The involvement of TGF-β1 /FAK/α-SMA pathway in the antifibrotic impact of rice bran oil on thioacetamide-induced liver fibrosis in rats

Autor: Rehab F. Abdel-Rahman, Hany M. Fayed, Gihan F. Asaad, Hanan A. Ogaly, Alyaa F. Hessin, Abeer A. A. Salama, Sahar S. Abd El-Rahman, Mahmoud S. Arbid, Marawan Abd Elbaset Mohamed
Rok vydání: 2021
Předmět:
Liver Cirrhosis
Male
Cell signaling
Physiology
Becaplermin
Thioacetamide
Signal transduction
Biochemistry
Malondialdehyde
Immune Physiology
Medicine and Health Sciences
Immune Response
Innate Immune System
Multidisciplinary
Liver Diseases
NF-kappa B
Signaling cascades
Eukaryota
Plants
Glutathione
Lipids
Hydroxyproline
Liver
Experimental Organism Systems
Medicine
Cytokines
Liver Fibrosis
Inflammation Mediators
Research Article
Cell biology
Science
Immunology
Gastroenterology and Hepatology
Research and Analysis Methods
Collagen Type I
Gas Chromatography-Mass Spectrometry
Rice Bran Oil
Transforming Growth Factor beta1
Signs and Symptoms
Plant and Algal Models
Albumins
Animals
Grasses
Rats
Wistar
Transaminases
Inflammation
Biology and life sciences
Connective Tissue Growth Factor
Organisms
Proteins
Globulins
Molecular Development
Fibrosis
Actins
Oxidative Stress
TGF-beta signaling cascade
Cyclooxygenase 2
Focal Adhesion Protein-Tyrosine Kinases
Immune System
Animal Studies
Rice
Clinical Medicine
Proto-Oncogene Proteins c-akt
Collagens
Oils
Biomarkers
Developmental Biology
Zdroj: PLoS ONE
PLoS ONE, Vol 16, Iss 12, p e0260130 (2021)
ISSN: 1932-6203
Popis: The objective of the current study is to investigate the effect of rice bran oil (RBO) on hepatic fibrosis as a characteristic response to persistent liver injuries. Rats were randomly allocated into five groups: the negative control group, thioacetamide (TAA) group (thioacetamide 100 mg/kg thrice weekly for two successive weeks, ip), RBO 0.2 and 0.4 groups (RBO 0.2mL and 0.4 mL/rat/day, po) and standard group (silymarin 100 mg/kg/day, po) for two weeks after TAA injection. Blood and liver tissue samples were collected for biochemical, molecular, and histological analyses. Liver functions, oxidative stress, inflammation, liver fibrosis markers were assessed. The obtained results showed that RBO reduced TAA-induced liver fibrosis and suppressed the extracellular matrix formation. Compared to the positive control group, RBO dramatically reduced total bilirubin, AST, and ALT blood levels. Furthermore, RBO reduced MDA and increased GSH contents in the liver. Simultaneously RBO downregulated the NF-κβ signaling pathway, which in turn inhibited the expression of some inflammatory mediators, including Cox-2, IL-1β, and TNF-α. RBO attenuated liver fibrosis by suppressing the biological effects of TGF-β1, α-SMA, collagen I, hydroxyproline, CTGF, and focal adhesion kinase (FAK). RBO reduced liver fibrosis by inhibiting hepatic stellate cell activation and modulating the interplay among the TGF-β1 and FAK signal transduction. The greater dosage of 0.4 mL/kg has a more substantial impact. Hence, this investigation presents RBO as a promising antifibrotic agent in the TAA model through inhibition of TGF-β1 /FAK/α-SMA.
Databáze: OpenAIRE
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