Chen An-Shu, Taguchi Tadao, Sakai Kazuo, Matahira Yoshiharu, Wang Min-Wei, Miwa Ichitomo
Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University; Nagoya 468-8503, Japan.
Biol Pharm Bull. 2005 Oct;28(10):1971-3. doi: 10.1248/bpb.28.1971.
The purpose of the present study was to examine whether chitobiose and chitotriose can protect rats from CCl4-induced hepatic toxicity when given orally. We studied the effects of the 2 chitooligosaccharides given orally to rats on the acute hepatotoxicity induced by CCl4-dependent lipid peroxidation. The increase in the sum of malondialdehyde and 4-hydroxy-2-alkenals, a marker of lipid peroxidation, in both plasma and liver of CCl4-treated rats was suppressed by oral administration of chitobiose or chitotriose. The elevation in the levels of plasma aspartate transaminase and alanine transaminase activities, markers of hepatic injury, induced by CCl4 intoxication was also counteracted by oral administration of either chitooligosaccharide. The results indicate that chitobiose and chitotriose have the ability to exert a protective action against CCl4-induced acute hepatoxicity, probably by their antioxidant activity.
本研究的目的是检测口服壳二糖和壳三糖是否能保护大鼠免受四氯化碳诱导的肝毒性。我们研究了口服给予大鼠这两种低聚壳聚糖对四氯化碳依赖性脂质过氧化诱导的急性肝毒性的影响。口服壳二糖或壳三糖可抑制四氯化碳处理大鼠血浆和肝脏中脂质过氧化标志物丙二醛和4-羟基-2-烯醛总和的增加。口服任何一种低聚壳聚糖也可抵消四氯化碳中毒诱导的肝损伤标志物血浆天冬氨酸转氨酶和丙氨酸转氨酶活性水平的升高。结果表明,壳二糖和壳三糖可能通过其抗氧化活性对四氯化碳诱导的急性肝毒性发挥保护作用。