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Selenium (Se) and vitamin B2 (VitB2) all play essential roles in participating in hepatic lipid metabolism regulation. In this study, we aimed to identify whether Se combined with VitB2 could meliorate nonalcoholic fatty liver disease (NAFLD) caused by high‐fat (HF) diet in rats. To this end, 50 SD male rats were randomly allotted into five groups equally after receiving a HF diet for 2 weeks. Rats were fed high‐fat diets and gavaged daily with 0.83 or 8.33 µg kg–1 Se combined with 0.70 or 3.50 mg kg–1 VitB2 for 8 weeks. Another 10 rats were given a conventional diet as a control group. The result showed that Se combined with VitB2 decreased NAFLD activity score and liver lipid's levels, relieved hepatic steatosis and lipid deposition and promoted the balance of ApoA1/ApoB ratio. The hepatic 3‐hydroxy‐3‐methyl glutaryl coenzyme A reductase (HMGR) level was declined, and the serum HL level was increased in NAFLD rats through the combined intervention. In addition, Se and VitB2 regulated hepatic metabolism factor's (FAS, ACC, ACAT1, PPARγ, and SREBP‐1c) expression level. Taken together, the combined intervention of Se and VitB2 can alleviate HF‐diet‐induced NAFLD in rats. The molecular mechanism may be related to affecting the activities of lipid metabolic enzymes such as FAS, ACC, HMGR, ACAT1, and HL by inhibiting the expression of PPARγ and SREBP‐1c. Practical Applications: The present study showed that a combination of Se and VitB2 can effectively reduce hepatic lipid accumulations, exert hepatoprotective effects and regulate hepatic lipid metabolism in NAFLD rats caused by a high‐fat diet. The possible molecular mechanism may be related to affecting the activities of lipid metabolic enzymes such as FAS, ACC, HMGR, ACAT1, and HL, and inhibiting the expression of PPARγ and SREBP‐1c. Se and VitB2 cosupplementation may be a potential therapeutic strategy in overcoming hepatic lipid disorders' adverse effects beyond pharmacological interventions to ameliorate NAFLD. [ABSTRACT FROM AUTHOR]

In this experiment, the effects of polypropylene thick fiber (PPTF) with different volume admixtures (0, 0.05%, 0.10%, 0.15%, 0.20%, 0.25%) on the compressive strength, splitting tensile strength and bending strength of large admixture of slag fly ash concrete were investigated with short-cut basalt fiber (BF) as a reference. The results show that the polypropylene thick fiber can work well with basalt fiber and improve its strengthening effect of single admixture. And 0.10% of polypropylene thick fiber and 0.10% of basalt fibers by volume have the best strengthening effect on the mechanical properties of the large amount of slag fly ash concret.

Highlights • Maternal folic acid deficient increased neuronal apoptosis. • Maternal folic acid deficiency stimulated the intrinsic apoptotic pathway (Bcl-2 pathway). • This effect associate with maternal folic acid deficiency upregulates miR-34a. Abstract Embryonic development is a critical period wherein brain neurons are generated and organized. Maternal dietary folate, a cofactor in one-carbon metabolism, modulates neurogenesis and apoptosis in foetal brain neurons. We hypothesized that aberrant neuronal apoptosis may affect the development of the central nervous system during maternal folic acid deficiency, with evident effects because maternal folic acid deficiency modulates the microRNA-34a associated with Bcl-2 pathway during embryonic development. Four-week-old female Sprague-Dawley rats were divided randomly into two groups (10 rats per group): a folate-deficient diet group and a folate-normal diet group. The diets were administered to the rats 60 d before mating, which was continued for the pregnant dams until parturition. Maternal folic acid deficiency increased neuronal apoptosis in the hippocampus and the cortex in the offspring. Furthermore, maternal folic acid deficiency increased the ratio of cleaved caspase-3/caspase-3, followed by an increase in caspase-3 activity. Moreover, maternal folic acid deficiency downregulated Bcl-2 and upregulated Bax, and this effect associate with maternal folic acid deficient increases expression of microRNA-34a. Together, the present results indicate that maternal folic acid deficiency stimulates neuronal apoptosis via microRNA-34a associated with Bcl-2 signalling in rat offspring. [ABSTRACT FROM AUTHOR]

BackgroundMethodsResultsConclusionMedium-chain fatty acids (MCFAs) and docosahexaenoic acid (DHA) could affect the occurrence of mild cognitive impairment (MCI). β-hydroxybutyrate (BHB), mitochondrial DNA copy number (mtDNAcn) and mitochondrial DNA (mtDNA) deletions might be their potential mechanisms. This study aimed to explore the relationship between MCFAs, DHA and MCI, and potential mechanisms.This study used data from Tianjin Elderly Nutrition and Cognition (TENC) cohort study, 120 individuals were identified with new onset MCI during follow-up, 120 individuals without MCI were selected by 1:1 matching sex, age, and education levels as the control group from TENC. Conditional logistic regression analysis and mediation effect analysis were used to explore their relationship.Higher serum octanoic acid levels (OR: 0.633, 95% CI: 0.520, 0.769), higher serum DHA levels (OR: 0.962, 95% CI: 0.942, 0.981), and more mtDNAcn (OR: 0.436, 95% CI: 0.240, 0.794) were associated with lower MCI risk, while more mtDNA deletions was associated with higher MCI risk (OR: 8.833, 95% CI: 3.909, 19.960). Mediation analysis suggested that BHB and mtDNAcn, in series, have mediation roles in the association between octanoic acid and MCI risk, and mtDNA deletions have mediation roles in the association between DHA and MCI risk.Higher serum octanoic acid and DHA levels were associated with lower MCI risk. Octanoic acid could affect the incidence of MCI through BHB, then mitochondria function, or through mitochondria function, or directly. Serum DHA level could affect the incidence of MCI through mitochondria function, or directly. [ABSTRACT FROM AUTHOR]

Astrocytes are the most widely distributed cells in the brain, and astrocyte apoptosis may play an important role in the pathogenesis of neurodegenerative diseases. Folate is required for the normal development of the nervous system, but its effect on astrocyte apoptosis is unclear. In this study, we hypothesized that folic acid (the therapeutic form of folate) decreases astrocyte apoptosis by preventing oxidative stress-induced telomere attrition. Primary cultures of astrocytes were incubated for 12 days with various concentrations of folic acid (0–40 μmol/L), then cell proliferation, apoptosis, intracellular folate concentration, intracellular homocysteine (Hcy) concentration, intracellular reactive oxygen species (ROS) levels, telomeric DNA oxidative damage, and telomere length were determined. The results showed that folic acid deficiency decreased intracellular folate, cell proliferation, and telomere length, whereas it increased Hcy concentration, ROS levels, telomeric DNA oxidative damage, and apoptosis. In contrast, folic acid dose-dependently increased intracellular folate, cell proliferation, and telomere length but it decreased Hcy concentration, ROS levels, telomeric DNA oxidative damage, and apoptosis. In conclusion, folic acid inhibited apoptosis in astrocytes. The underlying mechanism for this protective effect may be that folic acid decreased oxidative stress and thereby prevented telomeric DNA oxidative damage and telomere attrition. [ABSTRACT FROM AUTHOR]

Introduction: Cardiometabolic disease (CMD) is the leading cause of mortality in China. A healthy diet plays an essential role in the occurrence and development of CMD. Although the Chinese heart-healthy diet is the first diet with cardiovascular benefits, a healthy dietary pattern that fits Chinese food culture that can effectively reduce the risk of CMD has not been found., Methods/design: The study is a single-centre, open-label, randomised controlled trial aimed at evaluating the effect of the Reducing Cardiometabolic Diseases Risk (RCMDR) dietary pattern in reducing the risk of CMDs in people with dyslipidaemia and providing a reference basis for constructing a dietary pattern suitable for the prevention of CMDs in the Chinese population. Participants are men and women aged 35-45 years with dyslipidaemia in Tianjin. The target sample size is 100. After the run-in period, the participants will be randomised to the RCMDR dietary pattern intervention group or the general health education control group with a 1:1 ratio. The intervention phases will last 12 weeks, with a dietary intervention of 5 working days per week for participants in the intervention group. The primary outcome variable is the cardiometabolic risk score. The secondary outcome variables are blood lipid, blood pressure, blood glucose, body composition indices, insulin resistance and 10-year risk of cardiovascular diseases., Ethics and Dissemination: The study complies with the Measures for Ethical Review of Life Sciences and Medical Research Involving Human Beings and the Declaration of Helsinki. Signed informed consent will be obtained from all participants. The study has been approved by the Medical Ethics Committee of the Second Hospital of Tianjin Medical University (approval number: KY2023020). The results from the study will be disseminated through publications in a peer-reviewed journal., Trial Registration Number: Chinese Clinical Trial Registry (ChiCTR2300072472)., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Recent findings suggest that both dietary protein intake and hand grip strength (HGS) were associated with cognitive function, however, few studies have been devoted specifically to the mediation effect of HGS on the association of dietary protein with cognitive function., Objectives: To confirm the hypothesis that HGS mediated the association of dietary protein intake with cognitive function in the elderly, which was modified by triglyceride level and methylenetetrahydrofolate reductase (MTHFR) gene status., Methods: This cross-sectional study included 3,268 participants. Dietary protein intake, HGS, and cognitive function were collected by food frequency questionnaires (FFQ), grip measurements and mini mental state examination (MMSE), respectively. In this mediation analysis, dietary protein intake was entered as independent variable, HGS was entered as mediator, and cognitive function was entered as dependent variable., Results: HGS significantly mediated the associations of dietary protein (β = 0.0013, 95% CI: 0.0007, 0.0022), animal protein (β = 0.0024, 95% CI: 0.0012, 0.0037), and plant protein intake (β = 0.0011, 95% CI: 0.0001, 0.0023) with cognitive function in total participants, with the mediated proportion of 16.19%, 12.45% and 20.57%, respectively. Furthermore, significant mediation effects of HGS on the associations of dietary protein, animal protein, and plant protein intake with MMSE score were found in the elderly without hypertriglyceridemia or in MTHFR C677T CC/CT carriers., Conclusion: This study suggested that HGS mediated the association of dietary protein intake with cognitive function, and this mediation effect was modified by triglyceride level and MTHFR C677T gene status., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To establish an effective method of primary and passage cultured cerebral cortical astrocyte of SD neonatal rat in vitro., Methods: Cerebral cortex of two 2-day-old SD rats were taken with aseptic operation and then were cut to pieces. After stripped the pia mater, digested by 500 μL 0. 25% trypsin at 37 ℃ for 15 min. Next, dispersed cell suspension was made by mechanical method and filtered. Cell suspensions were incubated in an uncoated culture bottle at 37 ℃ for 15 min. The cells were inoculated at 5×10~6/m L in the T75 culture flask coated with L-polylysine. The cells were shaken at 200 r/min 37 ℃ for 18 h, then added 1 m L of trypsin to digest cells and then collected the cells. The morphology of the passage cells was observed under inverted phase contrast microscope, and the purity of astrocytes was identified by immunofluorescence staining of GFAP. The proliferate activity of passage cells was determined by MTS assay., Results: The purity of astrocytes was( 97. 86 ± 0. 91) %, and the growth and proliferation activity of astrocytes were good after passage., Conclusion: A rapid, economical and effective method for obtaining astrocytes in the cerebral cortex of newborn rats was established.