Protection of curcumin against amyloid-ß-induced cell damage and death involves the prevention from NMDA receptor-mediated intracellular Ca2+ elevation.

Alzheimer's disease (AD) is one of the common neurodegenerative diseases and amyloid-ß (Aß) is thought to be a key molecule contributing to AD pathology. Recently, curcumin is supposed to be beneficial to AD treatment. This study investigates the inhibitory effects of curcumin on Aß-induced cell damage and death involving NMDA receptor-mediated intracellular Ca(2+) elevation in human neuroblastoma SH-SY5Y cells. Cells were impaired significantly in Aß-damaged group compared with the control group, and cell viability was decreased while the released LDH from the cytosol was increased. Curcumin promotes cell growth and decreases cell impairment induced by Aß. Curcmin attenuates Aß-induced elevation of the ratio of cellular glutamate/γ-aminobutyric acid (GABA) with a concentration-dependent manner. Curcumin inhibits Aß-induced increase of cellular Ca(2+) and depresses Aß-induced phosphorylations of both NMDA receptor and cyclic AMP response element-binding protein (CREB) and activating transcription factor 1 (ATF-1). These results indicated that curcumin inhibits Aß-induced neuronal damage and cell death involving the prevention from intracellular Ca(2+) elevation mediated by the NMDA receptor.

Endoplasmic reticulum stress as a novel neuronal mediator in Alzheimer's disease.

Alzheimer's disease (AD) is one of the most common types of progressive dementias. The typical neuropathological changes in AD include extracellular senile plaques, intracellular neurofibrillary tangles, and loss of neurons. The pathogenetic mechanism of this disease is not comprehensively understood yet. Recently, endoplasmic reticulum stress (ER stress) has been considered as a potential event involved in AD development. Some AD-related factors, such as misfolded protein and Ca(2+) depletion, could disrupt the homeostasis of ER lumen. In AD, the aggregated amyloid-beta peptide (Abeta) could induce ER stress in an assembly dependent way. The presenilin has been identified as a Ca(2+) channel. Mutations of presenilin could change the balance of Ca(2+) in ER lumen and thus disrupts the ER homeostasis. Furthermore, the ER stress could lead to cellular disorders like inflammation. Through activating the expression of inflammatory factors, ER stress triggers inflammatory response in AD pathology. Herein, we reviewed the recent progress of ER stress-induced unfolded protein response (UPR) and the roles of ER stress in AD pathological process.

Chitooligosaccharides attenuate Cu2+-induced cellular oxidative damage and cell apoptosis involving Nrf2 activation.

Alzheimer's disease (AD) is one of the common neurodegenerative diseases. Increase of labile copper pool plays an important role in the pathogenesis of AD. Nrf2(NF-E2-related factor-2)-ARE (antioxidant response element) signaling is an important intracellular manner to defend against oxidative stress. In this study, we used SH-SY5Y cells as a model of neuron to test the effect of chitooligosaccharides (COSs) on Cu(2+)-induced oxidative damage. SH-SY5Y cells were treated with different concentrations of COSs (100-800 mg/L) before incubated with Cu(2+). Cell viability and cell damage and apoptosis were assessed. Both extracellular H(2)O(2) and intracellular ROS were measured and the relative levels of Nrf2, phosphorylated Nrf2, and HO-1 were analyzed by Western blotting, and further HO-1 mRNA was relatively quantified by real-time quantitative PCR. The results indicated that Cu(2+)-induced decrease of cell viability and increase of LDH release. In cell-free solution, COSs alone or with Cu(2+) cannot scavenge O(2)(-); however, COSs downregulate the levels of cellular oxidative stress and activated Caspase-3 induced by Cu(2+). Further, the levels of pSer40-Nrf2 protein and both the transcription and the translation of HO-1 gene are dramatically increased in COSs-protective group compared with Cu(2+) damage group. Therefore, these results indicate that Nrf2 activation might be involved in the protection of COSs against Cu(2+)-induced cellular oxidative damage. COSs contribute to the attenuation of oxidative damage and could be used as a nutritional agent for AD treatment.

[A survey on reproductive health related sexual behavior among middle school students in Luoyang city].

OBJECTIVE: To explore the appropriate ways and contents of reproductive health education for middle school students and to understand reproductive health related sexual behavior and influencing factors among middle school students. METHODS: Reproductive health related sexual behavior was evaluated among junior and senior middle school students in Luoyang by cluster sampling. The statistical software of SAS 8.1 was adopted for data analyses. Sexual behavior and influencing factors were analyzed by logistic regression. RESULTS: Critical sexual behaviors were found significantly higher in senior students, including masturbation, sexual fantasy and sexual intercourse than that in junior students (P < 0.05), and boys had higher prevalence than girls (P < 0.05). Results from multivariate logistic regression model analyses indicated that incidence rate of sexual behavior among those who ever having had experiences was higher than those who were inexperienced (OR = 2.62, 95%CI: 1.21 - 5.66). Incidence rate of sexual behavior was related to access of reproductive health and STD/AIDS knowledge (OR = 3.09, 95%CI: 1.43 - 6.51). In addition, incidence rate of sexual behavior was related to attitude and relation of amour between boys and girls (OR = 2.24, 95%CI: 1.32 - 3.75). CONCLUSION: Awareness on reproductive health knowledge among middle school students was not enough. Marginal sexual behaviors as masturbation and sexual fantasy had not been correctly and openly discussed to avoid inappropriate sexual activities.