[Dihydromyricetin mediates epithelial mesenchymal transformation and regulates the proliferation and apoptosis of esophageal squamous cell carcinoma cells].

Objective: To study the effects of dihydromyricetin (DMY) on the proliferation, apoptosis and epithelial mesenchymal transition (EMT) of esophageal squamous cell carcinoma (ESCC) cell KYSE150 and KYSE410. Methods: KYSE150 and KYSE410 cells were treated with different concentrations of DMY (0, 25, 50, 100, 150, 200 µmol/L) for 24 hours. The median inhibition concentration (IC50) values of KYSE150 and KYSE410 were detected by cell counting kit-8 (CCK-8) method. Then 0.5‰ dimethyl sulfoxide (DMSO) was used as control group, dihydromyricetin (DMY), dihydromyricetin and transforming growth factor-ß1 (DMY+ TGF-ß1), transforming growth factor-ß1 (TGF-ß1) were used as experimental group. Cell proliferation and apoptosis rates were measured by clonal formation and flow cytometry. Transwell invasion and wound healing assay were used to detect cell invasion and migration. The protein expression levels of Caspase-3, Caspase-9, Bcl-2, Bax, Smad2/3, phosphorylation-Smad2/3 (p-Smad2/3) and Vimentin were detected by western blot. Results: The IC50 values of DMY on KYSE410 and KYSE150 cells were 100.51 and 101.27 µmol/L. The clone formation numbers of KYSE150 and KYSE410 in DMY group [(0.53±0.03) and (0.31±0.03)] were lower than those in DMSO group [(1.00±0.10) and (1.00±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in DMY group [(1.84±0.22)% and (2.80±0.07)%] were higher than those in DMSO group [(1.00±0.18)% and (1.00±0.07)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in DMY group [(0.42±0.03) and (0.29±0.05)] were lower than those in DMSO group [(1.00±0.08) and (1.00±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in DMY group [(0.65±0.14)% and (0.40±0.17)%] were lower than those in DMSO group [(1.00±0.10)% and (1.00±0.08)%, P<0.05]. The clone formation numbers of KYSE150 and KYSE410 in TGF-ß1 group [(1.01±0.08) and (0.99±0.25)] were higher than those in DMY+ TGF-ß1 group [(0.73±0.10) and (0.58±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in TGF-ß1 group [(0.81±0.14)% and (1.18±0.10)%] were lower than those in DMY+ TGF-ß1 group [(1.38±0.22)% and (1.85±0.04)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in TGF-ß1 group [(1.19±0.11) and (1.39±0.11)] were higher than those in DMY+ TGF-ß1 group [(0.93±0.09) and (0.93±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in TGF-ß1 group [(1.87±0.19)% and (1.32±0.04)%] were higher than those in DMY+ TGF-ß1 group [(0.86±0.16)% and (0.77±0.12)%, P<0.05]. The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY group were higher than those in DMSO group, while the protein expression level of Bcl-2 was lower than that in DMSO group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in DMY group were lower than those in DMSO group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in TGF-ß1 group were lower than those in DMY+ TGF-ß1 group, and the protein expression level of Bcl-2 was higher than that in DMY+ TGF-ß1 group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY+ TGF-ß1 group were lower than those in DMY group, and the protein expression level of Bcl-2 was higher than that in DMY group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in TGF-ß1 group were higher than those in DMY+ TGF-ß1 group (P<0.05). Conclusion: DMY can inhibit the proliferation and EMT of ESCC mediated by TGF-ß1 and promote cell apoptosis.

[Identifying immunization strategy for preventing mother-to-child transmission of hepatitis B virus].

In 2016, the World Health Assembly endorsed the Global Health Sector Strategy on viral hepatitis, with aim to eliminate viral hepatitis as a public health threat by 2030, which may reduce the number of new cases of chronic hepatitis B by 90% (0.1% HBsAg prevalence among children) and mortality rate by 65%. In order to achieve this goal, blocking mother-to-child transmission of hepatitis B virus (HBV) is of paramount importance, especially in underdeveloped areas with high prevalence of HBV. In this paper, we discussed the status of chronic HBV infection and its serological and virological characteristics in women of childbearing age in China as well as the optimal dose of immunoglobulin in the combined passive-active immunoprophylaxis in infants born to HBsAg-positive mothers. In addition, the strategies for preventing mother-to-child transmission of HBV in terms of post-immunization testing, increased-dose vaccination (certainty/uncertainty) and follow-up of these infants.

[Correlation between serum HBV DNA level and HBsAg titer in HBeAg-positive pregnant women and impact of genomic variability of hepatitis B virus pre S/S regions on their correlations].

Objective: To analyze the correlation between serum HBV DNA level and HBsAg titer in hepatitis B e antigen positive pregnant women without antiviral therapy, and investigate the impact of genomic variability of preS/S regions on their correlations. Methods: Prenatal serum samples from 882 pregnant women with chronic HBV infection who were positive for HBsAg, HBeAg and HBV DNA and were not on antiviral therapy were included in the analysis. The Abbott i2000 and m2000 systems were used to qualitatively or quantitatively detect HBsAg, HBeAg and HBV DNA levels, respectively. HBV genotyping was performed using a type-specific primer nested polymerase chain reaction (nPCR). In addition, serum samples of pregnant women with HBV DNA levels correlated with HBsAg titer and HBV DNA levels higher than HBsAg titers were used to perform preS/S region amplification by nPCR method. PCR products were directly sequenced and mutation sites were analyzed by MEGA6.0 stasticial software. Mann-Whitney U test was used for the measurement data, and 2-test test for count data. Correlations between variables were analyzed using Spearman's rank correlation. Results: Serum HBsAg titer of HBeAg-positive pregnant women was positively correlated with HBV DNA level (r = 0.754, P < 0.01). Compared with the control group, mutation sites A60V (100% vs. 15.38%, χ(2) = 7.61, P < 0.01), V90A (100% vs. 30.77%, χ(2) = 4.43, P < 0.05) and I161T of HBV preS/S region (80.00% vs. 0, χ(2) = 9.14, P < 0.01) showed a significant decrease in HBsAg titer. Conclusion: Serum HBV DNA levels were positively correlated with HBsAg titer in HBeAg-positive pregnant women. Therefore, serum HBsAg titer may be used as a surrogate marker of serum HBV DNA. Single or multiple amino acid mutations sites A60V, V90A, and I161T in preS/S region may be one of the reasons that lead to a significant drop in HBsAg titer and affect its correlation with HBV DNA levels.