Keap1Nrf2启动子区甲基化及其对Nrf2下游抗氧化基因转录调控在燃煤型砷中毒的作用.pdfVIP

Keap1Nrf2启动子区甲基化及其对Nrf2下游抗氧化基因转录调控在燃煤型砷中毒的作用.pdf

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Keap1Nrf2启动子区甲基化及其对Nrf2下游抗氧化基因转录调控在燃煤型砷中毒的作用

data.Result:1.Methylation status of Keap:①the size of positive PCR products is 132 bp;②The Keap1 gene methylation rate of arsenic exposure observation object is 22.7% (47/207).Methylation positive rate of normal control group was 0.016 (1/64), exposure group is significantly higher than normal control group (P 0.05).③Methylation positive rate of healthy group in endemic area was 4.3% (2/46); Mild arsenic poisoning group methylation positive rate was 15.3% (7/46); Moderate arsenic poisoning methylation positive rate was 28.3% (17/60); High levels of arsenic poisoning group methylation positive rate was 38.2% (21/55). Keap1 methylation positive rate of arsenic exposure group was obviously higher than that of normal control group; And with the degree of arsenic poisoning, methylation positive rate in exposed group gradually increased trend.2.Methylation status of Nrf2:①the size of positive PCR products is 148 bp;②Exposed group methylation positive rate was 1.9% (4/207), normal control group methylation positive rate of 0 (0/64), the normal control of arsenic exposure observed Nrf2 gene methylation rate there was no statistically significant difference.③The methylation positive rate of healthy group in endemic area was 0 (0/46); Mild arsenic poisoning group methylation positive rate was 2.2% (1/46); Moderate arsenic poisoning methylation positive rate was 3.3% (2/60); High levels of arsenic poisoning group methylation positive rate was 1.8% (1/55).After statistics analysis: normal controls with ward patients and patients with light, medium and high levels of arsenic poisoning incidence of Nrf2 gene methylation differences had no statistical significance.3.the mRNA expression of GCLC and GCLM.Conclusion: the high arsenic exposure may cause the Keap1 gene promoter region methylation, Keap1 methylation may be inhibit one of the main reasons for its mRNA expression. Arsenic can cut Keap1 and raised by Nrf2 expression, regulate th

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