N-acetylcysteine inhibits atherosclerosis by correcting glutathione-dependent methylglyoxal elimination and dicarbonyl/oxidative stress in the aorta of diabetic mice
https://pmc.ncbi.nlm.nih.gov/articles/PMC7821347
At present, no specific antioxidant treatment has been recommended to prevent atherosclerotic progression (49). The present study confirmed that NAC possessed anti-atherosclerotic potential in experimental DM via the elevation of GSH in the aorta to inhibit dicarbonyl and oxidative stress. This finding may lead to a novel antioxidant strategy in the treatment of atherosclerosis in DM, in addition to the treatment of established risk factors.
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N-Acetylcysteine Improves Liver Function in Patients with Non-Alcoholic Fatty Liver Disease
Conclusions
N-acetylcysteine can improve liver function in patients with non-alcoholic fatty liver disease. Better results may be achievable in a longer follow up.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3270338
Long term N-acetylcysteine administration rescues liver steatosis via endoplasmic reticulum stress with unfolded protein response in mice
https://lipidworld.biomedcentral.com/articles/10.1186/s12944-020-01274-y
Conclusion
HF diet for 12 months induces significant liver steatosis via altered ER stress and UPR pathway activity, as well as liver apoptosis. NAC treatment rescues the liver steatosis and apoptosis induced by HF diet.
The efficacy of N-acetylcysteine in improving liver function: A systematic review and meta-analysis of controlled clinical trials
Conclusion
Although NAC might have favorable effect on ALB and bilirubin levels, larger trials assessing liver function as primary outcome are required.
https://www.sciencedirect.com/science/article/abs/pii/S2213434423000154
A Comparative Study of N-Acetyl Cysteine, Rosuvastatin, and Vitamin E in the Management of Patients with Non-Alcoholic Steatohepatitis: A Randomized Controlled Trial
Conclusions
NAC represents a promising therapeutic agent for NASH, attributed to its multifaceted benefits. This approach improves steatosis, fibrosis, and metabolic parameters, indicating a potential new strategy for managing NASH. NAC exhibits superior anti-inflammatory and anti-apoptotic effects relative to RSV or VE, with significant antifibrotic activity evidenced by liver stiffness measurements and non-invasive fibrosis scores. NAC distinctly enhances various metabolic parameters and improves HRQoL with few adverse effects. NAC has shown considerable enhancement in liver and kidney functions. Therefore, NAC is considered an old drug with new applications in the management of NASH.