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Effects of carnosic acid on arsenic-induced liver injury in mice: A comparative transcriptomics analysis
Baiming Jin1, Haonan Li2, Hua Zhang2
1Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, PR China; National Health Commission & Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University (23618504), Harbin 150081, PR China; Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health，Harbin Medical University, Harbin 150081, PR China; Institute of Cell Biotechnology, China and Russia Medical Research Center, Harbin Medical University, Harbin 150081, PR China; Department of Preventive Medicine, Qiqihar Medical University, Qiqihar 161006, PR China.
Background:
Long-term chronic exposure to arsenic can cause different degrees of liver injury. Till date, its molecular mechanism has not meant fully elucidated. Evidence indicates that Carnosic acid (CA) has a protective role in arsenic-induced liver injury. This study aimed to reveal the potential targets and evaluate the potential effect of CA intervention at transcriptional level, and provide reference for the intervention of arsenic-induced liver injury.
Methods:
Arsenic-induced liver injury and CA intervention models were established in C57BL/6 mice. RNA sequencing technique was carried out to obtain the differentially expressed gene (DEG) profiles. The common covariant DEGs between arsenic induction and CA intervention was screened by comparative transcriptomic analysis methods. QRT-PCR was used to verify the covariant DEGs.
Results:
Transcriptome results showed that 220 DEGs were identified after arsenic induction. 267 DEGs were identified after CA intervention (|fold change| > 2.0 and adjusted P < 0.05). 42 covariant DEGs were discovered between the comparison of "AS vs Control" and "AS & CA vs AS". In addition, hub gene analysis revealed a total of 8 covariant DEGs (Ehhadh, Fgf21, Cyp2b10, Plin2, Aacs, Cyp7a1, Per2 and Mylip). The mRNA expressions of Fgf21 and Plin2 were significantly increased (P < 0.05) and the mRNA expressions of Cyp2b10, Cyp7a1, Per2 and Mylip were significantly decreased (P < 0.05) after arsenic induction. On the contrary, the changes of these DEGs were reversed after CA intervention.
Conclusion:
The present study would be helpful to understand the potential health effects of arsenic-induced liver injury and identify new potential targets, and provide a reference for the intervention of CA.
