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The aim of the present study was to measure the expression of microRNA (miR)-146a in liver tissues, peripheral blood mononuclear cells (PMBC) and serum from patients with Hepatitis B and either liver fibrosis or cirrhosis, as well as to determine the regulatory mechanism of miR-146a. A total of 36 patients with Hepatitis B and liver fibrosis and 25 patients with hepatitis B and liver cirrhosis admitted to Linyi People's Hospital (Shandong, China) between June 2012 and February 2016 were included in the present study. Reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of miR-146a and interleukin (IL)-6 mRNA in the liver tissue, PBMCs and serum. Western blotting was used to assess the expression of IL-6 in liver tissues and PBMCs. An enzyme-linked immunosorbent assay was conducted to measure IL-6 levels in serum. To identify the direct interaction between IL-6 and miR-146a, a dual luciferase reporter assay was performed. IL-6 mRNA expression in liver tissues, PBMCs and serum from patients with liver cirrhosis was significantly higher than that from patients with liver fibrosis (P<0.05). Furthermore, IL-6 expression in liver tissues and PBMCs from patients with liver cirrhosis was enhanced and levels of IL-6 protein in the serum of patients with liver cirrhosis were significantly elevated compared with patients with liver fibrosis (P<0.05). By contrast, levels of miR-146a in liver tissues, PBMCs and serum from patients with liver cirrhosis were significantly downregulated (P<0.05) compared with patients with liver fibrosis. miR-146a regulated the expression of IL-6 by binding to its 3'-untranslated region. Thus, in the transformation from liver fibrosis to cirrhosis, the upregulation of IL-6 in liver tissues, PBMCs and serum may be associated with the downregulation of miR-146a. miR-146a directly targets IL-6, which may regulate the occurrence and immune responses of Hepatitis B.
RESUMO
BACKGROUND: Esophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This study investigated the etiological relationship between HPV infection and the occurrence of esophageal carcinoma at Tangshan City of the Hebei province in China. METHODS: 189 samples of esophageal carcinoma patients were collected. DNA and RNA were isolated from samples, HPV DNA was detected by polymerase chain reaction (PCR) using My09/11 for HPV L1, and HPV16 was determined using type-specific primer sets for HPV16 E6. The HPV16 integration site was verified by amplification of papillomavirus oncogene transcripts, and HPV16 oncogene transcript products were ligated to the pMD-18 T vector and sequenced to confirm the physical location of HPV16 integration. RESULTS: 168 HPV-positive samples were detected in 189 samples, and among them 76 specimens were HPV16 positive. Approximately 600 bp of the HPV16 oncogene transcript were detected in nine esophageal cancer samples. Sequence analysis revealed that HPV16 E7 integrated into human chromosome 2 in three samples, into human chromosome 5 in one sample, into human chromosome 6 in one sample, into human chromosome 8 in two samples, and into human chromosome 17 in two samples. The results verified that the integrated HPV16 E7 in five samples harbored one mutation of viral DNA compared with the HPV16 sequence provided in GenBank (K02718). CONCLUSIONS: The high prevalence of HPV16 suggests that HPV16 may play an etiological role in the development of esophageal cancer. The integration of HPV16 into host cell chromosomes suggests that persistent HPV infection is key for esophageal epithelial cell malignant transformation and carcinogenesis.
RESUMO
BACKGROUND The aim of this study was to investigate the value of plasma intermedin (IMD) in assessing severity and treatment efficacy of septic shock. MATERIAL AND METHODS Healthy male Sprague-Dawley (SD) rats were chosen and divided into a normal control group (n=15) and a shock model group (n=27) that received intravenous injection of lipopolysaccharide (LPS). Then, 3 specimens were taken from each group. The shock model group rats were divided into an LPS group and a treatment group with 12 rats each. The treatment group received intravenous injection of compound sodium lactate solution. Plasma IMD and IMD1-47 mRNA expressions were compared and analyzed. RESULTS Mean arterial pressure (MAP) was lower while white blood cell count and TNF-α were higher in the shock model group than in the normal control group (P<0.05). After 10 h and 20 h, the treatment group had lower plasma IMD and IMD1-47 mRNA expressions compared with the LPS group (P<0.05). Plasma IMD and IMD1-47 mRNA expressions in the LPS group after 20 h were significantly higher than after 10 h (P<0.05). IMD was positively correlated with interleukins (IL-3, IL-6, and IL-8), white blood cell count, and body temperature (all P<0.05), but were negatively correlated with systolic pressure (r=-0.8474, P=0.0040). CONCLUSIONS Plasma IMD level can effectively reflect the severity of septic shock and can be used as an important indicator of septic shock treatment effectiveness.
