Maruyama H, Furukawa K, Onda M
First Department of Surgery, Nippon Medical School, Tokyo, Japan.
Nihon Ika Daigaku Zasshi. 1995 Jun;62(3):271-82. doi: 10.1272/jnms1923.62.271.
The effect of coenzyme Q10 (CoQ10) on hepatocyte injury during endotoxin (ET) shock in rats was studied with special reference to the role of polymorphonuclear neutrophils (PMN). ET shock was induced by intravenous administration of 5 mg/kg ET, and CoQ10 was given at 20 mg/kg once or 3 times orally or intravenously. We examined plasma glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and glutamate dehydrogenase (GLDH) levels, superoxide production by PMN, the phagocytic activity of PMN, the cytotoxicity of PMN to liver cells, and histological changes in the liver. The CoQ10-treated rats showed lower levels of GOT, GPT, and GLDH than rats treated with ET only. When compared to the group given ET only superoxide production by PMN induced by 2-methyl-6-phenyl-3,7-dihydroimidazol [1,2-alpha]pyrazin-3-one (MCLA) was significantly inhibited in the group given CoQ10 intravenously and 3 times orally, but there was no significant difference in the group given CoQ10 once orally. However, the level of superoxide production by PMN stimulated by phorbol myristate acetate (PMA) was lower in all CoQ10-treated rats than in those given ET only. There was no difference in either peripheral PMN counts or PMN phagocytes between the CoQ10-treated group and the group given ET only. Histologically, the hepatocyte injury in all groups that received CoQ10 was milder than that in the ET-only group. No hepatocyte cytotoxicity by PMN was observed in any group that received CoQ10. These results suggest that both intravenous and oral administration of CoQ10 can modulate the endotoxin-activated PMN, and is useful for preventing hepatocyte injury during ET shock.
研究了辅酶Q10（CoQ10）对大鼠内毒素（ET）休克期间肝细胞损伤的影响，并特别参考了多形核中性粒细胞（PMN）的作用。通过静脉注射5mg/kg ET诱导ET休克，CoQ10以20mg/kg的剂量口服或静脉注射一次或三次。我们检测了血浆谷草转氨酶（GOT）、谷丙转氨酶（GPT）和谷氨酸脱氢酶（GLDH）水平、PMN产生的超氧化物、PMN的吞噬活性、PMN对肝细胞的细胞毒性以及肝脏的组织学变化。CoQ10处理的大鼠的GOT、GPT和GLDH水平低于仅接受ET处理的大鼠。与仅给予ET的组相比，静脉注射CoQ10和口服三次CoQ10的组中，由2-甲基-6-苯基-3,7-二氢咪唑[1,2-α]吡嗪-3-酮（MCLA）诱导的PMN产生的超氧化物显著受到抑制，但口服一次CoQ10的组中没有显著差异。然而，所有CoQ10处理的大鼠中，由佛波酯（PMA）刺激的PMN产生的超氧化物水平低于仅给予ET的大鼠。CoQ10处理组和仅给予ET的组在外周PMN计数或PMN吞噬细胞方面没有差异。组织学上，所有接受CoQ10的组中的肝细胞损伤均比仅接受ET的组轻。在任何接受CoQ10的组中均未观察到PMN对肝细胞的细胞毒性。这些结果表明，静脉注射和口服CoQ10均可调节内毒素激活的PMN，对预防ET休克期间的肝细胞损伤有用。
