Key result
Rosmarinic acid protects H9c2 cardiomyocytes from TNF-α-induced inflammatory injury by up-regulating miR-344a-3p and subsequently inhibiting CCR1 expression.
Why the study?
It was unclear whether rosmarinic acid protects cardiomyocytes from inflammatory damage through miRNAs.
Does rosmarinic acid protect cardiomyocytes from TNF-α-induced inflammatory damage via regulating miRNAs?
Does rosmarinic acid protect cardiomyocytes from TNF-α-induced inflammatory damage via regulating miRNAs?
Rosmarinic acid protects cardiomyocytes from TNF-α-induced inflammatory injury by up-regulating miR-344a-3p and inhibiting CCR1 expression, suggesting CCR1 as a potential therapeutic target.
Supports CCR1 as target in TNF-α cardiomyocyte injury; leaves open translation to in vivo or clinical settings.
To investigate whether rosmarinic acid protects cardiomyocytes from inflammatory damage through miRNAs, high-throughput sequencing and bioinformatics analysis were performed to identify TNF-α-induced inflammatory damage in cardiomyocytes and miRNAs differentially expressed in TNF-α-induced inflammatory injury in cardiomyocytes, and the bioinformatics analysis shown that the expression levels of 10 miRNAs were significantly up-regulated, and the expression levels of 6 miRNAs were significantly down-regulated. Among them, the expression level of miR-344a-3p was significantly up-regulated in the experimental group, while the expression level of miR-449c-5p was significantly down-regulated in experimental group of cells. The target genes of miR-344a-3p and miR-449c-5p were CCR1 and ATP2B4 respectively. The luciferase reporter system showed that luciferase activity in the WT-CCR1+miR-344a-3p mimic group was significantly decreased, and the expression of CCR1 was significantly decreased at mRNA and protein level after miR-344a-3p was transfected into H9C2 cells, indicating that TNF-α-induced inflammatory injury in cardiomyocytes, rosmarinic acid may up-regulate the expression of miR-344a-3p, thereby inhibiting the expression of CCR1 and ultimately protecting the cardiomyocytes from inflammatory damage. Thus, we thought that CCR1 might be a new therapeutic target for cardiomyocyte injury.
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Zhang et al. (2024) studied Cardiomyocyte injury. Rosmarinic acid vs. TNF-α alone (250 ng/mL) was evaluated on Cell viability and apoptosis (p=<0.05). Rosmarinic acid protects H9c2 cardiomyocytes from TNF-α-induced inflammatory injury by up-regulating miR-344a-3p and subsequently inhibiting CCR1 expression.
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