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자료유형
학술저널
저자정보
저널정보
한국실험동물학회 Laboratory Animal Research Laboratory Animal Research Vol.23 No.3
발행연도
2007.9
수록면
299 - 304 (6page)

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Liver transplantation is essential for patients with liver failure. Pig is known to be a most suitable species in xeno-transplantation of human organs. Hepatocytes are important sites in the body's metabolism and function. Glucose transporter in hepatocytes plays a role in regulation of blood glucose homeostasis. Epidermal growth factor (EGF) is known to be a regulator of physiological function in various cell systems. However, the effect of EGF on glucose activity in pig hepatocytes was not clearly elucidated. Thus, this study investigated the effect of EGF on glucose transporter and its related signal cascades in primary cultured pig hepatocytes. EGF inhibited glucose uptake in a dose (> 1 ng/㎖) dependent manner. EGF-induced decrease of [³H]-deoxyglucose uptake was blocked by AG 1478 (10-? M, an EGF receptor antagonist) genistein and herbymycin A (tyrosine kinase inhibitors, 10?? M), suggesting the role of activation and tyrosine phosphorylation of EGF receptor. In addition, EGF-induced decrease of [³H]-deoxyglucose uptake was prevented by mepacrine, AACOCF₃ (phospholipase A₂ inhibitors), indomethacin and ibuprofen (cyclooxygenase inhibitors). Indeed, EGF increased [³H]-arachidonic acid release and cyclooxygenase-2 (COX-2) expression. Moreover, EGF-induced stimulation of [³H]-arachidonic acid release was blocked by PD 98059 (a p44/42 mitogen activated protein kinase [MAPK] inhibitor) and SB 203580 (a p38 MAPK inhibitor). EGF-induced decrease of [³H]-deoxyglucose uptake was also prevented by these two MAPKs. However, EGF-induced stimulation of p44/42 MAPK and p38 MAPK was not blocked by mepacrine and indomethacin. In conclusion, EGF decreases glucose uptake via MAPK-COX-2 signal cascades in cultured pig hepatocytes.

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