Sex Hormones Enhance Gingival Inflammation without Affecting IL-1ß and TNF-α in Periodontally Healthy Women during Pregnancy.

Hormones (progesterone and estradiol) change greatly during pregnancy; however, the mechanism of hormonal changes on gingival inflammation is still unclear. This study is to evaluate the effects of hormonal changes during pregnancy on gingival inflammation and interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in gingival crevicular fluid (GCF). 30 periodontally healthy pregnant women were evaluated in the first, second, and third trimesters. 20 periodontally healthy nonpregnant women were evaluated twice (once per subsequent month). Clinical parameters including probing pocket depth (PPD), bleeding index (BI), gingival index (GI), clinical attachment level (CAL), and plaque index (PLI) were recorded. GCF levels of IL-1ß and TNF-α and serum levels of progesterone and estradiol were measured. From the data, despite low PLI, BI and GI increased significantly during pregnancy; however, no significant changes in PLI, CAL, IL-1ß, or TNF-α GCF levels were observed. Although IL-1ß, not TNF-α, was higher in pregnant group than in nonpregnant group, they showed no correlation with serum hormone levels during pregnancy. GI and BI showed significant positive correlation with serum hormone levels during pregnancy. This study suggests that sex hormone increase during pregnancy might have an effect on inflammatory status of gingiva, independent of IL-1ß and TNF-α in GCF.

Metabolomic profiling of serum and tongue coating of pregnant women with intrahepatic cholestasis in pregnancy.

Intrahepatic cholestasis of pregnancy (ICP) is associated with an increased risk of cesarean section and adverse fetal outcomes. Currently, ICP diagnosis depends largely on serum levels of bile acids and lacks sensitivity and specificity for accurate diagnosis. Tongue diagnosis is an important diagnostic tool in traditional Chinese medicine (TCM) and is used in our clinic as complementary treatment and personalized medicine for ICP. However, the molecular basis of the manifestation of greasy white tongue coatings in ICP remains unknown. In this study, we performed untargeted metabolomic profiling of the serum, tongue coating, and saliva of 66 pregnant women, including 22 with ICP. The metabolomic profiles of the serum and tongue coatings showed marked differences between the two clinical groups. Forty-six differentially abundant metabolites were identified, and their relative concentrations correlated with total bile acid levels. These differential metabolites included bile acids, lipids, microbiota- and diet-related metabolites, and exposomes. Conventional biochemical markers, including serum aminotransferases and bilirubin, were not significantly increased in the ICP group, whereas the total cholesterol and triglyceride levels were significantly increased as early as the first trimester. Our data provide insights into the pathophysiology of ICP and implicate the gut-liver axis and environmental exposure. Tongue coating has the potential to be a non-invasive diagnostic approach. Further studies are required to validate the clinical utility of these findings.

MicroRNA­532­5p regulates oxidative stress and insulin secretion damage in high glucose­induced pancreatic ß cells by downregulating the expression levels of CCND1.

Diabetes mellitus is a metabolic disorder caused by insufficient insulin secretion. The expression of microRNA (miR)­532­5P is downregulated in diabetes, but its specific role in diabetes has not yet been elucidated. The present study aimed to investigate the specific mechanism underlying the effects of miR­532­5p on diabetes. Cell viability was determined using an MTT assay. The expression levels of miR­532­5P, cyclin D1 (CCND1), Insulin1 and Insulin2 were detected using reverse transcription­quantitative PCR. The expression of miR­532­5p and CCND1 were overexpressed in cells by cell transfection. ELISA was used to detect insulin secretion. 2',7'­dichlorodihydrofluorescein diacetate was used to quantify reactive oxygen species levels in cells. Apoptosis was detected using a TUNEL assay. Western blotting was performed to detect the expression of apoptosis­related proteins, CCND1 and p53. A dual­luciferase reporter assay was conducted, and verified the targeted binding of miR­532­5p and CCND1. The expression of miR­532­5p was downregulated in high glucose (HG)­induced MIN6 cells. Overexpression of miR­532­5p could improve the HG­induced decline in insulin secretion and inhibit HG­induced oxidative stress and apoptosis in cells. miR­532­5p can target and regulate the expression of CCND1. Overexpression of miR­532­5p downregulated HG­induced cell insulin secretion, oxidative stress and apoptosis by downregulating CCND1, which is involved in regulating the expression of p53. To conclude, miR­532­5p regulated oxidative stress and insulin secretion damage in HG­induced pancreatic ß cells by downregulating the expression of CCND1, which is involved in the upregulation of the expression of p53.