.
Ifekt pan subarachnoid hemorrhage: Subarachnoid hemorrhage (SAH) na akyu nyurolכjik kכndishכn wit hεy mכtaliti εn rεkכvεshכn fεil rεt. As wan drɔg we dɛn kin yuz fɔ trit strok, inklud SAH, di ifɛkt dɛn we Cerebrolysin gɛt pan SAH pasɛnt dɛn dɔn drɔ atɛnshɔn. Wan sistamat rivyu ɛn mɛta-analysis fɔ yuz Cerebrolysin insay SAH pasɛnt dɛn sho se di data sho se Cerebrolysin gɛt fayn impak pan di mɔtaliti insay SAH pasɛnt dɛn.
di ifekt dεm pan nyu bכbi haypoksik-ischemik εnεsεfalopathy (HIE): HIE na bren disfכnkshכn we de kכz fכ pεrinatal asfiksia, εn dεn nכ כndastand in pathophysiological mεkanism dεm fכ fulכp yet. Di standad tritmɛnt we dɛn de gi naw na di tritmɛnt haypotɛmia, bɔt di we aw i de wok nɔ bɔku. Sεribrolaysin, as nyuroprotεktiv tritmεnt, de sho pכtεnshal insay di mεnejmεnt fכ HIE. Sεribrolaysin gεt tritmεnt winda we de te siks mכnt afta di ischemic injuri. if yu gi 0.1 ml/kg bכdi wet fכ Sεribrolysin tu tεm insay di wik i kin impruv di gros mכtalman εn langwej fכnshכn dεfisit insay bebi dεm, we de gi fayn ifekt pan di כvala autkam dεm.
Pɔtɛnɛshɛl rol fɔ traumatik bren injuri: Traumatik bren injuri (TBI) na kɔmɔn nyurolɔjik injuri we kin mek nyuronal damej ɛn day, we kin mek bɔku nyurolɔjik disfɔkshɔn. bays pan Cerebrolysin in nyuroprotεktiv εn nyurotrofik prכpati dεm, i de ol pכtεnshal aplikεshכn valyu bak fכ di tritmεnt fכ TBI. animal εkspεriεns stכdi dεn sho se di yus כf Sεribrolysin kin ridyus nyuronal apoptosis afta TBI εn protεkt di rεkכvri fכ nyurolכjik fכnshכn. in mεkanism fכ akshכn kin riliyt to mכltipכl mεkanism dεm, inklud fכ miks nyurotrofik fכktכ fכnshכn, rεgεl nyurotransmit sistεm, antioksidant strεs, εn inhεbit inflammatory rεspכns. tru dεn mεkanism dεm ya, i de εliviet sεkכnd dεmεj afta TBI εn i de protεkt nyural ripa εn rigεnεreshכn.
di efεkt dεm we kin apin pan dimεnshכn: Dimεnshכn na nyurodijεnεraytiv sik we dεn kכl prכgrεsiv kכgnitiv impεryans, wit in patכjεnεsis we involv nyuronal dεjεnεrayshכn εn day, nyurotransmitta imbalans, inflammatory rεspכns, εn כksidεtiv strεs. di mכltipכl mεkanism dεm we sεribrolaysin de du de mek i bi wan pכtεnshal tεrapi ejen fכ dimεnshכn. i kin mek di nyuron dεm liv εn gro bay we i de falamakata di wok we nyurotrofik fכktכ dεm de du, we de protεkt di nyuron dεm we dεn dכn pwεl. bay we i de rεgεl di nyurotransmitta sistεm, i de impruv di nyurotransmitta imbalans, lεk fכ inkrεs di asetilkolin rilis, we de mek di kכgnitiv fכnshכn bכku. di antioxidant εn anti-inflammatory ifekt dεm we i de gi de εp bak fכ ridyus nyuroinflammation εn oxidative damej na di bren fכ di wan dεm we gεt dimεnshכn, we de mek di sik slo.
Dɔn
As dכg we gεt nyuroprotεktiv εn nyurotrofik prכpati dεm, Sεribrolysin dεn dכn sho se i de trit nyurolכjik dizכrd dεm.
Rifrɛns dɛn
[1] Kojder K, Jarosz K, Bosiacki M, ɛn ɔda pipul dɛn. Sεribrolysin in Patiεnt dεm wit Subarachnoid εmoraji: Wan Sistεmatik Rivyu εn Mεta-Analysis[J]. J ɔ rnal ɔ f Klinik Mɛdisin, 2023,12. Di s://api.semanticscholar.org/KɔpɔsID:264397999. Di wan dɛn we de stɔdi bɔt di Baybul
[2] Mureșanu D. F., Livinț P. L., Chira D., ɛn ɔda pipul dɛn. Rol εn Impεkt כf Sεribrolysin fכ Ischemic Stroke Kεr[J]. J ɔ rnal ov Klinik Mɛdisin, 2022,11(5).DOI:10.3390/jcm11051273.
[3] Fiani B, Chacon D, Jarrah R, ɛn ɔda pipul dɛn. Nyuroprotεktiv stratεji dεm fכ sεribrolaysin fכ di tritmεnt fכ bεlε pikin dεm wit nyu bכbi haypoksik-ischemik εnεsεfalopati[J]. Akta Nyurɔlɔjika Bɛljika, 2021,121(6):1401-1406.DOI:10.1007/s13760-021-01795-y.
[4] Al-Mosawi A J. Klinik yus fɔ Sɛribrolaysin insay Pidiatrik Nyurosaykayatri[J]. Sayns Wɔl Jɔnal fɔ Famasiutik Sayns, 2020. https://api.semanticscholar.org/CorpusID:235912686
[5] Brainin M. Cerebrolysin: na mכlti-target dכg fכ rεkכvεshכn afta strok[J]. Ekspɛkt Rivyu fɔ Nyurotɛrapi, 2018,18(8):681-687.DOI:10.1080/14737175.2018.1500459.
[6] Ziganshina LE, Abakumova T. Sεribrolaysin fכ akyu ischemik strכk[J]. Cochrane Database of Sistɛmatik Rivyu, 2015(6):CD7026.DOI:10.1002/14651858.CD007026.pub3.
[7] Hartwig K, Fackler V, Jaksch-Bogensperger H, ɛn ɔda pipul dɛn. sεribrolaysin de protεkt PC12 sεl dεm frכm CoCl2-indyus haypoksia we de employ GSK3β signal[J]. Int ɛ rnash ɔ nal J ɔ rnal ɔ f Divɛlɔpmɛnt Nyurosayns, 2014,38:52-58.DOI:10.1016/j.ijdevneu.2014.07.005.
Prodak we de fɔ yuz fɔ risach nɔmɔ:
