HNK ameliorated NASH mainly by activating the CFLAR-JNK pathway, which not only alleviated fat deposition by promoting the efflux and β-oxidation of fatty acids in the liver but also attenuated hepatic oxidative damage and insulin resistance by upregulating the expression of NRF2 and pIRS1.
Keyphrases
- oxidative stress
- signaling pathway
- induced apoptosis
- fatty acid
- insulin resistance
- high fat diet induced
- adipose tissue
- cell death
- poor prognosis
- type diabetes
- metabolic syndrome
- dna damage
- ischemia reperfusion injury
- high fat diet
- endoplasmic reticulum stress
- hydrogen peroxide
- mouse model
- binding protein
- long non coding rna
- amino acid
- heat stress