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首页> 外文期刊>Biological & pharmaceutical bulletin >Effect of Ginsenoside Rb_1 on Rat Liver Phosphoproteins Induced by Carbon Tetrachloride
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Effect of Ginsenoside Rb_1 on Rat Liver Phosphoproteins Induced by Carbon Tetrachloride

机译:人参皂苷Rb_1对四氯化碳诱导的大鼠肝脏磷酸化蛋白的影响

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摘要

We investigated the effects of ginsenoside Rbt (G-Rbj), a major saponin from Panax ginseng C. A. Meyer, on rat liver protein phosphorylation after intraperitoneal administration of CCI4 alone or together with G-Rbt. We found that 118, 63, and 34kDa proteins were prominently phosphorylated in liver homogenates prepared from CG4-administered rats, while these protein-phosphorylations were inhibited in the homogenate prepared from the G-Rb! plus CCl4-administration group. When inhibitors of protein kinases were exogenously added to the homogenates from either the CCl4-administered group or the G-Rb! plus CCl4-administered group, their phosphorylations were inhibited much more by W-7, an inhibitor of Ca2+/calmodulin-dependent protein kinase (CaM-PK), than by H-7, an inhibitor of protein kinase C {C-kinase). Interestingly, only 34 kDa was phosphorylated in homogenates prepared from the corn oil-, G-Rbr, and G-Rbi plus CCl4-administered groups by the exogenous addition of sodium fluoride (NaF), an inhibitor of glycogen synthase. Additionally, G-Rbi inhibited the Ca2+-accumulation induced by CC14 both in liver homogenates and microsomes. The above results imply that G-Rb, inhibits the CCl4-induced protein phosphorylations by modulating CaM-PK rather than C-kinase, and that 34 kDa protein may play a different biological role in cellular environment from 118 and 63 kDa proteins. Therefore, a study in which G-Rbj is employed as a modulator of critical CCl4-induced phenomena ranging from the disturbance of Ca2+ concentration to protein phosphorylation may be successfully applicable to investigate the diverse physiological functions of liver.
机译:我们研究了人参皂甙Rbt(G-Rbj),一种来自人参C. A. Meyer的主要皂苷,对单独或与G-Rbt腹膜内给药后大鼠肝脏蛋白质磷酸化的影响。我们发现118、63和34kDa蛋白在从施用CG4的大鼠制备的肝匀浆中显着磷酸化,而这些蛋白的磷酸化在从G-Rb!制备的匀浆中被抑制。加上CCl4-给药组。当蛋白激酶抑制剂被外源添加至来自施用CCl4的组或G-Rb 1的匀浆中。加上CCl4给药组,Ca2 + /钙调蛋白依赖性蛋白激酶(CaM-PK)抑制剂W-7比蛋白激酶C(C-激酶)抑制剂H-7更能抑制其磷酸化。有趣的是,通过外源添加糖原合酶抑制剂氟化钠(NaF),在由玉米油,G-Rbr和G-Rbi加CCl4施用的组中制备的匀浆中,只有34 kDa被磷酸化。此外,G-Rbi抑制了CC14在肝匀浆和微粒体中诱导的Ca2 +积累。以上结果表明,G-Rb通过调节CaM-PK而不是C激酶来抑制CCl4诱导的蛋白磷酸化,并且34 kDa蛋白可能在细胞环境中起着不同于118和63 kDa蛋白的生物学作用。因此,将G-Rbj用作关键CCl4诱导的现象(从Ca2 +浓度的干扰到蛋白质磷酸化)的调节剂的研究可能成功地用于研究肝脏的多种生理功能。

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