Cardiogen 20 mg

▎ Cardiogen Structure

▎ Cardiogen Kev Tshawb Fawb

Kev tshawb fawb keeb kwm ntawm Cardiogen yog dab tsi?  

Tsav los ntawm cov kev xav tau ntawm kev tiv thaiv qog nqaij hlav / kev kho mob thiab kho cov kab mob plawv, kev tshawb fawb ntawm Cardiogen tau txais kev saib xyuas tseem ceeb. Cov kws tshawb fawb tau pom tias Cardiogen peptide inhibits transplantable M-1 sarcoma, inducing qog cell apoptosis thiab hemorrhagic necrosis, muab cov kev taw qhia tshiab rau kev kho mob qog. Lub caij no, nws cov txiaj ntsig muaj peev xwm hauv kev tswj hwm cov kab mob plawv thiab txhawb nqa myocardial regeneration kuj tau coj txoj hauv kev tshiab rau kev tshawb fawb txog kev kho mob plawv.  

Nrog rau kev loj hlob ntawm bioactive peptide tshuaj, txoj kev tshawb fawb ntawm Cardiogen cov qauv thiab kev ua haujlwm yog qhov tseem ceeb ntawm kev siv tshuaj lom neeg peptide nrog cov khoom tshwj xeeb. Txoj kev loj hlob ntawm cov thev naus laus zis xws li genetic engineering thiab proteomics tau muab kev txhawb nqa rau kev tshawb nrhiav qhov tob ntawm Cardiogen lub hauv paus chiv keeb thiab qhia meej txog nws cov txheej txheem ntawm kev nqis tes ua, tsav cov kev tshawb fawb txog kev mus tom ntej.  

Yuav ua li cas yog lub mechanism ntawm kev txiav txim ntawm Cardiogen?

Induction ntawm Tumor Cell Apoptosis: Cov kev tshawb fawb qhia tau hais tias tom qab txhaj Cardiogen rau nas nrog transplantable M-1 sarcoma, theem ntawm cov qog cell apoptosis nyob rau hauv tag nrho cov kev sim pab pawg neeg yog siab tshaj li nyob rau hauv pawg tswj. Qhov no qhia tau hais tias Cardiogen tuaj yeem ua rau cov txheej txheem apoptosis hauv cov qog hlwb los ntawm qee txoj hauv kev, ua rau cov qog nqaij hlav mus rau qhov programmed cell tuag. Apoptosis yog ib txoj hauv kev uas cov hlwb ua haujlwm kawg lawv lub neej tom qab lawv tus kheej cov kev pab cuam nyob rau hauv qee yam kev mob physiological lossis pathological. Feem ntau, apoptosis yog tswj hwm los ntawm cov noob caj noob ces thiab cov kev taw qhia. Cardiogen tuaj yeem qhib cov noob caj noob ces los yog txoj hauv kev taw qhia, xws li ua haujlwm ntawm Bcl-2 tsev neeg cov protein kom nce qhov kev qhia ntawm pro-apoptotic proteins (piv txwv li, Bax) los yog inhibit qhov kev ua haujlwm ntawm cov tshuaj tiv thaiv apoptotic (xws li, Bcl-2), yog li inducing tso tawm ntawm cytochrome C los ntawm mitochondria casse ua rau cov tshuaj tiv thaiv qhov kawg. rau qog cell apoptosis ^[1] .

Daim duab 1. Epigenetic mechanisms hauv plawv plawv. Lub plawv (chaw) txuas mus rau peb qhov tseem ceeb ntawm kev tswj hwm kev tswj hwm kev tswj hwm ntawm cov hlab plawv pathophysiology.

Source: MDPI ^[5]

Induction ntawm Tumor Hemorrhagic Necrosis: Cov koob tshuaj-raws li inhibition ntawm M-1 sarcoma kev loj hlob tom qab txhaj tshuaj Cardiogen yog ib feem ntawm cov qog hemorrhagic necrosis. Cov qog loj hlob nyob ntawm neovascularization rau cov as-ham thiab oxygen. Cardiogen tuaj yeem ua tiav cov txiaj ntsig no los ntawm kev cuam tshuam kev ua haujlwm ntawm cov qog vascular network. Nws tuaj yeem ua rau cov qog nqaij hlav vascular endothelial, cuam tshuam nrog cov cim qhia ntawm angiogenesis ntsig txog yam tshwm sim (xws li vascular endothelial loj hlob yam VEGF), cuam tshuam kev loj hlob, kev tsiv teb tsaws, thiab lumen tsim muaj peev xwm ntawm vascular endothelial hlwb, ua rau cov qog nqaij hlav angiogenesis, hauv zos ischemia, thiab hypoxia hauv cov nqaij mos. Nyob rau tib lub sijhawm, nws tuaj yeem cuam tshuam ncaj qha rau cov hlab ntsha uas twb muaj lawm, ua rau vascular rupture thiab los ntshav, ntxiv rau cov qog nqaij hlav necrosis ntau ntxiv ^[1].

Non-Direct Cytostatic Effect: Los ntawm qhov kev xav ntawm kev ua haujlwm ntawm kev loj hlob, cov qog loj hlob inhibition tsis tshwm sim los ntawm cov nyhuv cytostatic ncaj qha ntawm Cardiogen ntawm cov qog hlwb. Qhov no txhais tau tias nws tsis ncaj qha cuam tshuam cov txheej txheem metabolic xws li qog cell DNA synthesis lossis protein synthesis xws li tshuaj cytotoxic tshuaj los tiv thaiv qog cell proliferation. Es tsis txhob, nws inhibits qog loj hlob los ntawm indirect mechanisms xws li inducing apoptosis thiab ua rau qog hemorrhagic necrosis. Cov yam ntxwv ntawm kev ua tsis ncaj cytostatic no tuaj yeem ua rau Cardiogen muaj kev nyab xeeb dua nrog cov tshuaj toxicity tsawg rau cov hlwb li qub thaum siv los tiv thaiv qog nqaij hlav ^[1].  

Kev Ua Los Ntawm Tumor Vascular Network: Cov pov thawj morphological qhia tias Cardiogen qhov kev ua cuam tshuam nrog cov txheej txheem tshwj xeeb los ntawm cov qog vascular network. Cov qog vascular network tsis tsuas yog muab cov as-ham rau cov qog hlwb tab sis kuj tseem ua lub luag haujlwm tseem ceeb hauv cov qog metastasis thiab lwm yam txheej txheem. Cardiogen tuaj yeem khi rau cov receptors tshwj xeeb ntawm cov hlwb (xws li cov hlwb endothelial thiab pericytes) hauv cov qog vascular network, ua kom cov teeb liab hloov mus rau hauv lub cev thiab ua rau muaj kev cuam tshuam txog kev lom neeg, xws li tswj hwm vascular permeability thiab cuam tshuam rau kev cog lus thiab so ntawm vascular du leeg nqaij hlwb, yog li cuam tshuam rau cov ntaub so ntswg. kev loj hlob, apoptosis, thiab lwm yam txheej txheem.

Tsis tas li ntawd, cov qauv txawv txav thiab kev ua haujlwm ntawm cov qog vascular network muab lub hauv paus rau Cardiogen lub hom phiaj ua haujlwm, ua rau nws ua haujlwm tshwj xeeb rau cov qog nqaij hlav nrog kev cuam tshuam tsawg heev rau cov hlab ntsha ib txwm muaj ^[1]  

Cov ntawv thov ntawm Cardiogen yog dab tsi?  

Cov txiaj ntsig ntawm Cardiac-Related Indices: Hauv cov xwm txheej kev ntxhov siab, Cardiogen ua lub luag haujlwm tseem ceeb hauv kev tswj lub plawv dhia thiab lub cev qhov hnyav hauv cov nas. Cov kev tshawb fawb tau pom tias kev txhaj tshuaj Cardiogen tuaj yeem them rov qab rau cov teebmeem kev ntxhov siab ntawm adrenaline ntawm cov txheeb ze hloov pauv ntawm lub plawv, qog adrenal, thiab tus po, normalizing cov txheeb ze ntawm cov kabmob no. Nyob rau tib lub sijhawm, nws pab txo lub plawv dhia kom tswj tau qhov tseem ceeb thiab txo qhov tshwm sim ntawm arrhythmia nyob rau hauv kev ntxhov siab. Qhov no qhia tau hais tias Cardiogen tuaj yeem tswj hwm lub cev lub cev ntawm lub plawv thiab cov kabmob muaj feem xyuam rau hauv ib puag ncig kev ntxhov siab, ua rau muaj txiaj ntsig zoo rau stabilizing cov hlab plawv ^[2].  

Daim ntawv thov hauv Kev Kho Mob Mob plawv  

Kev Kho Mob Myocardial Infarction: Cardiogenin, ib qho kev tivthaiv tawm los ntawm cov nroj tsuag rho tawm (tejzaum nws muaj feem xyuam rau Cardiogen lossis ib qho ntawm nws cov khoom xyaw nquag), tau pom tias muaj txiaj ntsig zoo hauv tsiaj cov qauv ntawm myocardial infarction. Cov kev tshawb fawb tau pom tias cardiogenin tuaj yeem kho lub siab mob plawv, nrog rau cov kab mob endogenous mesenchymal qia hlwb (MSCs) tau pom kom sib txawv rau hauv cov cardiomyocytes tshiab hauv thaj chaw infarcted, nrog rau kev txhim kho tseem ceeb hauv plawv kev ua haujlwm. 

Hloov MSCs ua ntej kho nrog EGJ (ib tsob nroj extract uas muaj cardiogenin) los yog cardiogenin rau hauv myocardial infarction tsiaj qauv kuj txhawb nqa kev tsim kho ntawm myocardium ua haujlwm. Qhov no qhia tau hais tias cardiogenin tsis tsuas yog muaj peev xwm txhawb nqa myocardial regeneration tab sis kuj tseem tuaj yeem qhib MSCs, muab cov xwm txheej tsim nyog rau myocardial regeneration thiab qhib txoj hauv kev tshiab rau kev kho mob myocardial infarction. Tsis tas li ntawd, kev tswj hwm qhov ncauj ntawm cardiogenin kuj tau pom tias muaj cov txiaj ntsig kho mob tseem ceeb ntawm myocardial infarction, nrog cov pob txha pob txha-derived endogenous MSCs tau lees paub tias yog thawj lub xov tooj ntawm tes rau kev tsim kho myocardium. Kev tshawb fawb txog kev siv tshuab ua ntej qhia tias miR-9 thiab nws lub hom phiaj E-cadherin tuaj yeem koom nrog hauv kev tsim cov discs intercalated ^{[3, 4]}.  

Cov ntawv thov hauv Kev Kho Mob Cancer: Cardiogen peptide nthuav tawm cov qog hloov pauv hauv cov nas uas hloov pauv M-1 sarcoma. Cov kev tshawb fawb tau pom tias tom qab txhaj tshuaj Cardiogen, theem ntawm cov qog cell apoptosis nyob rau hauv tag nrho cov pab pawg neeg sim yog siab dua li nyob rau hauv pawg tswj, thiab cov tshuaj inhibited M-1 sarcoma kev loj hlob nyob rau hauv ib tug npaum li cas ntawm cov tshuaj. Cov nyhuv inhibitory no tsis yog los ntawm cov tshuaj ncaj qha cytostatic nkaus rau cov qog nqaij hlav tab sis los ntawm kev ua rau cov qog hemorrhagic necrosis thiab txhawb cov qog cell apoptosis. Morphologically, Cardiogen tuaj yeem siv nws cov txheej txheem tshwj xeeb ntawm kev ua los ntawm cov qog vascular network, muab lub tswv yim tshiab rau kev kho mob qog noj ntshav los ntawm kev tswj cov qog microenvironment thiab inducing qog cell apoptosis ^{[3, 4]}.  

Xaus  

Hauv cov ntsiab lus, Cardiogen tuaj yeem tswj hwm cov hlab plawv, txhim kho kev ua haujlwm ntawm lub plawv thiab cov kabmob muaj feem xyuam nrog kev ntxhov siab, thiab txhawb kev kho myocardial infarction. Lub caij no, nws daim ntawv peptide tuaj yeem tsim cov qog cell apoptosis, ua rau hemorrhagic necrosis, thiab inhibit qog kev loj hlob, muab cov lus qhia tshiab rau kev kho mob.

Hais Txog Tus Sau

Cov ntaub ntawv hais saum toj no yog txhua yam tshawb fawb, kho thiab sau los ntawm Cocer Peptides.

Scientific Journal Author

Cheng, Lei yog ib tug kws tshaj lij nrog kev tshawb fawb txog kev ua neej nyob thiab cov ntaub ntawv tshawb fawb. Koom nrog cov tsev kawm muaj koob npe xws li Hong Kong Polytechnic University, Dali University, thiab Suav University of Hong Kong, nws tau qhia txog keeb kwm kev kawm sib txawv thiab tob tob. Nws txoj kev tshawb fawb nthuav dav thoob plaws Biochemistry & Molecular Biology, Cell Biology, thiab Materials Science, uas yog nyob rau hauv lub hauv ntej ntawm kev tshawb fawb niaj hnub thiab tuav cov peev txheej tseem ceeb. Cheng, Lei txoj hauj lwm tsom tsis yog rau kev tshawb fawb txog kev tshawb fawb nkaus xwb tab sis kuj yog kev koom ua ke ntawm kev tshawb fawb thiab thev naus laus zis, muab kev txhawb nqa zoo rau kev txhim kho theoretical thiab thev naus laus zis tshiab hauv cov haujlwm muaj feem xyuam. Nws txoj kev sib koom tes nrog ntau lub tsev kawm ntawv kuj tseem yog qhov tseem ceeb hauv kev txhawb nqa kev sib pauv kev kawm thiab kev tshawb fawb kev koom tes.. Cheng, Lei tau teev nyob rau hauv kev siv cov ntaub ntawv pov thawj [3].

▎ Cov Lus Qhia Tseem Ceeb

[1] Levdik NV, Knyazkin I V. Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent nas[J]. Bulletin of Experimental Biology and Medicine, 2009,148(3):433-436.DOI:10.1007/s10517-010-0730-9.

[2] Mendzheritckiy AM, Vovk AN, Isachkina NS, et al. Kev cuam tshuam ntawm kev txhaj tshuaj cardiogen hauv cov qauv kev ntxhov siab adrenaline ntawm tus nqi ntawm lub plawv Performance index thiab qhov hnyav ntawm cov nas lub cev [M]. 2020: 35-37.10.23947/interagro.2020.2.35-37.

[3] Cheng L, Chen H, Yao X, et al. Ib tsob nroj-derived tshuaj kho mob plawv [J]. PLoS Ib, 2009,4(2):e4461.DOI:10.1371/journal.pone.0004461.

[4] Lin X, Peng P, Cheng L, et al. Lub ntuj sib xyaw ua rau kev sib txawv cardiogenic ntawm endogenous MSCs rau kev kho mob plawv [J]. Differentiation, 2012,83(1):1-9.DOI:10.1016/j.diff.2011.09.001.

[5] Martínez-Iglesias O, Naidoo V, Carrera I, et al. Ntuj Bioproducts nrog Epigenetic Properties rau Kev Kho Mob plawv [J]. Genes, 2025,16(5},ARTICLE-NUMBER= {566).DOI:10.3390/genes16050566.

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.