ABSTRACT
Female Wistar rats were treated with orally administered soy isoflavones at concentrations of 0, 25, 50, or 100mg/kg body weight from weaning until sexual maturity (3 mo.), and ovarian steroidogenesis was evaluated. After soy isoflavones were administered, a significant (P<0.05) decrease (44%) in the serum estrodial levels of the high-dose (HD) group were observed. Cultured granulosa cells from the middle- (MD) and HD groups showed significantly (P<0.05) reduced (31%, 45%, respectively) in vitro estradiol secretion, and those from the HD group showed significantly (P<0.05) reduced progesterone (25%) secretion. Compared with the control group, the mRNA expression of the steroidogenic acute regulatory protein (Star), cytochromeP450 cholesterol side chain cleavage (Cyp11a1 and Cyp19a1), and hydroxysteroid dehydrogenase 3b (Hsd3b) genes also decreased. Real-time quantitative PCR and Western blotting revealed a significant (P<0.05) decrease in key transcription factor steroidogenic factor-1 (SF-1) expression in the HD group. The detection of DNA methylation using bisulfitesequencing PCR (BSP) suggested a significantly (P<0.05) increased total methylation rate in the proximal SF-1 promoter in the HD group. Further studies showed that treatment with soy isoflavones can significantly (P<0.05) increase the mRNA expression of DNA methyltransferase (DNMT) 1 and DNMT3a. This study proved that soy isoflavone administration from weaning until sexual maturity could inhibit ovarian steroidogenesis, suggesting that SF-1 might play an important role in this effect. In addition, DNA methylation might play a role in the downregulation of SF-1 gene expression induced by soy isoflavones.
Subject(s)
DNA Methylation/drug effects , Isoflavones/pharmacology , Steroidogenic Factor 1/metabolism , Weaning , Animals , Aromatase/genetics , Aromatase/metabolism , Cholesterol Side-Chain Cleavage Enzyme/genetics , Cholesterol Side-Chain Cleavage Enzyme/metabolism , DNA (Cytosine-5-)-Methyltransferase 1 , DNA (Cytosine-5-)-Methyltransferases/genetics , DNA (Cytosine-5-)-Methyltransferases/metabolism , DNA Methyltransferase 3A , Dose-Response Relationship, Drug , Down-Regulation , Estradiol/blood , Female , Ovary/drug effects , Ovary/metabolism , Phosphoproteins/genetics , Phosphoproteins/metabolism , Promoter Regions, Genetic , Rats , Rats, Wistar , Glycine max/chemistry , Steroidogenic Factor 1/genetics , Transcription Factors/genetics , Transcription Factors/metabolismABSTRACT
This study aims to evaluate the independent and joint effects of tea and milk consumption on oral cancer risk among non-smokers and non-drinkers (NS/ND). A hospital-based case-control study was performed in Fujian, China. 421 cases and frequency-matched 1398 controls were included without tobacco smoking and alcohol drinking habits. Unconditional logistic regression model was used to assess the relationship of tea and milk consumption with oral cancer risk. Tea and milk consumption were significantly associated with decreased risk of oral cancer, the adjusted odds ratios (aORs) were 0.73 (95% CI: 0.54-0.97) and 0.69 (95% CI: 0.55-0.88), respectively. According to subgroup analysis, the inverse associations between tea consumption and oral cancer risk were only observed among the elders (>60 years) and urban residents. While the protect effect of milk drinking was more obvious in males, normal body mass index population (18.5-23.9), urban residents and those age ≤ 60 years. Additionally, a significantly multiplicative interaction between tea and milk consumption was observed for oral cancer risk (P = 0.001). The present study is the first to simultaneously assess the association of tea consumption and milk drinking with oral cancer risk. The results suggest that tea and milk consumption are independent protective factors for oral cancer among NS/ND, with a joint effect between them.
Subject(s)
Milk/chemistry , Mouth Neoplasms/etiology , Tea/chemistry , Animals , Case-Control Studies , China , Female , Humans , Male , Middle Aged , Risk Factors , Surveys and QuestionnairesABSTRACT
This study investigated the effects of polysaccharides from Enteromorpha prolifera (PEP) on glucose metabolism in a rat model of diabetes mellitus (DM). PEP (0, 150, 300, and 600 mg/kg) was administered intragastrically to rats for four weeks. After treatment, fasting blood glucose (FBG) and insulin (INS) levels were measured, and the insulin sensitivity index (ISI) was calculated. The morphopathological changes in the pancreas were observed. Serum samples were collected to measure the oxidant-antioxidant status. The mRNA expression levels of glucokinase (GCK) and insulin receptor (InsR) in liver tissue and glucose transporter type 4 (GLUT-4) and adiponectin (APN) in adipose tissue were determined. Compared with the model group, the FBG and INS levels were lower, the ISI was higher, and the number of islet ß-cells was significantly increased in all the PEP groups. In the medium- and high-dose PEP groups, MDA levels decreased, and the enzymatic activities of SOD and GSH-Px increased. The mRNA expression of InsR and GCK increased in all the PEP groups; APN mRNA expression increased in the high-dose PEP group, and GLUT-4 mRNA expression increased in adipose tissue. These findings suggest that PEP is a potential therapeutic agent that can be utilized to treat DM.