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001-es BibID:BIBFORM059782
035-os BibID:(WOS)000363822600014 (Scopus)84940040945
Első szerző:Csépányi Evelin (gyógyszerész)
Cím:Cardiovascular effects of low versus high-dose beta-carotene in a rat model / Evelin Csepanyi, Attila Czompa, David Haines, Istvan Lekli, Edina Bakondi, Gyorgy Balla, Arpad Tosaki, Istvan Bak
Dátum:2015
ISSN:1043-6618
Megjegyzések:?-carotene (BC), a lipid-soluble tetraterpene precursor to vitamin A, widely distributed in plants, including many used in human diet, has well-known health-enhancing properties, including reducing risk of and treatment for certain diseases. Nevertheless, BC may also act to promote disease through the activity of BC derivatives that form in the presence of external toxicants such as cigarette smoke and endogenously-produced reactive oxygen species. The present investigation evaluates the dose-dependent cardioprotective and possibly harmful properties of BC in a rat model. Adult male rats, were gavage-fed BC for 4 weeks, at dosages of either 0, 30 or 150 mg/kg/day. Then hearts excised from the animals were mounted in a "working heart" apparatus and subjected to 30 minutes of global ischemia, followed by 120 minutes of reperfusion. A panel of cardiac functional evaluations was conducted on each heart. Infarct size and total antioxidant capacity of the myocardium were assessed. Heart tissue content of heme oxygenase-1 (HO-1) by Western blot analysis; and potential direct cytotoxic effects of BC by MTT assay were evaluated. Hearts taken from rats receiving 30 mg/kg/day BC exhibited significantly improved heart function at lower reperfusion times, but lost this protection at higher BC dosage and longer reperfusion times. Myocardial HO-1 content was significantly elevated dose-responsively to both BC dosage. Finally, in vitro evaluation of BC on H9c2 cells showed that the agent significantly improved vitality of these cells in a dose range of 2.5-10 ?M.Although data presented here do not allow for a comprehensive mechanistic explanation for reduced cardioprotection at high dose BC, it is speculated that since Fe2+ produced as a metabolite of HO-1 activity, may determine whether BC acts as an antioxidant or prooxidant agent, the strong induction of this enzyme in response to ischemia/reperfusion-induced oxidative stress may account for the high-dose BC loss of cardioprotection.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
beta-carotene
heart
ischemia/reperfusion
heme-oxygenase-1
Megjelenés:Pharmacological Research. - 100 (2015), p. 148-156. -
További szerzők:Czompa Attila (1985-) (gyógyszerész) Haines, David Donald (1981-) (gyógyszerész) Lekli István (1981-) (gyógyszerész) Bakondi Edina (1975-) (biokémikus, vegyész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus)
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001-es BibID:BIBFORM020518
Első szerző:Oroszi Gábor (Pécs)
Cím:Interplay between nitric oxide and CGRP by capsaicin in isolated guinea-pig heart / Gabor Oroszi, Zoltan Szilvassy, Joseph Nemeth, Arpad Tosaki, Janos Szolcsanyi
Dátum:1999
ISSN:1043-6618
Megjegyzések:AbstractCapsaicin at a concentration of 10(-7)m induced a significant increase in heart rate and increased coronary flow in isolated Langendorff-perfused guinea-pig hearts. This effect was completely blocked by 30 microm of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. Additional incubation with 3 m m L-Arg antagonized the inhibitory effect of L-NAME. In the presence of 1 microm of a human calcitonin gene-related peptide fragment (hCGRP 8-37), a CGRP-receptor antagonist, L-Arg was without effect. We conclude that a capsaicin-induced increase in coronary flow and heart rate is dependent from an interplay between CGRP and NO in guinea-pig hearts. 1999 Academic Press.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nitric oxide
CGRP
capsaicin
Megjelenés:Pharmacological Research 40 : 2 (1999), p. 125-128. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (Pécs) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Szolcsányi János (Pécs)
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