Naringenin Prevents Oxidative Stress and Inflammation in LPS-Induced Liver Injury through the Regulation of LncRNA-mRNA in Male Mice

Abstract

Inflammation accompanies hepatic dysfunction resulting from tissue oxidative damage. Naringenin (Nar), a natural flavanone, has known antioxidant and anti-inflammatory activities, but its mechanism of action in the regulation of liver dysfunction requires further investigation. In this study, the role of naringenin in lipopolysaccharide (LPS)-induced hepatic oxidative stress and inflammation was explored, as well as its mechanism by transcriptome sequencing. The results indicated that compared with the LPS group, Nar treatment caused a significant increase in the mRNA levels of antioxidant factors glutamate-cysteine ligase catalytic subunit (GCLC) and glutamate-cysteine ligase modifier subunit (GCLM), yet the expression of related inflammatory factors (MCP1, TNFα, IL-1β and IL-6) showed less of an increase. RNA sequencing identified 36 differentially expressed lncRNAs and 603 differentially expressed mRNAs. KEGG enrichment analysis indicated that oxidative stress and inflammation pathways are meticulously linked with naringenin treatment. The Co-lncRNA-mRNA network was also constructed. Tissue expression profiles showed that lncRNA played a higher role in the liver. Subsequently, expression levels of inflammatory factors indicated that lncRNAs and target mRNAs were significantly reduced after naringenin treatment in mouse liver AML12 cells and obese mouse. These results suggest that naringenin helps to prevent liver dysfunction through the regulation of lncRNA-mRNA axis to reduce oxidative stress and inflammatory factors.

Antioxidative and Anti-Inflammatory Protective Effects of Fucoxanthin against Paracetamol-Induced Hepatotoxicity in Rats

“…There was a dose-dependent modulation in the expression of the above-mentioned genes and proteins in the rats with PAC-induced liver injury after treatment with F100 (100 mg/kg), F200 (200 mg/kg), and F500 (500 mg/kg). Previously, it was reported that liver inflammation is a sign of almost all liver disease and a major contributor to liver damage, and PAC toxicity causes damage to the liver's central lobule region, which results in the release of reactive oxygen species (ROS) and the generation of proinflammatory cytokines [1]. The biological system includes two categories of free radicals: reactive oxygen species (ROS) that are derived from O 2 metabolism and reactive nitrogen species (RNS) that are derived from nitric oxide and superoxide [31].…”

“…The liver plays a crucial role in the homeostasis maintenance of the human body. Liver damage is linked to oxidative stress and the immune system's inflammatory response [1]. Detoxification, metabolism, protein synthesis, host defense, and immunological response are just some of the many essential functions maintained by the liver [1].…”

“…Liver damage is linked to oxidative stress and the immune system's inflammatory response [1]. Detoxification, metabolism, protein synthesis, host defense, and immunological response are just some of the many essential functions maintained by the liver [1]. Acute liver failure is characterized by severe liver dysfunction manifested by coagulopathy, jaundice, and encephalopathy, typically in the absence of underlying liver disease [2].…”

LanGui tea, an herbal medicine formula, protects against binge alcohol-induced acute liver injury by activating AMPK-NLRP3 signaling

“…For in vitro ethanol or inflammation modeling and subsequent cell experiments, the AML-12 cells were cultured in DMEM-F12, and then subjected to ethanol (500 mM) [ 33 ] or LPS (100 ng.mL −1 ) [ 34 ] with or without the addition of DMSO (0.1%), CC (10 μM), and the ELG at specified concentrations for 24 h.…”