Protective effects of extracts of Schisandra chinensis stems against acetaminophen-induced hepatotoxicity via regulation of MAPK and caspase-3 signaling pathways.
10.1016/S1875-5364(18)30110-9
- Author:
Yan-Zi LI
1
;
Zhi-Na MA
1
;
Yin-Shi SUN
2
;
Shen REN
1
;
Shuang JIANG
1
;
Wei-Zhe ZHANG
1
;
Zi WANG
3
;
Wei LI
4
Author Information
1. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
2. Institute of Special Wild Economic Animals and Plant, Chinese Academy of Agricultural Sciences (CAAS), Changchun 132109, China.
3. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China. Electronic address: wangzi8020@126.com.
4. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China. Electronic address: liwei7727@126.com.
- Publication Type:Journal Article
- Keywords:
APAP-induced hepatotoxicity;
Anti-apoptosis;
Anti-inflammation;
Anti-oxidation;
MAPK and caspase-3 signaling pathways;
Schisandra chinensis
- MeSH:
Acetaminophen;
adverse effects;
Alanine Transaminase;
metabolism;
Animals;
Apoptosis;
drug effects;
Aspartate Aminotransferases;
metabolism;
Caspase 3;
genetics;
metabolism;
Chemical and Drug Induced Liver Injury;
genetics;
metabolism;
physiopathology;
prevention & control;
Drugs, Chinese Herbal;
administration & dosage;
chemistry;
Glutathione;
metabolism;
Humans;
Liver;
drug effects;
metabolism;
Male;
Malondialdehyde;
metabolism;
Mice;
Mice, Inbred ICR;
Mitogen-Activated Protein Kinases;
chemistry;
genetics;
metabolism;
Oxidative Stress;
drug effects;
Schisandra;
chemistry;
Signal Transduction;
drug effects
- From:
Chinese Journal of Natural Medicines (English Ed.)
2018;16(9):700-713
- CountryChina
- Language:English
-
Abstract:
The present study was designed to evaluate protective activity of an ethanol extract of the stems of Schisandra chinensis (SCE) and explore its possible molecular mechanisms on acetaminophen (APAP) induced hepatotoxicity in a mouse model. The results of HPLC analysis showed that the main components of SCE included schisandrol A, schisandrol B, deoxyschisandrin, schisandrin B, and schisandrin C and their contents were 5.83, 7.11, 2.13, 4.86, 0.42 mg·g, respectively. SCE extract was given for 7 consecutive days before a single hepatotoxic dose of APAP (250 mg·kg) was injected to mice. Our results showed that SCE pretreatment ameliorated liver dysfunction and oxidative stress, which was evidenced by significant decreases in aspartate transaminase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA) contents and elevations in reduced glutathione (GSH) and superoxide dismutase (SOD) levels. These findings were associated with the result that the SCE pretreatment significantly decreased expression levels of 4-hydroxynonenal (4-HNE) and 3-nitrotyrosine (3-NT). SCE also significantly decreased the expression levels of Bax, mitogen- activated protein kinase (MAPK), and cleaved caspase-3 by APAP exposure. Furthermore, supplementation with SCE suppressed the expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), suggesting alleviation of inflammatory response. In summary, these findings from the present study clearly demonstrated that SCE exerted significant alleviation in APAP-induced oxidative stress, inflammation and apoptosis mainly via regulating MAPK and caspase-3 signaling pathways.
