Myocardial ischemia/reperfusion (I/R) causes serious threats to human life. Naringenin, a polyphenolic compound naturally occurring in citrus fruit, has cardioprotective effects against myocardial I/R injury. Besides, miR-24-3p is also reported to have cardioprotective effects. We intended to explore whether the cardioprotective effects of naringenin relate to miR-24-3p and its underlying mechanism. In this study, we used an in vivo rat myocardial I/R model and an in vitro cardiomyocyte H9c2 hypoxia/reoxygenation (H/R) model. Myocardial injury was detected by hematoxylin-eosin staining and ELISA for creatine kinase (CK), malondialdehyde (MDA), and lactate dehydrogenase (LDH). miR-24-3p and cell death inducing p53 target 1 (Cdip1) mRNA expressions were examined by RT-PCR. We find that naringenin pretreatment significantly relieves myocardial I/R injury, reduces LDH, CD, and MDA levels, and increases miR-24-3p expression. Furthermore, miR-24-3p alleviates myocardial I/R injury partially through regulating Cdip1. Moreover, naringenin protects myocardial I/R injury partially by regulating miR-24-3p to inhibit Cdip1 expression. In conclusion, our data suggest naringenin protects myocardial I/R injury partially through miR-24-3p/Cdip1 axis.
Shoufen Yu,Xueyuan Yu,Junchang Liu,Muzhen Guan,Zhongheng Wang,Xiaosa Li
Background The blood–brain barrier (BBB) is essential for maintaining normal brain function and is involved in the progression of major depressive disorder (MDD). This study investigated the abnormal expression and regulatory role of miR-24-3p in neuronal injury and BBB dysfunction during MDD pathogenesis.Methods The expression of miR-24-3p was examined in serum samples from patients with MDD and from chronic unpredictable mild stress and lipopolysaccharide mouse models, as well as in hippocampal tissue from mice. A loss-of-function assay was conducted to explore the role of miR-24-3p in brain injury, assessing neuronal cell viability, apoptosis, inflammatory response, oxidative stress, and astrocyte activation. Exosomes were then isolated to evaluate the regulatory role and function of miR-24-3p in BBB dysfunction. Behavioural tests were performed to assess depressive-like behaviours in mice.Results miR-24-3p was significantly upregulated in MDD samples. Inhibiting miR-24-3p suppressed LPS-induced neuronal apoptosis and inflammation, while promoting the secretion of neurofunctional factors. Further analysis revealed that inhibiting exosomal miR-24-3p alleviated depressive-like behaviour in MDD model mice, reduced BBB permeability, and improved BBB function.Conclusion miR-24-3p inhibition attenuated neuronal damage, reduced astrocyte activation, and enhanced BBB stability through exosome-mediated regulation, thereby alleviating neurobehavioural abnormalities and the progression of MDD.
Sili Chen,Liqin Xiong,Xinlan Wu,Lu Chen,Junwei Zhang,Guanqing Jiang,Xin Li,Qiaoyuan Yang
We investigated the toxicity of benzo[ghi]perylene (BghiP), a prevalent polycyclic aromatic hydrocarbon (PAH). Transcriptome analysis of control and BghiP-exposed human bronchial epithelial cells (BEAS-2B) led to the identification of a novel chimeric RNA (chRNA), TVP23C-CDRT4, whose expression is significantly downregulated by BghiP in vitro and in vivo. Funcionally, overexpression of TVP23C-CDRT4 inhibited BghiP-induced cell proliferation and DNA damage, whereas its knockdown exacerbated these detrimental effects. Mechanistically, TVP23C-CDRT4 acts as a molecular decoy for miR-24-3p. Thus, BghiP-induced suppression of TVP23C-CDRT4 unveils a novel mechanism of PAH toxicity, highlighting its anti-proliferative and genome-protective roles relevant to the early stages of carcinogenesis.
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