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首页> 外文期刊>Journal of Cellular Physiology >High glucose-induced inhibition of alpha-methyl-D-glucopyranoside uptake is mediated by protein kinase C-dependent activation of arachidonic acid release in primary cultured rabbit renal proximal tubule cells.
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High glucose-induced inhibition of alpha-methyl-D-glucopyranoside uptake is mediated by protein kinase C-dependent activation of arachidonic acid release in primary cultured rabbit renal proximal tubule cells.

机译：高glucose-induced抑制alpha-methyl-D-glucopyranoside吸收是介导通过蛋白激酶C-dependent激活的花生四烯酸释放主要讲究的兔肾近端小管细胞。

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摘要

Abnormal glucose handling in the proximal tubule may play an important role in the development of diabetic nephropathy. Thus, the present study was designed to examine the effect of high glucose on alpha-methyl-D-glucopyranoside (alpha-MG) uptake and its signaling pathways in the primary cultured rabbit renal proximal tubule cells (PTCs). When PTCs were preincubated with 25 or 50 mM glucose for 4 h, 25 or 50 mM glucose significantly inhibited alpha-MG uptake, while 25 or 50 mM mannitol and L-glucose did not affect. Actinomycin D and cycloheximide did not block the effect of high glucose on alpha-MG uptake. Twenty-five millimoles glucose-induced inhibition of alpha-MG uptake was blocked by mepacrine and AACOCF(3), phospholipase A(2) (PLA(2)) inhibitors. Twenty-five millimoles of glucose, not mannitol or L-glucose, significantly increased the [(3)H]-arachidonic acid (AA) release compared to control. In addition, the 25 mM glucose-induced [(3)H]-AA release was completely blocked by mepacrine or AACOCF(3). Indomethacin, a cyclooxygenase inhibitor, blocked the high glucose-induced inhibition of alpha-MG uptake, although econazole, cytochrome P-450 a epoxygenase inhibitor, and nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, did not. On the other hand, staurosporine and bisindolylmaleimide I, protein kinase C (PKC) inhibitors, blocked 25 mM glucose-induced increase of [(3)H]-AA release and inhibition of alpha-MG uptake. However, neomycin, U 73122, and phospholipase c(PLC) inhibitors did not block the effect of 25 mM glucose on [(3)H]-AA release and alpha-MG uptake. Pretreatment of methoxyverapamil, an L-type Ca(2+) channel blocker, abolished 25 mM glucose-induced increase of [(3)H]-AA release. Indeed, 25 mM glucose increased translocation of cPLA(2) from cytosolic fraction to membrane fraction. In conclusion, the present results demonstrate that high glucose inhibits alpha-MG uptake by the increase of AA release via the activation of PKC. Copyright 2000 Wiley-Liss, Inc.
机译：不正常的葡萄糖处理在近端小管可能发挥重要作用的发展糖尿病肾病。旨在研究高葡萄糖的影响alpha-methyl-D-glucopyranoside (alpha-MG)吸收在初选中及其信号通路培养兔肾近端小管细胞(ptc)。毫米为4 h葡萄糖,葡萄糖25或50毫米显著抑制alpha-MG吸收,而25或50 mM甘露醇和L-glucose并不影响。放线菌素D和环己酰亚胺不阻止高葡萄糖对alpha-MG吸收的影响。25毫克分子glucose-induced抑制的alpha-MG吸收被阿的平抑制剂。明显不是甘露醇或L-glucose,((3) H)增加了花生四烯酸(AA)释放控制相比。mM glucose-induced [(3) H] aa释放完全被阿的平或AACOCF(3)。环氧酶抑制剂吲哚美辛,屏蔽alpha-MG glucose-induced抑制高吸收,虽然益康唑,细胞色素p - 450 aepoxygenase抑制剂和去甲二氢愈创木酸(NDGA),脂氧合酶抑制剂,没有。另一方面,staurosporine和bisindolylmaleimide我,蛋白激酶C (PKC)抑制剂,阻塞glucose-induced 25毫米增加[(3)H] aa的释放和抑制alpha-MG吸收。磷脂酶c (PLC)抑制剂没有阻止25毫米葡萄糖的影响[(3)H] aa和释放alpha-MG吸收。methoxyverapamil, l型钙通道(2 +)杀杀杀,废除了25毫米glucose-induced增加(3) H aa的释放。从胞质cPLA易位的增加(2)膜分数分数。目前的结果表明,高葡萄糖抑制alpha-MG吸收增加的AA通过激活PKC释放。Wiley-Liss公司。

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