Ukusebenza okuqhelekileyo komzimba womntu kufuna ukuhamba ngokukhawuleza kwamandla ngendlela ye-adenosine triphosphate (ATP). Umjikelezo we-tricarboxylic acid (TCA), inkqubo ebalulekileyo yokuvelisa i-ATP kwi-mitochondria, i-hub enkulu ye-metabolites kwaye iqinisekisa ukulingana okuhle phakathi kwe-cyclic intermediates, ebizwa ngokuba 'yi-metabolic flux.' Le ntsholongwane ikholelwa ukuba iphazamisekile kwiingxaki ezinxulumene nentliziyo njenge-myocardial ischemia (MI), apho ukuhamba kwegazi ukuya entliziyweni kuyancipha, imisipha yentliziyo, okanye i-cardiomyocytes, ekufumaneni ioksijini eyaneleyo. Ukunciphisa i-ATP synthesis kunye nokunyuka kwe-glucose breakdown, okanye "glycolysis," phawula i-MI, kodwa ukuxhaphaza umjikelo we-TCA kwizicwangciso zonyango kunzima.
I-Ginkgo biloba L. isicatshulwa (i-GBE), equlethe i-bilobalide esebenzayo, isetyenziswe ngokuqhelekileyo njengeyeza eliqhelekileyo lokunyanga izifo zentliziyo ye-ischemic, kodwa indlela yokusebenza kwayo ayaziwa. Izazinzulu ezikhokelwa nguProf. Jinlan Zhang ovela kwiZiko laseTshayina leMateria Medica zatyhila ngempumelelo isayensi emva kweziphumo ze-GBE ze-cardioprotective kwisifundo esitsha. "Ulawulo lwe-GBE lwe-metabolism yamandla yatsala ingqalelo yethu kuba intliziyo isebenza ngokuqhubekayo kwaye idinga amandla ukunika amandla inkqubo yokujikeleza," utsho uProf. Zhang.
Uphononongo, olwapapashwa kwi-Journal of Pharmaceutical Analysis, lubonisa indlela ukuhanjiswa kwekhabhoni ukusuka kwi-glycolysis ukuya kumjikelezo we-TCA kuvaliwe kwi-cardiomyocytes echaphazelekayo ye-MI. Oososayensi bafumanisa ukuba i-TCA flux yaphazamiseka ngokucacileyo kula maseli, akhetha ukusebenzisa enye imithombo yekhabhoni kunokuba i-glucose ibonelele ngokuqhubekayo amandla. Nangona kunjalo, ukuvinjelwa kunye nokuphazamiseka kwemveliso ye-ATP ayinakuthintelwa kwiiseli ezilimele. I-Ischemic cardiomyocytes iqulethe ubuninzi bee-enzymes eziguqule imithombo yekhabhoni kwi-metabolites, kokubili ngaphambi nangexesha lokujikeleza kwe-TCA, enokuthi ibangele ukuba i-metabolites iqokelele kwaye iphazamise i-metabolism flux, ekubeni ingenako ukungena kumjikelezo ngokugqithisileyo.
Okubangela umdla kukuba, ekuphatheni iiseli ezonzakeleyo nge-GBE, ababhali bafumanisa ukuba i-bilobalide inokukhusela i-mitochondria kwaye igcine isizukulwana se-ATP. Amanqanaba e-enzyme kwiiseli eziphathwayo ehla kwaye anqanda ukuqokelelwa kwe-metabolite, ukuphuculwa kwe-metabolic flux, kunye nokunciphisa uxinzelelo kwiiseli zentliziyo. Oku kuguqulwa kwe-metabolic flux kwiiseli eziphathwe nge-GBE zahlukile kwiindlela ezichazwe ngaphambili.
Baye bavavanya izicubu ze-myocardial zeempuku eziphathwe nge-GBE, ezibonise iimpawu zomonakalo ongaphantsi we-MI kuneisampulu zezicubu ezinganyangekanga. Iziphumo zazihambelana nezo ze-ISO-enzakeleyo iiseli, ebonisa ukuba i-bilobalide ikhusela imisipha yentliziyo.
Nangona uphando lweziyobisi lwe-metabolic kwi-MI lusanda kufumana ukuthamba, impumelelo isekude kakhulu. Iziphumo zonyango lwe-bilobalide ezifunyenwe kolu phononongo aziboneleli kuphela ngobungqina obuninzi be-MI's metabolic pathology, kodwa zikwanika inkuthazo kunyango olutsha lwamayeza.
"I-MI iyingozi enkulu kwimpilo yabantu emhlabeni jikelele kwaye icacise i-pathophysiology yayo kunye nonyango olunokubakho luyimfuneko," kusho uProf. Zhang. "Iziphumo zethu zibonakala zithembisa, kwaye silindele ukufumana inkuthazo kolu phando kwindlela ye-metabolic kunye nesiseko sezinto kunyango lwe-MI," uqukumbela ngelitshoyo.
INTO ONOKUYITHATHA KWELI NQAKU:
- The tricarboxylic acid (TCA) cycle, an important ATP-producing process in the mitochondria, is a major hub of metabolites and ensures a fine balance between its cyclic intermediates, referred to as the ‘metabolic flux.
- Ischemic cardiomyocytes contained larger quantities of enzymes that converted carbon sources to metabolites, both before and during the TCA cycle, which might have caused the metabolites to accumulate and disturb the metabolic flux, since they could not enter the cycle in excess.
- The study, which was published in the Journal of Pharmaceutical Analysis, reveals how carbon transfer from glycolysis to the TCA cycle is blocked in MI-affected cardiomyocytes.
