Yoshioka Hiroki, Usuda Haruki, Fujii Hirohisa, Nonogaki Tsunemasa
College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyamaku, Nagoya, Aichi, 463-8521, Japan.
Department of Pharmacology, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo, Shimane, 693-8501, Japan.
Environ Health Prev Med. 2017 Jun 12;22(1):54. doi: 10.1186/s12199-017-0662-3.
The aim of this study was to investigate the therapeutic effects of a Sasa veitchii leaf extract (SE) on acetaminophen (APAP)-induced hepatotoxicity.
Seven-week-old male ddY mice were orally administered SE or saline (0.2 mL) once a day for a week. Twenty-four hours after the last pretreatment, the mice were intraperitoneally injected with 550 mg/kg APAP or saline under fasting conditions. The mice from each group were euthanized and bled for plasma analysis 2, 6, 24, and 72 h after the injection.
We found that pretreatment with SE significantly decreased hepatic injury markers (i.e., alanine aminotransferase and aspartate aminotransferase), oxidative stress (malondialdehyde and glutathione level), inflammatory cytokines, histological damage, c-jun N-terminal kinase activation, and receptor-interacting protein-1 activation. Further, SE pretreatment decreased Cyp2e1 expression and increased total antioxidant capacity in the liver.
Our findings demonstrate that prophylactic SE treatment protects mice from APAP-induced hepatotoxicity through modulation of Cyp2e1 expression and antioxidant capacity.
本研究旨在探讨茶树叶提取物（SE）对乙酰氨基酚（APAP）诱导的肝毒性的治疗作用。
7周龄雄性ddY小鼠每天口服一次SE或生理盐水（0.2 mL），持续一周。在最后一次预处理24小时后，小鼠在禁食条件下腹腔注射550 mg/kg APAP或生理盐水。注射后2、6、24和72小时，对每组小鼠实施安乐死并采血进行血浆分析。
我们发现，SE预处理显著降低了肝损伤标志物（即丙氨酸转氨酶和天冬氨酸转氨酶）、氧化应激（丙二醛和谷胱甘肽水平）、炎性细胞因子、组织学损伤、c-jun氨基末端激酶激活和受体相互作用蛋白-1激活。此外，SE预处理降低了肝脏中Cyp2e1的表达，并提高了总抗氧化能力。
我们的研究结果表明，预防性SE治疗通过调节Cyp2e1表达和抗氧化能力，保护小鼠免受APAP诱导的肝毒性。
