Schisandra chinensis essential oil attenuates acetaminophen-induced liver injury through alleviating oxidative stress and activating autophagy

被引:17
作者
Zhao, Jing [1 ,2 ,3 ]
Ding, Kaixin [2 ,3 ]
Hou, Manting [2 ,3 ]
Li, Yuanhua [1 ,2 ,3 ]
Hou, Xiaorong [2 ,3 ]
Dai, Wenzhang [1 ,2 ,3 ]
Li, Zhiyong [2 ,3 ]
Zhao, Jun [2 ]
Liu, Wenlong [1 ]
Bai, Zhaofang [2 ,3 ]
机构
[1] Hunan Univ Chinese Med, Sch Pharm, 300 Bachelor St, Changsha 410208, Peoples R China
[2] Chinese Peoples Liberat Army Gen Hosp, Dept Hepatol, Med Ctr 5, 100 West Fourth Ring Rd, Beijing 100039, Peoples R China
[3] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 5, China Mil Inst Chinese Mat, 100 West Fourth Ring Rd, Beijing 100039, Peoples R China
基金
中国国家自然科学基金;
关键词
Drug-induced liver injury; oxidative stress; essential oil; antioxidant; autophagy; INDUCED HEPATOTOXICITY; THERAPEUTIC TARGET; IN-VIVO; PROTECTS; MICE; NECROSIS; SYSTEM;
D O I
10.1080/13880209.2022.2067569
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context Schisandra chinensis (Turcz.) Baill. (Magnoliaceae) essential oil (SCEO) composition is rich in lignans that are believed to perform protective effects in the liver. Objective This study investigates the effects of SCEO in the treatment of acetaminophen (APAP)-induced liver injury in mice. Materials and methods C57BL/6 mice (n = 56) were randomly divided into seven groups: normal; APAP (300 mg/kg); APAP plus bicyclol (200 mg/kg); APAP plus SCEO (0.25, 0.5, 1, 2 g/kg). Serum biochemical parameters for liver function, inflammatory factors, and antioxidant activities were determined. The protein expression levels of Nrf2, GCLC, GCLM, HO-1, p62, and LC3 were assessed by western blotting. Nrf2, GCLC, HO-1, p62, and LC3 mRNA were detected by real-time PCR. Results Compared to APAP overdose, SCEO (2 g/kg) pre-treatment reduced the serum levels of AST (79.4%), ALT (84.6%), TNF-alpha (57.3%), and IL-6 (53.0%). In addition, SCEO (2 g/kg) markedly suppressed cytochrome P450 2E1 (CYP2E1) (15.4%) and attenuated the exhaustion of GSH (43.6%) and SOD (16.8%), and the accumulation of MDA (22.6%) in the liver, to inhibit the occurrence of oxidative stress. Moreover, hepatic tissues from our experiment revealed that SCEO pre-treatment mitigated liver injury caused by oxidative stress by increasing Nrf2, HO-1, and GCL. Additionally, SCEO activated autophagy, which upregulated hepatic LC3-II and decreased p62 in APAP overdose mice (p < 0.05). Discussion and conclusions Our evidence demonstrated that SCEO protects hepatocytes from APAP-induced liver injury in vivo and the findings will provide a reliable theoretical basis for developing novel therapeutics.
引用
收藏
页码:958 / 967
页数:10
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