Schisandra chinensis essential oil attenuates acetaminophen-induced liver injury through alleviating oxidative stress and activating autophagy. (31st December 2022)

• Record Type: Journal Article
• Authors: Zhao, Jing; Ding, Kaixin; Hou, Manting; Li, Yuanhua; Hou, Xiaorong; Dai, Wenzhang; Li, Zhiyong; Zhao, Jun; Liu, Wenlong; Bai, Zhaofang
• Is Part Of: Pharmaceutical biology. Volume 60:Number 1(2022)
• Page Start: 958
• Page End: 967
• Publication Date: 2022-12-31
• Subjects: Drug-induced liver injury -- oxidative stress -- essential oil -- antioxidant -- autophagy; Pharmacognosy -- Periodicals; Materia medica, Vegetable -- Periodicals; 615.321
• DOI: 10.1080/13880209.2022.2067569
• Languages: English
• ISSNs: 1388-0209

Abstract

Abstract: 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-α (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.