Low miR-92a-3p in oocytes mediates the multigenerational and transgenerational inheritance of poor cartilage quality in rat induced by prenatal dexamethasone exposure.

An adverse environment during pregnancy leads to intrauterine programming changes in multiple generations, resulting in the multigenerational inheritance of abnormal phenotype. Here, we reported the multigenerational inheritance of poor articular cartilage quality induced by prenatal dexamethasone exposure (PDE) with 0.2 mg/kg·d dexamethasone from gestational day (GD) 9 to GD20 in Wistar rats and investigated its intrauterine epigenetic programming mechanism.

Activation of α-7 Nicotinic Acetylcholine Receptor Attenuates Cardiac Inflammation Through NLRP3/Caspase-1/IL-18 Pathway.

Activation of α-7 nicotinic acetylcholine receptor (α7nAChR) receptor might induce cardiac inflammation, cardiac remodeling, and dysfunction. In this regard, this study aims to clarify the role and mechanism of α7nAChR in the process of cardiac inflammation and damage. Normal male C57BL/6J and NLRP3-knockout mice were used to evaluate the effect of PHA-543613, a selective agonist of α7nAChR, on cardiac inflammation and possible involvement of NLRP3/Caspase-1/IL-18 using western blotting and ELISA.

[Effects of curcumol on liver function and fibrosis in rats of nonalcoholic fatty liver disease and its mechanism].

To investigate the effects and mechanism of curcumol (CC) on liver function and fibrosis in rats of nonalcoholic fatty liver disease (NAFLD). The rat models of nonalcoholic steatohepatitis (NASH) combined with liver fibrosis were constructed by high-fat diet. Sixty SD rats were randomly divided into blank control group, model group (NASH), NASH + Compound Biejiarangan Troche (CBT) group (positive control group), and NASH + CC groups (25, 50, 100 mg/kg) , 10 rats in each group.

Prenatal dexamethasone exposure programs the decreased testosterone synthesis in offspring rats by low level of endogenous glucocorticoids.

Prenatal dexamethasone exposure (PDE) can decrease maternal endogenous glucocorticoid level and induce testicular dysplasia in male offspring rats. In this study we investigated low level endogenous glucocorticoid-mediated testicular dysplasia in PDE offspring and elucidated the intrauterine epigenetic programming mechanisms. Pregnant rats were injected with dexamethasone (0.

Articular damages in multi-generational female offspring due to prenatal caffeine exposure correlates with H3K9 deacetylation of TGFβ signaling pathway.

Adverse environment during pregnancy could lead to maternal glucocorticoid overexposure in utero, and then induce the intrauterine growth retardation (IUGR) and the programmed change in cartilage development. The transforming growth factor β (TGFβ) signaling pathway plays a crucial role in the process of chondrogenesis, cartilage growth, development, maturation, and phenotype maintenance. Our previous results had shown that prenatal caffeine exposure (PCE) could result in the damaged articular cartilage in offspring rats.

Prenatal ethanol exposure induced disorder of hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolic programming alteration and dysfunction of glucose and lipid metabolism in 40-week-old female offspring rats.

This study was designed to demonstrate disorder of hypothalamic-pituitary-adrenal (HPA) axis-associated neuroendocrine metabolic programming alteration and dysfunction of glucose and lipid metabolism induced by prenatal ethanol exposure (PEE) in postnatal week 40 (PW40) female offspring rats. Pregnant Wistar rats were administrated 4  g/kg·d ethanol intragastrically from gestational day 11 until term delivery. After weaning, the female offspring were fed with high-fat diet until PW24, and suffered to unpredictable chronic stress (UCS) during PW38-40.

Reduced testicular steroidogenesis in rat offspring by prenatal nicotine exposure: Epigenetic programming and heritability via nAChR/HDAC4.

Prenatal nicotine exposure (PNE) may lead to offspring's testicular dysplasia. Here, we confirmed the intergenerational effect of PNE on testosterone synthetic function and explored its epigenetic programming mechanism. Pregnant Wistar rats were injected subcutaneously with nicotine (2 mg/kg.

Prenatal ethanol exposure induces susceptibility to premature ovarian insufficiency.

Prenatal ethanol exposure (PEE) adversely affects the offspring reproductive system. We aimed to confirm the susceptibility to premature ovarian insufficiency (POI) in female PEE offspring and elucidate its intrauterine programming mechanism. The pregnant Wistar female rats were intragastrically administered with 4 g/kg×d of ethanol from gestational day (GD) 9 to 20.

The GC-IGF1 axis-mediated testicular dysplasia caused by prenatal caffeine exposure.

Prenatal caffeine exposure (PCE) can induce testicular developmental toxicity. Here, we aimed to explore the underlying mechanism of this process in reference to its intrauterine origin. Pregnant rats were intragastrically administrated caffeine (30 and 120 mg/kg/day) from gestational days 9 to 20.

Corticosterone rather than ethanol epigenetic programmed testicular dysplasia caused by prenatal ethanol exposure in male offspring rats.

Prenatal ethanol exposure (PEE) could affect offspring's testicular development. This study aimed to illuminate its intrauterine origin and the programming mechanism caused by PEE. Pregnant Wistar rats were given ethanol (4 g/kg.

Excitotoxicity and compensatory upregulation of GAD67 in fetal rat hippocampus caused by prenatal nicotine exposure are associated with inhibition of the BDNF pathway.

Prenatal nicotine exposure (PNE) can cause hypersensitivity of hypothalamic-pituitary-adrenal (HPA) axis in offspring with intrauterine growth retardation. The purpose of this study was to explore the original mechanism of intrauterine development that mediates hypersensitivity of the HPA axis in offspring due to PNE. Pregnant Wistar rats were injected subcutaneously with 2 mg/kg·d of nicotine on the 9th to the 20th gestational day (GD9-GD20) and the fetuses were extracted at GD20.

Decreased H3K9ac level of AT2R mediates the developmental origin of glomerulosclerosis induced by prenatal dexamethasone exposure in male offspring rats.

This study aimed to demonstrate that prenatal dexamethasone exposure (PDE) can induce kidney dysplasia in utero and adult glomerulosclerosis in male offspring, and to explore the underlying intrauterine programming mechanisms. Pregnant rats were subcutaneously administered dexamethasone 0.2 mg/kg.

Decreased H3K9ac level of StAR mediated testicular dysplasia induced by prenatal dexamethasone exposure in male offspring rats.

Prenatal dexamethasone exposure (PDE) could induce testicular developmental toxicity in adults. The present study aims to confirm its intrauterine origination, and to explore its potential intrauterine programming mechanism. The pregnant rats were respectively injected subcutaneously with 0.

cAMP/PKA/EGR1 signaling mediates the molecular mechanism of ethanol-induced inhibition of placental 11β-HSD2 expression.

It is known that inhibiting 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) expression in the placenta can cause fetal over-exposure to maternal glucocorticoids and induce intrauterine growth restriction (IUGR); these effects ultimately increase the risk of adult chronic diseases. This study aimed to investigate the molecular mechanism of the prenatal ethanol exposure (PEE)-induced inhibition of placental 11β-HSD2 expression. Pregnant Wistar rats were intragastrically administered ethanol (4 g/kg/d) from gestational days 9 to 20.

Prenatal nicotine exposure intergenerationally programs imperfect articular cartilage via histone deacetylation through maternal lineage.

Accumulating evidence has shown that the impact of prenatal environmental factors on the organs of the offspring could last until the adulthood. Here, we aimed to investigate these effects and the potential mechanism of prenatal nicotine exposure (PNE) on the female adult cartilage of the first generation (PNE-F1) and the second generation (PNE-F2). Pregnant Wistar rats were injected with 2.

Prenatal Dexamethasone Exposure Induced Ovarian Developmental Toxicity and Transgenerational Effect in Rat Offspring.

Prenatal dexamethasone exposure (PDE) induces multiorgan developmental toxicities in offspring. Here we verified the transgenerational inheritance effect of ovarian developmental toxicity by PDE and explored its intrauterine programming mechanism. Pregnant rats subcutaneously received 0.

Effects of prenatal caffeine exposure on glucose homeostasis of adult offspring rats.

Epidemiological evidences show that prenatal caffeine exposure (PCE) could induce intrauterine growth retardation (IUGR). The IUGR offspring also present glucose intolerance and type 2 diabetes mellitus after maturity. We have previously demonstrated that PCE induced IUGR and increased susceptibility to adult metabolic syndrome in rats.

Prenatal caffeine exposure induced high susceptibility to metabolic syndrome in adult female offspring rats and its underlying mechanisms.

Our previous studies have demonstrated that prenatal caffeine exposure (PCE) induced an intrauterine programming of hypothalamic-pituitary-adrenal axis (HPAA)-associated neuroendocrine metabolism in 3-month-old offspring rats. In this study, we aimed to confirm this programming disorder and high susceptibility to metabolic syndrome (MS) in 10-month-old female PCE offspring with postnatal catch-up growth. We found that PCE female offspring rats showed decreased bodyweight but a higher rate of weight gain after birth.

Chest circumference and sitting height among children and adolescents from Lhasa, tibet compared to other high altitude populations.

Objectives: The adaptation of human beings to a high altitude environment during growth has been reported in several populations but is less known for Tibetans. The objective of this study was to investigate similarities and differences of Tibetans in patterns and characteristics of physical growth and development in comparison to other high altitude populations.

Methods: We measured the stature, weight, chest circumference and sitting height of 2,813 healthy children and adolescents aged 6- to 21-year-old living at 3,658-4,500 m in Tibet, China, and compared them with published data from other high altitude populations.

[Progress in individual identification of burned bones].

The burned bone DNA test have became more and more important in identifying the individuals and paternity involved in the fire, explosion disasters as well as burn corpse crimes. As an important genetic marker system, STR has been widely used in forensic individual identification, paternity test and other fields. In this article, the influence of burned temperature and time to STR typing was reviewed, the choice of STR locus and DNA extraction methods were discussed about burned bones.