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The expression of CLIC1 might be closely related to the carcinogenesis, clinical biological behaviors, and prognosis of pancreatic ductal adenocarcinomas.

Pseudorabies virus (PRV) infection leads to severe inflammatory responses and tissue damage, and many natural herbs exhibit protective effects against viral infection by modulating the inflammatory response. An ethyl acetate fraction of flavonoids from Polygonum hydropiper L. (FEA) was prepared through ethanol extraction and ethyl acetate fractional extraction. An inflammatory model was established in RAW264.7 cells with PRV infection to evaluate the anti-inflammatory activity of FEA by measuring cell viability, nitric oxide (NO) production, reactive oxygen species (ROS) release, and mRNA expression of inflammatory factors, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Its functional mechanism was investigated by analyzing the phosphorylation and nuclear translocation of key proteins in the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. Our findings indicate that PRV induced inflammatory responses in RAW264.7 cells, and the responses were similar to that in lipopolysaccharide (LPS)-stimulated cells. FEA significantly suppressed NO synthesis and down-regulated both expression and secretion of COX-2, iNOS, and inflammatory cytokines (P < 0.05 or P < 0.01). FEA also reduced NF-κB p65 translocation into the nucleus and decreased MAPK phosphorylation, indicating that the NF-κB/MAPK signaling pathway may be closely related to the inflammatory response during viral infection. The findings suggested the potential pharmaceutical application of FEA as a natural product that can treat viral infections due to its ability to mitigate inflammatory responses.

Objective. To compare the merits and demerits of PEG-IFNα-2a and PEG-IFNα-2b for the treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB). Methods. Clinical files from eighty-four CHB patients admitted to the Second Hospital of Shanxi Medical University between January 2018 and January 2019 were retrospectively analyzed and assigned to two groups: group 2a treated with PEG-IFNα-2a and group 2b treated with PEG-IFNα-2b. The clinical efficacy was compared between the above two arms, and the liver function (ALT, AST, HA, LN, and IV-C), HBV-DNA, HBsAg, HBeAg, and inflammatory factors (IFs, IL-1β, IL-6, IL-8, and TNF-α) were tested at 12 weeks (T1), 24 weeks (T2), and 48 weeks (T3). The alterations of hemodynamics (SBP, DBP, MAP, and CVP), cardiac function (LVEF and BNP), and the incidence of adverse reactions (ARs) during treatment were recorded. Finally, the patients were followed up for 2 years to investigate the quality of life (QOL) as well as the positive seroconversion rate of HBsAg and HBeAg. Results. The overall response rate was similar in the two arms ( P > 0.05 ). After treatment, the liver function, HBV-DNA, HBsAg, HBeAg, IFs, hemodynamics, and cardiac function were enormously improved ( P < 0.05 ), with faster improvement in group 2b compared with group 2a ( P < 0.05 ). The investigation of ARs identified notably lower incidence rates of alopecia, thrombocytopenia, and granulocytopenia in group 2a as compared to group 2b ( P < 0.05 ). The prognostic follow-up results revealed no distinct difference in the QOL score and the positive seroconversion rate of HBsAg and HBeAg ( P > 0.05 ); however, the quantitative results of HBV-DNA, HBsAg, and HBeAg in group 2b were lower than those in group 2a ( P < 0.05 ). Conclusions. Both PEG-IFNα-2a and PEG-IFNα-2b have excellent and stable therapeutic effects on HBeAg-positive CHB, among which PEG-IFNα-2b renders a faster treatment process but higher side effects, which can provide valuable references when choosing a treatment plan for CHB.

Abstract. The renin angiotensin system (RAS) plays a major role in liver fibrosis. A novel homologue of angiotensin converting enzyme, ACE2, was identified as a negative regulator of RAS as it degrades Ang II to Ang1-7. We investigated in vivo the expression of ACE2 in liver fibrosis. We evaluated the relationship between biochemical variables and liver tissue expression of ACE2, the correlation between a histological assessment of liver fibrosis and liver tissue expression of ACE2. Male SD rats were randomly divided into a CCL4 group which received injections of CCL4 and the control group which received injections of olive oil. Liver pathology was examined by H&E and Sirius red staining, and real-time PCR was performed to determine the gene expression levels of ACE2 and ACE. Real-time PCR analysis revealed that ACE2 mRNA was higher at the two-, four-, and six-week time points, respectively (p<0.01). Similarly, hepatic ACE mRNA was significantly increased after CCL4 injection. There was a significant correlation between ACE and ACE2 gene expression (r=0.750, P<0.001). ACE2 gene expression strongly correlated with ALT (r=0.669, P<0.0001) and AST levels (r=0.815, P<0.0001). There was a significant correlation between circulating ACE2 and histological scores of liver fibrosis. ACE2 and ACE gene expression correlated with the ISHAK score (r=0.850, P<0.001; r=0.806, P<0.001). There was a significant relationship between ACE2 gene expression and the degree of liver fibrosis. ACE2 plays a crucial role in liver fibrogenesis.

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Abstract. Hepatitis B virus (HBV) infection leads to the development of liver inflammation, causing morbidity and mortality. Multiple factors influence HBV progression, including genetic factors. Toll-like receptor (TLR)9 plays a key role in innate immunity, and mutations in the genes encoding this receptor have been associated with liver damage progression. Our study aimed to investigate one-tag single nucleotide polymorphisms (rs187084) representing the majority of common variations in TLR9 in a population-based study of Chinese patients. A total of 209 Chinese patients with HBV infection (130 with chronic hepatitis and 79 with liver cirrhosis) and 193 healthy individuals were studied. Our results showed that the frequencies of the C/C genotype and C allele were statistically higher in patients with HBV-related liver cirrhosis than in the healthy controls (26.6 vs. 15.5%; OR=1.97, 95% CI 1.05-3.71, ¯2=4.483, P=0.034/43.1 vs. 37.8%; OR=1.49, 95% CI 1.02-2.16, ¯2=4.323, P=0.038). No significant differences in the frequencies of alleles or genotypes were found between patients with chronic hepatitis B and the control subjects. In conclusion, this study is the first to show that small effects within TLR9 contribute towards the development of HBV, supporting the hypothesis that little is currently known regarding the contribution of genetic factors to HBV.

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