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    Wyświetlanie 1-3 z 3
    Tytuł:
    The effects of dexamethasone and minocycline alone and combined with N-acetylcysteine and vitamin E on serum matrix metalloproteinase-9 and coenzyme Q10 levels in aflatoxin B1 administered rats
    Autorzy:
    Tras, B.
    Eser Faki, H.
    Ozdemir Kutahya, Z.
    Bahcivan, E.
    Dik, B.
    Uney, K.
    Powiązania:
    https://bibliotekanauki.pl/articles/16539322.pdf
    Data publikacji:
    2022
    Wydawca:
    Polska Akademia Nauk. Czasopisma i Monografie PAN
    Tematy:
    aflatoxin B1
    coenzyme Q10
    matrix metalloproteinase-9
    rat
    treatment
    Opis:
    This study aimed to determine the effects of dexamethasone and minocycline alone and combined treatment with N-acetylcysteine (NAC) and vitamin E on serum coenzyme Q10 (CoQ10) and matrix metalloproteinase-9 (MMP-9) levels in rats administered aflatoxin B1 (AFB1). The study was carried out on 66 male Wistar rats. Following the intraperitoneal (IP) administration of AFB1 at dose of 2 mg/kg, minocycline (45 and 90 mg/kg, IP) and dexamethasone (5 and 20 mg/kg, IP) were administered alone and combined with NAC (200 mg/kg, IP) and vitamin E (600 mg/kg, IP). CoQ10 and MMP-9 levels were analyzed using the HPLC-UV method and a commercial kit by ELISA, respectively. AFB1 increased MMP-9 level and decreased CoQ10 level compared to the control group. After dexamethasone and minocycline administration, there is no increase in CoQ10 level, which is caused by AFB1. However, dexamethasone and minocycline combined with NAC+vitamin E caused significant increases in CoQ10 levels. Dexamethasone and minocycline alone and combined with NAC+vitamin E decreased MMP-9 levels compared to the single AFB1 treated group. The use of MMPs inhibitors and oxidative stress-reducing agents is anticipated to be beneficial in the poisoning with AFB1.
    Źródło:
    Polish Journal of Veterinary Sciences; 2022, 25, 3; 419-427
    1505-1773
    Pojawia się w:
    Polish Journal of Veterinary Sciences
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Prostaglandin-J2 upregulates expression of matrix metalloproteinase-1 independently of activation of peroxisome proliferator-activated receptor-γ.
    Autorzy:
    Józkowicz, Alicja
    Huk, Ihor
    Nigisch, Anneliese
    Cisowski, Jarosław
    Weigel, Guenter
    Dulak, Józef
    Powiązania:
    https://bibliotekanauki.pl/articles/1043441.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    matrix metalloproteinase-1
    urokinase plasminogen activator
    prostaglandin-J2
    peroxisome proliferator-activated receptor-γ
    endothelial cells
    Opis:
    Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-inducible nuclear receptor that functions as a transcription factor involved in lipid metabolism, inflammatory response and angiogenesis. The most potent endogenous PPARγ activator is 15-deoxy-Δ12,14prostaglandin-J2 (15d-PGJ2), whereas synthetic ligands include the oral antidiabetic drugs thiazolidinediones (TZDs). Activation of PPARγ was reported to decrease the synthesis of matrix metalloproteinases (MMPs) in vascular smooth muscle cells and macrophages. We aimed to investigate the effect of PPARγ ligands on expression of MMP-1 and urokinase plasminogen activator (uPA) in human microvascular endothelial cells (HMEC-1). We found that treatment of HMEC-1 with 15d-PGJ2 increased the synthesis of MMP-1 protein up to 168% comparing to untreated cells. TZDs (ciglitazone and troglitazone), more potent activators of PPARγ in HMEC-1, did not influence MMP-1 production, arguing against the involvement of PPARγ in this process. Importantly, the stimulatory effect of 15d-PGJ2 was reversed by the antioxidant N-acetyl-cysteine (NAC), suggesting a contribution of oxidative stress. We demonstrated also that 15d-PGJ2 did not change the activity of MMP-1 promoter, but increased the stability of MMP-1 mRNA. In contrast, 15d-PGJ2 very potently inhibited the synthesis of uPA. This effect was in part mimicked by ciglitazone and troglitazone implying an involvement of PPARγ. Accordingly, NAC did not modify the inhibitory effect of 15d-PGJ2 on uPA expression. In conclusion, we postulate that 15d-PGJ2 may differently regulate the synthesis of proteases involved in angiogenesis : it upregulates MMP-1 expression in HMEC-1 through induction of oxidative stress, and inhibits uPA synthesis partly by activation of PPARγ.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 3; 677-689
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    In vitro reoxygenation following hypoxia increases MMP-2 and TIMP-2 secretion by human umbilical vein endothelial cells
    Autorzy:
    Cavdar, Zahide
    Oktay, Gulgun
    Egrilmez, Mehtap
    Genc, Sermin
    Genc, Kursad
    Altun, Zekiye
    Islekel, Huray
    Guner, Gul
    Powiązania:
    https://bibliotekanauki.pl/articles/1040424.pdf
    Data publikacji:
    2010
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    hypoxia
    reoxygenation
    matrix metalloproteinase-2
    tissue inhibitor of metalloproteinase-2
    membrane type-1 matrix metalloproteinase
    endothelial cell
    Opis:
    Endothelial cells lining the inner blood vessel walls play a key role in the response to hypoxia, which is frequently encountered in clinical conditions such as myocardial infarction, renal ischemia and cerebral ischemia. In the present study we investigated the effects of hypoxia and hypoxia/reoxygenation on gelatinases (matrix metalloproteinase-2 and -9), their inhibitor (TIMP-2) and activator (MT1-MMP), in human umbilical vein endothelial (HUVE) cells. HUVE cells were subjected to 4 h of hypoxia or hypoxia followed by 4 and 24 h of reoxygenation. The pro- and active forms of MMP-2 and MMP-9 were analyzed by gelatin zymography; TIMP-2 protein level was assayed using ELISA, while MT1-MMP activity was measured using an activity assay. The secretion of MMP-2 proform increased significantly in cells subjected to 4 h of hypoxia followed by 4 or 24 h of reoxygenation, compared with the normoxic group. TIMP-2 protein level also increased significantly in the hypoxia/reoxygenation groups, compared with the normoxic group. There were no statistically significant differences in the levels of active MT1-MMP in all groups. This study indicates that MMP-2 and TIMP-2 could be regarded as important components of a mechanism in the pathophysiology of ischemic injury following reperfusion.
    Źródło:
    Acta Biochimica Polonica; 2010, 57, 1; 69-73
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-3 z 3

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