Effects of Helicobacter pylori Infection on the Prognosis of Chronic Atrophic Gastritis by Inducing the Macrophage Polarization.

Background: Recently, the effects of Helicobacter pylori (H. pylori) infection on the prognosis of chronic atrophic gastritis (CAG) are still unclear. The aim of our study was to discuss the role of H. pylori infection on the prognosis of CAG by inducing the M1/M2 macrophage polarization. Methods: A total of 180 subjects as control (group 1), CAG patients without H. pylori infection (group 2) and H. pylori-associated CAG patients (group 3) were respectively recruited for this cross-sectional investigation in Daqing Oilfield General Hospital from May 2019 to July 2020. Their serum samples were collected to determine the concentrations of pro-inflammatory and anti-inflammatory cytokines. Meanwhile, the gastric mucosa was excised to determine the related gene expressions on the M1/M2 macrophage polarization. Then the prognosis of CAG was evaluated according to the status of clinical manifestations and endoscopic examination after the follow-up. Results: Notably, it was proved that compared with the control group, the expressions and concentrations of pro-inflammatory cytokines (M1 macrophage: inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin-6 (IL-6)) were significantly higher, while the anti-inflammatory cytokines (M2 macrophage: arginase-1 (Arg-1), IL-4 and IL-10) were apparently reduced in the group 2 and group 3 (P < 0.05). Moreover, more days were needed for the prognosis of CAG in group 3 than those in group 2, which was accompanied by higher expressions of pro-inflammatory and lower anti-inflammatory cytokines at the baseline (P < 0.05). Furthermore, negative correlations were shown between the concentrations of iNOS, TNF-α, IFN-γ and IL-6, and the prognosis of CAG (P < 0.05), while positive correlations were observed between the contents of IL-4 and IL-10, and prognosis of CAG (P < 0.05). Conclusion: These above results indicated that H. pylori infection-induced disorders of M1/M2 macrophage polarization could affect the prognosis of CAG.

Corticosteroid Therapy Might be Associated with the Development of Coronary Aneurysm in Children with Kawasaki Disease.

BACKGROUND: Coronary artery lesions (CALs) are known to be the main complication in children with Kawasaki disease (KD). Instead of intravenous immunoglobulin (IVIG), corticosteroid therapy has been accepted to be used for children with KD who are unresponsive to IVIG. This study aimed to evaluate risk factors for CALs in children with KD. METHODS: We retrospectively reviewed the clinical records of 2331 children with KD from January 2005 to December 2014. To identify the independent risk factors for CALs, multivariable logistic regression models were constructed using significant variables identified from univariate logistic regression analysis. RESULTS: The incidence of CALs was 36.0% (840 of 2331), including 625 (26.8%) coronary artery dilations and 215 (9.2%) coronary artery aneurysms (CAAs). Multivariable logistic regression analysis identified that male, incomplete KD, longer fever duration, and C-reactive protein (CRP) >100 mg/L were independent risk factors for coronary artery dilatations. On the other hand, male, incomplete KD, longer fever duration, prolonged days of illness at the initial treatment, corticosteroid therapy, sodium ≤133 mmol/L, and albumin <35 g/L were the independent risk factors for CAAs. In addition, corticosteroid therapy, prolonged days of illness at the initial treatment, and albumin <35 g/L were the independent risk factors for giant CAAs. CONCLUSIONS: CALs might be associated with male sex, incomplete KD, longer fever duration, prolonged days of illness at the initial treatment, albumin <35 g/L, sodium ≤133 mmol/L, CRP >100 mg/L, and corticosteroid therapy. Corticosteroid therapy was an independent risk factor for CAAs and giant CAAs. Thus, corticosteroids should be used with caution in the treatment of KD with the risk for CALs.

Effects of gene silencing of CypB on gastric cancer cells.

OBJECTIVE: To determine the effect of gene silencing of cyclophilin B (CypB) on growth and proliferation of gastric cancer cells. METHODS: CypB siRNA lentivirus (LV-CypB-si) and control lentivirus (LV-si-con) were produced. CypB expression in gastric cancer cell lines was detected by Western blot. BGC823 and SGC7901 cells were chosen to be infected with LV-si-con and LV-CypB-si, and stable transfectants were isolated. The cell groups transfected with LV-CypB-siRNA, LV-siRNA-con and transfected no carrier were served as the experimental group, the implicit control group and the blank control group respectively. MTT and colony formation assays were used to examine the effect of CypB on the cell growth and proliferation in vitro. Cell cycle was analyzed with flow cytometry. The expression of VEGFR of BGC823-si and SGC7901-si was detected by Western blot. RESULTS: Gene silencing of CypB can inhibit gastric cancer cell growth, proliferation, cell cycle progress and tumorigenesis. CypB expression level was obviously higher in SGC7901 and BGC823 than MKN28 and GES. These two cell lines were infected with LV-si-con and LV-CypB-si respectively. MTT and cloney formation assays showed a significantly decreased rate of cell proliferation from the forth day or the fifth day in cells transfected with LV-CypB-si (P<0.05). Down-regulation of CypB resulted in slightly decreased percentage of S phase and increased percentage of G1 (P<0.05). These findings indicated that CypB could promote the G1-S transition of gastric cancer cell. In addition, the expression of VEGF of BGC823 and SGC7901 transfected with CypB siRNA was reduced in comparison with the implicit control group and the blank control group. CONCLUSIONS: Gene silencing of CypB decreases gastric cancer cells proliferation and in vivo tumorigenesis. These findings indiccate CypB could be a potential biomarker and therapeutic target for gastric cancer.

Effects and mechanism of miR-214 on hepatocellular carcinoma.

OBJECTIVE: To explore the role of miR-214 in the progression of hepatocellular carcinoma (HCC) and its inhibitory mechanisms in depressing the signaling pathway of ß-catenin, this study was conducted. METHODS: We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2. Differences between the two cell lines were compared in cell growth, proliferation, colony forming ability and cell cycles. RT-PCR method was applied for the quantification of ß-catenin mRNA expression. Western-blot method was applied for the determination of the protein level of ß-catenin and their downstream targets (ie. Cyclin D1, c-Myc and TCF-1). The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression. RESULTS: In comparison with negative (Lv-control-HepG2) and blank (HepG2) control, a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48∼72h of cell culture experiments (P<0.05). The miR-214 treatment resulted in a colony forming efficiency of (23.28±3.26)%, which was significantly lower than that of negative control [(51.31±3.97)%] (P<0.05). According to FCM results, the experimental group, compared with control, showed a higher proportion of cells in G0/G1 phase [(70.32±3.12)%] but a lower proportion in S phase [(18.42±2.90)%] (P<0.05). The MTT assay demonstrated a significant inhibition of the proliferation and ß-catenin expression of HCC cells compared with control (P<0.05), while no significant difference was observed after HCC cells being transfected with ß-catenin overexpression plasmid (P>0.05). By comparing to the RT-PCR and Western-blot results of control, the miR-214 treatment led to a slightly decrease in the ß-catenin mRNA expression (P>0.05), but an extremely inhibition in the protein level of ß-catenin and its downstream targets Cyclin D1, c-Myc, and TCF-1 (P<0.05). CONCLUSIONS: miR-214 functions as a suppressor during the progression of HCC, and its inhibitory role was achieved by down-regulating ß-catenin signaling pathway.