Effects of dark chocolate on NOX‐2‐generated oxidative stress in patients with non‐alcoholic steatohepatitis

Abstract

Cocoa polyphenols exert an antioxidant activity via NOX2 down-regulation in NASH patients.

From Cocoa to Chocolate: The Impact of Processing on In Vitro Antioxidant Activity and the Effects of Chocolate on Antioxidant Markers In Vivo

“…It seems that all the different formulations that were used in the studies, such as tablets and chocolate drinks, failed to display any significant effect. Moreover, in agreement with previous evidences in vivo ( 1 ), milk chocolate does not produce any significant antioxidant effect in humans, and it has been utilized as control ( 57 ) in the only study where an effect was detected with dark chocolate.…”

“…An increase in plasma polyphenol levels, namely, epicatechin, catechin, epicatechin-3 O -methylether, and total phenolics, following a cocoa-based product supplementation period was detected in three studies out of seven. Increases were not correlated to any changes in markers of antioxidant function except for Loffredo et al ( 57 ).…”

Potential Therapeutic Benefits of Herbs and Supplements in Patients with NAFLD

“…Cocoa has gained interested based on its antioxidative potential and has been found to decrease NADPH oxidase levels in NASH patients and reduce oxidative stress [ 100 , 101 ]. Similarly, cinnamon has been studied for its antioxidative effects as well and a blinded trial in NAFLD patients by Askari et al reported that 1500 mg of cinnamon supplementation for 12 weeks reduced AST, ALT, and insulin resistance compared to the placebo group [ 102 ].…”

Five Constituents in Psoralea corylifolia L. Attenuate Palmitic Acid-Induced Hepatocyte Injury via Inhibiting the Protein Kinase C-α/Nicotinamide-Adenine Dinucleotide Phosphate Oxidase Pathway

“…Oxidative stress refers to a shift in the balance toward increased intracellular reactive oxygen species (ROS) generation, compared to breakdown (Mann et al, 2017). Nicotinamideadenine dinucleotide phosphate oxidase (NOX) is considered the major cellular ROS source (Loffredo et al, 2016;Long et al, 2017;Rabelo et al, 2018). Its activation has been associated with hepatic injury (Matsumoto et al, 2018;Zheng et al, 2018) and also plays a very plausible role as the starting point of extrahepatic damage, leading to inflammation and fibrosis through activation of Kupffer cells and hepatic stellate cells (HSCs) (Das et al, 2015;, thus causing a self-perpetuating circle of ROS formation and ROS-mediated damage (Masarone et al, 2018;Zhong and Liu, 2018).…”