ABSTRACT
OBJECTIVE: Arid2-IR is a long non-coding RNA (lncRNA) that promotes renal injury, while its role in lipopolysaccharides (LPS)-induced acute lung injury (ALI) is unknown. Our preliminary sequencing analysis revealed an inverse correlation of Arid2-IR and miR-132-3p, which is known to suppress LPS-induced ALI. Therefore, Arid2-IR and miR-132-3p may interact with each other to participate in LPS-induced ALI in pneumonia. This study aimed to investigate the interaction between Arid2-IR and miR-132-3p in ALI induced by pneumonia. MATERIALS AND METHODS: Plasma samples were obtained from patients with pneumonia (n = 98) and healthy controls (n = 98) to detect the expression of circulating Arid2-IR and miR-132-3p. The correlation between them was analyzed using Pearson's correlation coefficient. The crosstalk between them in human bronchial epithelial cells (HBEpC) was analyzed through overexpression assay. MSP was applied to determine the methylation of the miR-132-3p gene. Cell viability was evaluated by 2,5-diphenyl-2H-tetrazolium bromide assay. RESULTS: Arid2-IR was highly upregulated in pneumonia group, while the expression levels of miR-132-3p decreased in pneumonia group compared to that in the controls. Arid2-IR and miR-132-3p were inversely correlated across patient samples. Overexpression of Arid2-IR decreased the expression levels of miR-132-3p in HBEpCs and increased the methylation of miR-132-3p gene. Arid2-IR suppressed the role of miR-132-3p in increasing the viability of HBEpCs induced by LPS. DISCUSSION AND CONCLUSION: Arid2-IR is upregulated in pneumonia and may downregulate miR-132-3p by increasing its methylation to decrease cell viability, thereby promoting LPS-induced ALI in pneumonia.
Subject(s)
Acute Lung Injury , MicroRNAs , Pneumonia , RNA, Long Noncoding , Humans , Acute Lung Injury/genetics , Acute Lung Injury/metabolism , Apoptosis , Lipopolysaccharides/toxicity , Methylation , MicroRNAs/genetics , Pneumonia/genetics , RNA, Long Noncoding/genetics , Transcription Factors/genetics , Transcription Factors/metabolismABSTRACT
There was an outbreak of Dengue fever on September 5, 2019, in Hainan Province, which has not been endemic for 28 years. We aim to describe the clinical and epidemiological features of the 2019 outbreak in Hainan Province and identify the cause. All type 1 Dengue fever cases that occurred in this outbreak of Hainan exhibited mild clinical symptoms. The epidemiological investigations indicate that the outbreak might originate from workers in the Xiuying area, Haikou City, form a concentrated outbreak, and then spread out. Bayesian phylogenies results and epidemiological data were used to infer a likely series of events for the dengue virus's potential spread and trace the possible sources. The strains' sequences were close to a sequence from the nearby Guangdong province, supporting the hypothesis that the dengue virus was imported from Guangdong province and then spread across Hainan province. Furthermore, it is interesting that two other strains didn't group with this cluster, suggesting that additional introduction pathways might exist. The study indicated that the dengue fever epidemic presented two important modes in Hainan. Firstly, epidemics prevalence was caused by imported cases, and then endogenous epidemics broke out in the natural epidemic focus.
ABSTRACT
The aim of this study was to investigate the protective effect of chlorogenic acid (CA) on liver injury caused by bile duct ligation (BDL), as well as the potential mechanism. Permanent bile duct ligation induced liver injury was evaluated by liver index, liver function and pathological observation. Oral administration of CA for 3 weeks markedly attenuated liver swelling and fibrosis. Blood biochemistry results revealed that CA decreased alanine transaminase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, direct bilirubin and total bile acid. PCR analysis indicated that collagen I, collagen III, transforming growth factor and vascular endothelial growth factor mRNA were increased markedly by BDL treatment but these increases were suppressed by CA. Additionally, CA effectively alleviated the expression of α-smooth muscle actin induced by BDL. Taken together, our data indicate that CA can efficiently inhibit BDL-induced liver injury in rats, which is a candidate drug for preventing liver injury against cholestasis.