Objective: To investigate the concentration of serum bone resorption markers NTX and TRACP-5b of children aged 8-14 years in a coal-burning fluorosis area and its relationship with age, and to provide population data for the study of pathogenesis of skeletal fluorosis. Methods: Totally 123 children of 8-14 schoolage in the two primary schools in Doujing Township, Shuicheng County, Liupanshui City, Guizhou Province were randomly selected as the exposed group. According to the matching principle, 64 children were randomly selected as a control from a primary school in a nondisease area Huaga Town. The dental fluorosis was investigated, and the concentrations of serum NTX and TRACP-5b were measured. Results: The detection rate of dental fluorosis in the fluorosis area was 94.3% and 0 in the control area. The concentrations of serum NTX in fluorosis area children were 13.04 (10.76, 15.64), 14.82 (12.15, 18.26)nmol/L in the early adolescence and middle-aged period, which lower than the control area 15.73(14.36, 18.61), 16.45(15.45, 22.02)nmol/L( P <0.05); The serum TRACP-5b levels in children with fluorosis were 276.74(237.63, 312.75), 270.14(242.82, 321.97), 305.95(259.78, 339.87)nmol/L in prepubertal, early adolescence and middle youth, lower than the control area 370.88 (304.47, 452.84), 353.30 (262.05, 393.19), 420.22 (376.96, 544.60)nmol/L( Z =-3.03, -2.66, -3.10, P <0.05). Serum NTx and TRACP-5b in fluorosis area were negatively correlated with dental fluorosis in children( r =-0.51, -0.37, P <0.01). Conclusion Fluorosis can reduce the concentrations of serum bone resorption markers NTX and TRACP-5b in children of different age groups. TRACP-5b may be more sensitive to fluoride exposure than NTX, but the specific mechanism remains to be further studied.

Previous studies have shown that spinosin was implicated in the modulation of sedation and hypnosis, while its effects on learning and memory deficits were rarely reported. The aim of this study is to investigate the effects of spinosin on the improvement of cognitive impairment in model mice with Alzheimer’s disease (AD) induced by Aβ1–42 and determine the underlying mechanism. Spontaneous locomotion assessment and Morris water maze test were performed to investigate the impact of spinosin on behavioral activities, and the pathological changes were assayed by biochemical analyses and histological assay. After 7 days of intracerebroventricular (ICV) administration of spinosin (100 µg/kg/day), the cognitive impairment of mice induced by Aβ1–42 was significantly attenuated. Moreover, spinosin treatment effectively decreased the level of malondialdehyde (MDA) and Aβ1–42 accumulation in hippocampus. Aβ1–42 induced alterations in the expression of brain derived neurotrophic factor (BDNF) and B-cell lymphoma-2 (Bcl-2), as well as inflammatory response in brain were also reversed by spinosin treatment. These results indicated that the ameliorating effect of spinosin on cognitive impairment might be mediated through the regulation of oxidative stress, inflammatory process, apoptotic program and neurotrophic factor expression, suggesting that spinosin might be beneficial to treat learning and memory deficits in patients with AD via multi-targets.
Alzheimer Disease* ; Animals ; B-Lymphocytes ; Brain ; Brain-Derived Neurotrophic Factor ; Cognition Disorders ; Hippocampus ; Humans ; Hypnosis ; Learning* ; Locomotion ; Malondialdehyde ; Memory Disorders ; Memory* ; Mice* ; Neuroprotection ; Neuroprotective Agents* ; Oxidative Stress ; Water

Depression is a major mood disorder. Abnormal expression of glial glutamate transporter-1 (GLT-1) is associated with depression. Schisantherin B (STB) is one bioactive of lignans isolated from Schisandra chinensis (Turcz.) Baill which has been commonly used as a traditional herbal medicine for thousands of years. This paper was designed to investigate the effects of STB on depressive mice induced by forced swimming test (FST). Additionally, we also assessed the impairment of FST on cognitive function in mice with different ages. FST and open field test (OFT) were used for assessing depressive symptoms, and Y-maze was used for evaluating cognition processes. Our study showed that STB acting as an antidepressant, which increased GLT-1 levels by promoting PI3K/AKT/mTOR pathway. Although the damage is reversible, short-term learning and memory impairment caused by FST test is more serious in the aged mice, and STB also exerts cognition improvement ability in the meanwhile. Our findings suggested that STB might be a promising therapeutic agent of depression by regulating the GLT-1 restoration as well as activating PI3K/AKT/mTOR pathway.
Animals ; Cognition ; Cognition Disorders ; Depression ; Glutamic Acid ; Herbal Medicine ; Learning ; Lignans ; Memory ; Mice ; Mood Disorders ; Physical Exertion ; Schisandra

The present research work primarily investigated whether spinosin has the potential of improving the pathogenesis of Alzheimer’s disease (AD) driven by β-amyloid (Aβ) overproduction through impacting the procession of amyloid precursor protein (APP). Wild type mouse Neuro-2a cells (N2a/WT) and N2a stably expressing human APP695 (N2a/APP695) cells were treated with spinosin for 24 h. The levels of APP protein and secreted enzymes closely related to APP procession were examined by western blot analysis. Oxidative stress related proteins, such as nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) were detected by immunofluorescence assay and western blot analysis, respectively. The intracellular reactive oxygen species (ROS) level was analyzed by flow cytometry, the levels of Aβ1-42 were determined by ELISA kit, and Thioflavin T (ThT) assay was used to detect the effect of spinosin on Aβ1-42 aggregation. The results showed that ROS induced the expression of ADAM10 and reduced the expression of BACE1, while spinosin inhibited ROS production by activating Nrf2 and up-regulating the expression of HO-1. Additionally, spinosin reduced Aβ1-42 production by impacting the procession of APP. In addition, spinosin inhibited the aggregation of Aβ1-42. In conclusion, spinosin reduced Aβ1-42 production by activating the Nrf2/HO-1 pathway in N2a/WT and N2a/ APP695 cells. Therefore, spinosin is expected to be a promising treatment of AD.