Are N-Acetylcysteine and Resveratrol Effective Treatments for Liver Disease?

Chávez, Edgar; Galicia-Moreno, Marina; Muriel, Pablo

doi:10.1016/b978-0-12-804274-8.00052-7

Cited by 1 publication

(1 citation statement)

References 113 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, two of the most studied hepatoprotective compounds until now are resveratrol and N-acetylcysteine (NAC) [60]. On the one hand, resveratrol inhibits the formation of hepatocyte nodules in the DEN-induced HCC model plus phenobarbital administration; moreover, it is capable of modulating mitochondrial biogenesis [61]. On the other hand, NAC blocked phosphorylation of β-catenin, JNK, and c-jun activation, avoiding the development of liver damage in HCC transaldolase-deficient mice, a limiting enzyme for the non-oxidative branch of the pentose phosphate pathway, which is, at least in part, responsible for HCC generation [62]; furthermore, NAC stabilizes the mitochondrial membrane potential regulating mitochondrial dynamics [61].…”

Section: Dynamicsmentioning

confidence: 99%

Interaction of Mitochondrial and Epigenetic Regulation in Hepatocellular Carcinoma

Sánchez¹,

Chávez²,

Loyden³

et al. 2018

Liver Cancer

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is a pathology preceded mainly by cirrhosis of diverse etiology and is associated with uncontrolled dedifferentiation and cell proliferation processes. Many cellular functions are dependent on mitochondrial function, among which we can mention the enzymatic activity of PARP-1 and sirtuin 1, epigenetic regulation of gene expression, apoptosis, and so on. Mitochondrial dysfunction is related to liver diseases including cirrhosis and HCC; the energetic demand is not properly supplied and mitochondrial morphologic changes have been observed, resulting in an altered metabolism. There is a strong relationship between epigenetics and mitochondrion since the first one is dependent on the correct function of the last one. There is an interest to improve or to maintain mitochondrial integrity in order to prevent or reverse HCC; such is the case of IFC-305 that has a beneficial effect on mitochondrial function in a sequential model of cirrhosis-HCC. In this model, IFC-305 downregulates the expression of PCNA, thymidylate synthase, HGF and its receptor c-Met and upregulates the cell cycle inhibitor p27, thereby decreasing cell proliferation. Both effects, improvement of mitochondria function and reduction of tumor proliferation, suggest its use as HCC chemoprevention or as an adjuvant in chemotherapy.

show abstract