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Oral iron sulfide prevents acute alcohol intoxication by initiating the endogenous multienzymatic antioxidant defense system.
Sci Adv
January 2025
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Nankai University, Haihe Education Park, 38 Tongyan Road, Tianjin 300353, People's Republic of China.
Acute alcohol intoxication could cause multiorgan damage, including nervous, digestive, and cardiovascular systems, and in particular, irreversible damage to the brain and liver. Emerging studies have revealed that the endogenous multienzymatic antioxidant defense system (MEAODS) plays a central role in preventing oxidative stress and other toxicological compounds produced by alcohol. However, few available drugs could quickly regulate MEAODS.
View Article and Find Full Text PDFNLRP6 overexpression improves nonalcoholic fatty liver disease by promoting lipid oxidation and decomposition in hepatocytes through the AMPK/CPT1A/PGC1A pathway.
Nan Fang Yi Ke Da Xue Xue Bao
January 2025
Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang 550000, China.
Objectives: To investigate the regulatory role of nucleotide-bound oligomerized domain-like receptor containing pyrin-domain protein 6 (NLRP6) in liver lipid metabolism and non-alcoholic fatty liver disease (NAFLD).
Methods: Mouse models with high-fat diet (HFD) feeding for 16 weeks (=6) or with methionine choline-deficient diet (MCD) feeding for 8 weeks (=6) were examined for the development of NAFLD using HE and oil red O staining, and hepatic expressions of NLRP6 were detected with RT-qPCR, Western blotting, and immunohistochemical staining. Cultured human hepatocytes (LO2 cells) with adenovirus-mediated NLRP6 overexpression or knock-down were treated with palmitic acid (PA) in the presence or absence of compound C (an AMPK inhibitor), and the changes in cellular lipid metabolism were examined by measuring triglyceride, ATP and β-hydroxybutyrate levels and using oil red staining, RT-qPCR, and Western blotting.
Correlation between metabolic dysfunction-associated steatotic liver disease and subclinical coronary atherosclerosis in eastern China.
Diabetol Metab Syndr
January 2025
Department of Radiology, Shanghai Health and Medical Center, No. 67 Dajishan, Binhu District, Wuxi, 214065, China.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by the presence of at least one cardiovascular disease (CVD) risk factor, underscoring its potential to elevate CVD risk in affected individuals. However, evidence linking MASLD to subclinical coronary atherosclerosis remains scarce, and further investigations are necessary to elucidate the independent role of varying MASLD severities as a CVD risk factor.
Methods: This study analyzed 7,507 participants aged ≥ 40 who underwent comprehensive health evaluations at the Shanghai Health and Medical Center.
The association between immunoinflammatory biomarkers NLR, PLR, LMR and nonalcoholic fatty liver disease: a systematic review and meta-analysis.
Clin Exp Med
January 2025
Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, No. 110 Ganhe Road, Shanghai, 200437, China.
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disorder closely linked to metabolic syndrome. Identifying novel, easily measurable biomarkers could significantly enhance the diagnosis and management of NAFLD in clinical settings. Recent studies suggest that immunoinflammatory biomarkers-specifically, the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and lymphocyte-to-monocyte ratio (LMR)-may offer diagnostic value for NAFLD.
View Article and Find Full Text PDFFunctional mechanisms and potential therapeutic strategies for lactylation in liver diseases.
Life Sci
January 2025
Department of Hepatobiliary and Pancreatic Surgery, General Surgery Center, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China. Electronic address:
Lactylation, a novel form of lactate-mediated protein post-translational modification (PTM), has been identified as a crucial regulator of gene expression and protein function through the modification of both histone and non-histone proteins. Liver disease is frequently characterized by a reprogramming of glucose metabolism and subsequent lactate accumulation. Recent research has implicated lactylation in a diverse array of hepatic pathologies, including liver injury, non-alcoholic fatty liver disease, liver fibrosis, and hepatocellular carcinoma.
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