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Objective To explore the effect of plasma glucose management on placental ultrastructure in pregnant women with gestational diabetes mellitus, so as to provide scientific evidence for optimizing the management during pregnancy. Methods Pregnant women with gestational diabetes mellitus were divided into satisfied glucose control group and dissatisfied glucose control group; meanwhile, normal pregnant women were taken as controls. All the participants received antenatal care until delivery in the First People's Hospital of Nantong from January 2013 to December 2014. Plasma glucose levels of the three groups were examined and the placental ultrastructure was observed by transmission electron microscopy. Results (1) Finally 57 pregnant women were included in this study. There were 32 pregnant women with gestational diabetes mellitus (56.14%, 32/57) and 25 with normal glucose (43.86%, 25/57). The proportions of pregnant women with satisfied and dissatisfied glucose control were 35.09% (20/57) and 21.05% (12/57), respectively. (2) There were no significant differences in the age, gestational weeks of oral glucose tolerance test (OGTT), gestational weeks of labor, blood pressure or body mass index between the three groups (P>0.05). (3) After plasma glucose management, there was no significant difference in fasting blood glucose between the three groups (P=0.099). And no significant differences were found in 2 h postprandial blood glucose, nocturnal blood glucose, or glycosylated hemoglobin between satisfied glucose control group and healthy control group (P>0.05). The 2 h postprandial blood glucose, nocturnal blood glucose and glycosylated hemoglobin in the dissatisfied glucose control group were significantly higher than those in the other two groups (P0.05). The proportions of participants with placental ultrastructure changes in the dissatisfied glucose control group were significantly different from those of the other two groups (P<0.01).Conclusion Hyperglycemia is a risk factor for placental ultrastructure change in pregnant women with gestational diabetes mellitus; the management of plasma glucose should be strengthened during pregnancy, so as to avoid the placental ultrastructure change and to reduce adverse pregnancy.
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<p><b>OBJECTIVE</b>To determine the role of IGF-1/PI3K pathway and investigate the molecular mechanism of Fuzhenghuayu (FZHY) therapy in a spontaneous recovery rat model of liver fibrosis.</p><p><b>METHODS</b>The liver fibrosis model was induced in male Wistar rats by administering 8 weeks of twice weekly CCL4 intraperitoneal injections without (untreated model) or with once daily FZHY (treated model). Normal, untreated rats served as the control group. At weeks 4, 6 and 8 (fibrosis) and 10, 12 and 14 (spontaneous recovery) after modeling initiation, effects on protein (a-SMA, IGF-1, PI3K) and mRNA (IGF-1, PI3K) expression levels were evaluated by immunohistochemistry and RT-PCR, respectively. Serum markers of liver function (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)) and liver cell damage (alkaline hydrolysis, HYP) were measured. Histology was performed to assess the degree of inflammation and fibrosis (Ishak scoring system).</p><p><b>RESULTS</b>In the untreated model group, progression of liver fibrosis (weeks 4, 6 and 8) was accompanied by gradual increases in inflammation, necrosis, serum ALT and AST, and hepatic expression of a-SMA protein and IGF-1 and PI3K protein and mRNA; however, during the spontaneous recovery period (weeks 10, 12 and 14) the IGF-1 and PI3K protein and mRNA levels rapidly decreased and the HYP level, Ishak score, and a-SMA hepatic expression also decreased. The FZHY-treated model group showed significantly lower fibrosis-related up-regulation of IGF-1 and PI3K protein and mRNA expression, HYP level, Ishak score, and a-SMA hepatic expression at each time point (vs. untreated model group).</p><p><b>CONCLUSION</b>The IGF-1/PI3K pathway may contribute to progression of liver fibrosis. The mechanism by which FZHY prevents liver fibrosis in a rat model may involve blocking of the IGF/PI3K pathway and inhibiting HSC activation.</p>