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RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary
Dong Qu1, Kaikai Zhang1, Lijian Chen1
1Department of Forensic Pathology, School of Forensic Medicine, Southern Medical University, Guangzhou, China.
Abstract:
In this study, RNA-sequencing (RNA-seq) was utilized to investigate the effects of luteolin on hepatotoxicity caused by methamphetamine (METH). The rats in METH group were administrated with METH (15 mg/kg, two times per day) via intraperitoneal (i.p.) injections for four consecutive days. The rats in luteolin + METH group were firstly administrated with luteolin (100 mg/kg, once a day) by oral gavage for 3 days before METH treatment. Lueolin attenuated the hepatotoxicity induced by METH via histopathological and biochemical analysis. The results of RNA-seq showed that luteolin could regulate 497 differentially expressed genes (DEGs), and the selected DEGs were mainly enriched in eight pathways, according to KEGG analysis. Furthermore, qRT-PCR was utilized to verify the results of RNA-seq. Six genes were selected as follows: liver enriched antimicrobial peptide 2 (Leap2), fatty acid synthase (Fasn), fatty acid binding protein 5 (Fabp5), patatin like phospholipase domain containing 3 (Pnpla3), myelin basic protein (Mbp) and calmodulin 3 (Calm3). Though because of the design flaws, the luteolin group has not been included, this study demonstrated that luteolin might exert hepato-protective effects from METH via modulation of oxidative phosphorylation, cytochrome P450 and certain signaling pathways.
Insights
Luteolin, a natural compound, mitigates liver damage caused by methamphetamine (METH) by regulating key genes and pathways. This study reveals luteolin
Area of Science:
- Pharmacology and Toxicology
- Molecular Biology
- Hepatology
Background:
- Methamphetamine (METH) abuse is associated with significant hepatotoxicity.
- Luteolin is a natural flavonoid with potential antioxidant and anti-inflammatory properties.
- Understanding the molecular mechanisms underlying METH-induced liver injury and potential therapeutic interventions is crucial.
Purpose of the Study:
- To investigate the protective effects of luteolin against methamphetamine-induced hepatotoxicity in a rat model.
- To elucidate the molecular mechanisms underlying luteolin's hepatoprotective effects using RNA-sequencing (RNA-seq).
Main Methods:
- Hepatotoxicity was induced in rats using methamphetamine (METH).
- Rats were pre-treated with luteolin via oral gavage.
- Histopathological and biochemical analyses were performed to assess liver damage.
- RNA-sequencing (RNA-seq) was employed to identify differentially expressed genes (DEGs) and enriched pathways (KEGG analysis).
- Quantitative real-time PCR (qRT-PCR) was used to validate RNA-seq findings for selected genes (Leap2, Fasn, Fabp5, Pnpla3, Mbp, Calm3).
Main Results:
- Luteolin administration attenuated METH-induced hepatotoxicity, as evidenced by histopathological and biochemical markers.
- RNA-seq analysis identified 497 differentially expressed genes (DEGs) regulated by luteolin.
- KEGG pathway analysis indicated that these DEGs were primarily enriched in pathways related to oxidative phosphorylation, cytochrome P450, and other signaling pathways.
- qRT-PCR confirmed the differential expression of key genes involved in liver function and cellular processes.
Conclusions:
- Luteolin demonstrates significant hepatoprotective effects against METH-induced liver injury.
- The protective mechanism involves the modulation of oxidative phosphorylation, cytochrome P450 activity, and specific signaling pathways.
- Luteolin holds potential as a therapeutic agent for mitigating METH-related hepatotoxicity.
