Protection by different classes of dietary polyphenols against palmitic acid-induced steatosis, nitro-oxidative stress and endoplasmic reticulum stress in HepG2 hepatocytes

Increased load of electron donors (NADH and FADH2) originating from fat metabolism to the mitochondrial electron transport chain (ETC) results in increased ROS production due to leakage of electrons from complex I and III. These ROS further cause mitochondrial dysfunction and decrease mitochondrial content. Polyphenols improve the flow of electrons in the ETC possibly by inducing the expression of mitochondrial respiratory complex subunits and improving mitochondrial function leading to protection against the decline in mitochondrial membrane potential. Polyphenols also prevent induction of endoplasmic reticulum chaperones by palmitate, leading to lower expression of pro-apoptotic CHOP. By preventing the decline in ΔΨm and the expression of ER stress chaperones and CHOP, polyphenols may prevent apoptosis involved in the progression of NAFLD.