Tsuchida T, Yasuyama T, Higuchi K, Watanabe A, Urakami T, Akaike T, Sato K, Maeda H
Third Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
J Gastroenterol Hepatol. 1993 Jul-Aug;8(4):342-7. doi: 10.1111/j.1440-1746.1993.tb01525.x.
Pyrroloquinoline quinone (PQQ) and its derivative, oxazo pyrroloquinoline (OPQ-G), protected rats from experimental liver injury induced by carbon tetrachloride (CCl4) in vivo. This effect was observed after an intraperitoneal injection of 5 mg/kg PQQ or OPQ-G, which was given twice, 10 min and 1 h before CCl4 administration. Pyrroloquinoline quinone protected primary cultured rat hepatocytes from CCl4 toxicity in vitro. This protection was most effective at a concentration of 3 mumol/L PQQ. Pyrroloquinoline quinone derivatives (oxazo pyrroloquinoline, methyl-thioethyl oxazo pyrroloquinoline and PQQ-allylester) also protected the hepatocytes from CCl4 toxicity. Pyrroloquinoline quinone and its derivatives inhibited the lucigenin-enhanced chemiluminescence from isolated hepatocytes initiated by CCl4. These results suggest that eliminating free radicals is one of the protective mechanisms of PQQ and its derivatives against CCl4-induced liver injury.
吡咯喹啉醌（PQQ）及其衍生物恶唑吡咯喹啉（OPQ-G）在体内可保护大鼠免受四氯化碳（CCl4）诱导的实验性肝损伤。在腹腔注射5mg/kg PQQ或OPQ-G后观察到这种效果，该注射在CCl4给药前10分钟和1小时进行，共注射两次。吡咯喹啉醌在体外可保护原代培养的大鼠肝细胞免受CCl4毒性。这种保护在3μmol/L PQQ浓度时最为有效。吡咯喹啉醌衍生物（恶唑吡咯喹啉、甲硫乙基恶唑吡咯喹啉和PQQ-烯丙酯）也可保护肝细胞免受CCl4毒性。吡咯喹啉醌及其衍生物可抑制由CCl4引发的离体肝细胞的光泽精增强化学发光。这些结果表明，清除自由基是PQQ及其衍生物对抗CCl4诱导的肝损伤的保护机制之一。
