Objective. To observe the effects of resveratrol (Res) on the antioxidative function and estrogen level in an Alzheimer’s disease (AD) mouse model. Methods. First, we examined the effects of Res on an AD mice model. SAMP8 mice were selected as the model, and normal-aging SAMR1 mice were used as the control group. The model mice were randomly divided into three groups: a model group, high-dose Res group (40mg/kg, intraperitoneal (ip)), and low-dose Res group (20mg/kg, ip). After receiving medication for 15 days, the mice were subjected to the water maze test to assess their spatial discrimination. The spectrophotometric method was used to detect the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) as well as the malondialdehyde (MDA) content. Quantitative PCR (q-PCR) was used to detect SOD, GSH-Px, CAT, and heme oxygenase-1 (HO-1) mRNA level changes. Western blot analysis detected HO-1 and Nrf2 protein expression. Second, we researched the effect of Res on the estrogen level in the SAMP8 model mice. The model mice were randomly divided into four groups: a model group, estrogen replacement group (0.28 mg/kg, intramuscular (im), estradiol benzoate), high-dose Res group (5 mg/kg, im), and low-dose Res group (2.5 mg/kg, im). The mice were injected, once every three days, for 5 weeks. Q-PCR was used to detect brain tissue mRNA expression changes. Western blot analysis detected ERα, ERβ, and ChAT protein expression. An enzyme-linked immunosorbent assay (ELISA) kit was used to detect the expression of E2 and amyloid β protein (Aβ) in brain tissue. Results. Compared with the control treatment, Res could improve the spatial abilities of the mice to a certain extent and also increase the expression of SOD, GSH-Px, CAT, and HO-1 at the mRNA level (P<0.05). In addition, enhanced SOD, GSH-Px, and CAT activities and HO-1 protein levels and decreased MDA content (P<0.05) were detected in the brain tissue of the Res-treated mice. The cytoplasmic Nrf2 content in the Res-treated mice was also decreased while the nuclear Nrf2 content and the nuclear translation rate of Nrf2 were increased (P<0.05). Res could decrease the expression of ERβ in the brain tissue at the mRNA and protein levels and the expression of Aβ in the brain tissue at the protein level. Res could also increase the mRNA and protein expression of ERα and ChAT and the protein expression of estradiol in the brain tissue. Conclusion. Res can increase the antioxidant capacity of AD models through the Nrf2/HO-1 signaling pathway. In addition, Res can enhance estrogen levels in an AD model. These findings provide a new idea for the treatment of AD.

The structure of a back propagation neural network was optimized by a particle swarm optimization (PSO) algorithm, and a back propagation neural network model based on a PSO algorithm was constructed. By comparison with a general back propagation neural network and logistic regression, the fitting performance and prediction performance of the PSO algorithm is discussed. Furthermore, based on the back propagation neural network optimized by the PSO algorithm, the risk factors related to hypertension were further explored through the mean influence value algorithm to construct a risk prediction model. In the evaluation of the fitting effect, the root mean square error and coefficient of determination of the back propagation neural network based on the PSO algorithm were 0.09 and 0.29, respectively. In the comparison of prediction performance, the accuracy, sensitivity, specificity, and area under the receiver operating characteristic curve of the back propagation neural network based on PSO algorithm were 85.38%, 43.90%, 96.66%, and 0.86, respectively. The results showed that the backpropagation neural network optimized by PSO had the best fitting effect and prediction performance. Meanwhile, the mean impact value algorithm could screen out the risk factors related to hypertension and build a disease prediction model, which can provide clues for exploring the pathogenesis of hypertension and preventing hypertension.

Combination of betulinic acid and chidamide synergistically inhibits Epstein-Barr virus replication through over-generation of reactive oxygen species Combination of betulinic acid and chidamide synergistically inhibits epstein-barr virus replication through over-generation of reactive oxygen species

Vitamin C is an important micronutrient for human. Association between vitamin C and trouble sleeping was less studied. Therefore, the purpose of this study was to investigate the possible link between vitamin C in serum and trouble sleeping. The cross-sectional data was derived from the National Health and Nutrition Examination Survey (NHANES, 2017–2018). Trouble sleeping was measured by asking participants: “Have you ever told doctor had trouble sleeping”. Responses to this question was “yes” or “no”. vitamin C in serum was obtained by measuring the serum samples. We used multivariable binary logistic regressions to examine the possible link between vitamin C in serum and trouble sleeping, and then a subgroup analysis was performed. Moreover, the non-linear relationship between vitamin C in serum and trouble sleeping was further detected using a restricted cubic spline (RCS) model. A total of 3227 participants were included in the study. After adjusting all potential confounders, the results of multivariable logistic regression showed the significant negative association between vitamin C in serum and trouble sleeping(OR = 0.816; 95% CI:0.669 ~ 0.995). The significant inverse association was also found in female(OR = 0.713; 95% CI:0.546 ~ 0.931), age ≤ 65 years(OR = 0.773; 95% CI:0.600 ~ 0.996), and in participants with high cholesterol level(OR = 0.738; 95% CI:0.548 ~ 0.994). In addition, the RCS model demonstrated the significant non-linear relationship between vitamin C in serum and trouble sleeping (P value of nonlinear = 0.010). Our study demonstrates the significant negative association between vitamin C in serum and trouble sleeping.

The aim of the present study is to explored the relationship between ADIPO signalling pathway and T2DM, to provide clues for further study of the pathogenesis of T2DM and to determine the possible drug targets. This study employed a case-control study design. Twenty-three single nucleotide polymorphisms (SNPs) of 13 genes in the selected ADIPO signalling pathway were genotyped by SNPscan^TM kit. All statistical analysis was performed by SPSS 25.0, PLINK 1.07, R 2.14.2, Haploview 4.2, SNPstats, and other statistical software packages. In the association analysis based on a single SNPs, rs1044471 had statistical significance in the overdominant model without adjusting covariates. Rs1042531 had statistical significance in the overdominant model. Rs12718444 had statistical significance in the recessive model. There was a linkage disequilibrium between the loci within 9 genes, and the two loci in RXRA gene did not form blocks. Four kernel functions were used for SNPs set analysis based on ADIPO signalling pathway showed that there was no statistical significance whether covariates were added or not, P>0.05.According to our research results, it is found that some single nucleotide polymorphisms (ADIPOR2 rs1044471, PCK1 rs1042531, GLUT1 rs12718444) in the adiponectin signalling pathway may be associated with T2DM