Capparis spinosa improves non-alcoholic steatohepatitis through down-regulating SREBP-1c and a PPARα-independent pathway in high-fat diet-fed rats.
Rasoul AkbariHamid YaghootiMohammad Taha JalaliLaya Sadat KhorsandiNarges MohammadtaghvaeiPublished in: BMC research notes (2022)
In the rats (n = 40) model of NASH, biochemical and histopathological examinations showed that liver steatosis, inflammation, and hepatic fibrosis were markedly attenuated in response to CS and fenofibrate interventions. At the molecular level, CS treatment down-regulated sterol regulatory element-binding protein-1c (SREBP-1c) (p < 0.001), acetyl-CoA carboxylase (ACC) (p < 0.001), and up-regulated Carnitine palmitoyltransferase I (CPT1) expression (p < 0.001). In conclusion, CS has favorable therapeutic effects for NASH, which was associated with ameliorating steatosis and fibrosis via regulation of the DNL and β-oxidation pathway genes.
Keyphrases
- high fat diet
- insulin resistance
- binding protein
- transcription factor
- adipose tissue
- oxidative stress
- metabolic syndrome
- poor prognosis
- high fat diet induced
- liver fibrosis
- skeletal muscle
- fatty acid
- physical activity
- type diabetes
- genome wide identification
- liver injury
- dna methylation
- long non coding rna
- smoking cessation