Salvia hispanica L. (chia seeds) alleviates paracetamol-induced acute liver injury in mice by modulating oxidative stress and inflammation
Samya Mahmoud Ahmed, Marwa A. Masoud- Pharmacology, Toxicology and Pharmaceutics (miscellaneous)
- Pharmaceutical Science
- Toxicology
- Biochemistry, Genetics and Molecular Biology (miscellaneous)
- Applied Microbiology and Biotechnology
Background
Paracetamol [N-acetyl-p-aminophenol (APAP)] is one of the frequently prescribed antipyretics and analgesics; yet going over the recommended dose still poses a major clinical challenge and leads to serious drug-encouraged liver damage.
Objective
Our study aims to discover the hepatoprotective effect of
Materials and methods
Paracetamol (300 mg/kg bw, once a day for two successive days) was orally administered to establish a liver injury model. Forty male albino mice were randomly divided into four groups (10/group); control, APAP group, CS-4%+APAP group: was pretreated with CS (4%) for 21 days before receiving APAP, CS-20%+APAP group: was pretreated with CS (20%) for 21 days before receiving APAP. At the end of the experiment, the levels of liver injury indices, hepatic nitro-oxidative stress, and inflammatory-associated biomarkers along with histopathological examinations were determined. Additionally, inflammatory responses of some primer sequences (nuclear factor kappa B, p38 mitogen-activated protein kinases, monocyte chemoattractant protein-1, and toll-like receptor 4) were determined by quantitative real-time PCR in liver tissues.
Results
CS markedly stabilized the APAP-motivated alterations in liver function markers, cytochrome P450 2E1 level, hepatic nitro-oxidative stress, and pathological changes. The anti-inflammatory activity of CS improved tumor necrosis factor-alpha and myeloperoxidase production. Furthermore, mRNA expression of nuclear factor kappa B, monocyte chemoattractant protein-1, p38 mitogen-activated protein kinases, and toll-like receptor 4 were significantly downregulated. Such effects were found to be responsible for its hepatoprotective effect in a dose-dependent way.
Conclusion
Our results showed evidence that the hepatoprotective effect of CS against APAP-induced liver injury was mediated through the reduction of oxidative stress damage, enhancement of antioxidant status, and inhibition of different inflammatory markers.