1. Academic Validation
  2. Schisandra chinensis essential oil attenuates acetaminophen-induced liver injury through alleviating oxidative stress and activating autophagy

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

  • Pharm Biol. 2022 Dec;60(1):958-967. doi: 10.1080/13880209.2022.2067569.
Jing Zhao 1 2 3 Kaixin Ding 2 3 Manting Hou 2 3 Yuanhua Li 1 2 3 Xiaorong Hou 2 3 Wenzhang Dai 1 2 3 Zhiyong Li 2 3 Jun Zhao 2 Wenlong Liu 1 Zhaofang Bai 2 3
Affiliations

Affiliations

  • 1 School of Pharmacy, Hunan University of Chinese Medicine, Changsha, China.
  • 2 Department of Hepatology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, China.
  • 3 China Military Institute of Chinese Materia, the Fifth Medical Centre, Chinese PLA General Hospital, Beijing, China.
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.

Keywords

Drug-induced liver injury; antioxidant; autophagy; essential oil; oxidative stress.

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