CircRNA_1156 Attenuates Neodymium Nitrate-Induced Hepatocyte Ferroptosis by Inhibiting the ACSL4/PKCβII Signaling Pathway
- Ning Wang 1, Jing Leng 1, Jing Xu 1, Kelei Qian 1, Zhiqing Zheng 1, Gonghua Tao 1, Ping Xiao 1, Xinyu Hong 1
- 1Institute of Chemical Safety Evaluation, State Environmental Protection Key Laboratory of Health Impact Assessment on New Environmental Pollutants, Shanghai Municipal Center for Disease Control and Prevention, Shanghai 201107, China.
- 0Institute of Chemical Safety Evaluation, State Environmental Protection Key Laboratory of Health Impact Assessment on New Environmental Pollutants, Shanghai Municipal Center for Disease Control and Prevention, Shanghai 201107, China.
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View abstract on PubMed
Summary
This summary is machine-generated.CircRNA_1156 inhibits neodymium nitrate-induced ferroptosis in liver cells. This circular RNA protects against rare earth element compound hepatotoxicity by downregulating the ACSL4/PKCβII pathway.
Area Of Science
- Biochemistry
- Cell Biology
- Toxicology
Background
- Ferroptosis, a lipid peroxidation-driven cell death, contributes to liver disease pathogenesis.
- Rare earth element compounds, like neodymium nitrate, can induce hepatotoxicity.
- Circular RNAs (circRNAs) are emerging as critical regulators in cellular processes.
Purpose Of The Study
- To investigate the role of circRNA_1156 in neodymium nitrate-induced ferroptosis in hepatocytes.
- To elucidate the molecular mechanisms by which circRNA_1156 affects Nd(NO3)3-induced liver injury.
- To explore circRNA_1156 as a potential therapeutic target for rare earth element compound hepatotoxicity.
Main Methods
- In vitro studies using AML12 hepatocytes exposed to Nd(NO3)3.
- In vivo studies involving chronic Nd(NO3)3 administration in animal models.
- Assessment of cell viability, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) levels.
- Analysis of ACSL4 and PKCβII expression, hepatic iron deposition, and mitochondrial damage.
- Overexpression of circRNA_1156 to evaluate its protective effects.
Main Results
- Nd(NO3)3 exposure reduced hepatocyte viability, increased oxidative stress markers (ROS, MDA), and depleted GSH.
- Overexpression of circRNA_1156 reversed Nd(NO3)3-induced cellular damage and suppressed ACSL4/PKCβII expression.
- In vivo, Nd(NO3)3 induced hepatic iron deposition, mitochondrial damage, and activated the ACSL4/PKCβII pathway.
- CircRNA_1156 overexpression significantly ameliorated these in vivo adverse effects.
Conclusions
- CircRNA_1156 acts as a novel inhibitor of neodymium nitrate-induced ferroptosis.
- The protective mechanism involves the downregulation of the ACSL4/PKCβII pathway.
- CircRNA_1156 holds therapeutic potential for treating liver injury caused by rare earth element compounds.
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