3,3′-Iminodipropionitrile (IDPN), one of the nitrile derivatives, can induce persistent neurotoxicity, and therefore cause dyskinesia and cognitive impairments. Gastrodin, a main bioactive ingredient of Gastrodia elata Blume, is shown to greatly improve cognitive function. The aim of this study was to further determine whether administration of gastrodin can ameliorate IDPN-induced cognitive deficits in the Morris water maze (MWM) and novel object recognition (NOR) task, and to explore the underlying mechanisms. Results showed that exposure to IDPN (100 mg/kg/day, for 8 days) significantly impaired spatial and object recognition memory and that repeated treatment with gastrodin (150 mg/kg/day, for 6 weeks) could effectively alleviate the IDPN-induced cognitive impairments as indicated by increased spatial memory and discrimination ratio in the MWM and NOR tests. Gastrodin treatment also reverted IDPN-induced decreases of γ-aminobutyric acid (GABA) levels and increases of a2 GABAA receptor protein expression in the prefrontal cortex and hippocampus of IDPN-treated rats. These results suggest that gastrodin treatment may provide a novel pharmacological strategy for IDPN-induced cognitive deficits, which was mediated, at least in part, by normalizing the GABAergic system.
Oxidative damage promotes atherosclerosis. SOD2 is an important antioxidant enzyme. A case–control study and a meta-analysis
were performed to assess the association of C47T polymorphism in SOD2 gene with premature, late-onset and overall coronary artery disease (CAD) risk. A hospital-based case–control study was conducted
with 269 premature CAD cases, 278 late-onset CAD cases and 299 healthy controls. Polymerase chain reaction (PCR) and Pyrosequencing
were used to detect the polymorphism. Multinomial logistic regression model was performed to estimate odds ratio (OR) with
95% confidence intervals (CIs) and adjust potential confounders. A meta-analysis was performed using eight outcomes including
our result. Fixed or random effect pooled measure was selected on the basis of homogeneity test among studies. Heterogeneity
among studies was evaluated using I2. Meta-regression was used to explore potential sources of between-study heterogeneity. Publication bias was estimated using
Peters’s linear regression test. In our case–control study, compared with the TT as the reference, the mutant genotype of
CC + TC was significantly associated with a reduced premature CAD risk both in univariate (OR = 0.60, 95% CI = 0.41–0.87)
and multivariate (OR = 0.59, 95% CI = 0.40–0.87) logistic regressions, but not with late-onset CAD risk. After excluding one
article that deviated from Hardy–Weinberg equilibrium in controls, this meta-analysis showed a significant association of
the C allele with reduced risk of CAD in dominant (FEM: OR = 0.69, 95% CI = 0.61–0.78), recessive (OR = 0.64, 95% CI = 0.50–0.82),
and codominant (FEM: OR = 0.73, 95% CI = 0.65–0.80) models. Our study suggested that the mutant genotype of CC + TC was significantly
associated with a reduced CAD risk. 相似文献
正Dear Editor,Avian influenza viruses (AIVs) have posed a serious threat to poultry production and public health. To date, more than fourteen AIV subtypes that are able to infect human beings have been documented. Also, it is suggested that new subtypes may be reported in the future, owing to the migration of wild birds and live poultry transportation (Gao, 2018).Poultry may act as a potential incubator for novel subtypes of avian influenza virus (Bi et al., 2016a; Bi et al., 2016b; Liu et al., 2014a; Su et al., 2017). Up to date, the H7N9 AIV emerged in February 2013 has caused 1,567 human cases,with a fatality rate of 39.2%(http://www.who.int/influenza/ 相似文献
E-selectin (SELE) mediates the rolling and adhesion of leukocytes on activated endothelial cells and plays a critial role in the pathogenesis of coronary artery disease (CAD). Associatons between the A561C and G98T polymorphisms of the SELE gene and CAD risk were investigated broadly, but the results were inconsistent. In the present study, we performed a meta-analysis to systematically evaluate the associations between the two polymorphisms and the risk of CAD.
Methods
Comprehensive research was conducted to identify relevant studies. The fixed or random effect model was selected based on the heterogeneity among studies, which was evaluated with Q-test and Ι2. Meta-regression was used to explore the potential sources of between-study heterogeneity. Peters''s linear regression test was used to estimate the publication bias.
Results
Overall, 24 articles involving 3694 cases and 3469 controls were included. After excluding articles deviating from Hardy–Weinberg equilibrium in controls and sensitive analysis, our meta-analysis showed a significant association between the A561C ploymprphism and CAD in dominant (OR = 1.84, 95% CI = 1.56–2.16) and codominant (OR = 1.74, 95% CI = 1.49–2.03) models. As for the G98T polymorphism, significantly increased CAD risk was observed in dominant (OR = 1.47, 95% CI = 1.16–1.87) and codominant (OR = 1.48, 95% CI = 1.18–1.86) models, but after subgroup analysis, the association was not significant among Caucasians in dominant (OR = 1.58, 95% CI = 0.73–3.41) and codominant (OR = 1.58, 95% CI = 0.79–3.20) models.
Conclusions
Despite some limitations, our meta-analysis suggested that the SELE gene polymorphisms (A561C, G98T) were significantly associated with increased risk of CAD. However, after subgroup analysis no significant association was found among Caucasians for the G98T polymorphism, which may be due to the small sample size and other confounding factors. Future investigations with multicenter, large-scale, and multi-ethnic groups are needed. 相似文献