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Abstract Objectives: Observational studies suggested that obesity may promote the development of allergic rhinitis. The aim of this study was to explore the association of obesity, lipids and adipokines with this allergic disease at the genetic level using Mendelian randomization strategies. Methods: Summary data for three obesity indicators (such as body mass index), eight lipid indicators (such as triglycerides) and six adipokines (such as interleukin-6 and adipocyte fatty acid-binding protein) were collected, and suitable instrumental variables were extracted from these summary data according to the three main assumptions of Mendelian randomization. Three Mendelian randomization methods (such as inverse variance weighted) were used to detect the casual effect of the above indicators on allergic rhinitis risk. Sensitivity analyses were performed to assess heterogeneity and horizontal pleiotropy. Results: After Bonferroni correction, the inverse variance weighted reported that elevated levels of interleukin-6 and adipocyte fatty acid-binding protein were nominally associated with the decreased risk of allergic rhinitis (OR = 0.870, 95% CI 0.765-0.990, p = 0.035; OR = 0.732, 95% CI 0.551-0.973, p = 0.032). The other Mendelian randomization methods supported these results. Obesity, lipids and other adipokines were not related to this allergic disease. Sensitivity analyses found no heterogeneity and horizontal pleiotropy in the study. Conclusion: The study provided some interesting, but not sufficient, evidence to suggest that interleukin-6 and adipocyte fatty acid-binding protein might play a protective role in the development of allergic rhinitis at the genetic level. These findings should be validated by more research. Level of evidence: This was a Mendelian randomized study with a level of evidence second only to clinical randomized trials, and higher than cohort and case-control studies.
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Aim To explore the effects of corilagin on non-alcoholic fatty liver disease induced by high-fat and high-sugar diet in mice via regulating AMPK-autophagy signaling. Methods Healthy 8-week-old male C57BL/6J mice were randomly divided into control group, model group and corilagin group. The mice of model group and corilagin group were fed with a high-fat and high-sugar diet for four weeks at the age of eight weeks. The corilagin group mice were also intraperitoneally injected with corilagin (20 mg • k g
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Aim To explore the protective mechanism of tanshinone B on cognitive dysfunction in mice with vascular dementia.Methods C57BL/6 male mice were divided into control group, vascular dementia model group(VD group), tanshinone B group(TSB 2,4,8 mg·kg-1), donepezil hydrochloride group(1 mg·kg-1), according to the random number table method.The VD model was constructed by the coarctation of bilateral common carotid arteries in mice.Ten days after the successful modeling, the low, medium, and high-dose tanshinone B groups were intraperitoneally injected with tanshinone B, the positive control medicine group was intraperitoneally injected with donepezil hydrochloride, once a day, and the mice in control group and VD group were injected intraperitoneally with the same amount of normal saline for 20 d.Morris water maze test was used to detect the learning and memory ability of mice in each group; the cortex and hippocampus of each group were separated, and MDA, SOD and GSH-Px were determined by spectrophotometry; the pathological changes in the hippocampus of each group were observed by HE staining.The expression of p-LRP6, LRP6, Wnt1 and β-catenin protein in the hippocampus of each group of mice were detected by Western blot.Results Compared with control group, the ability of memory was reduced, the content MDA increased(P<0.01), SOD and GSH-Px activities decreased(P<0.01), and significant pathological damage in hippocampus, the expression of p-LRP6, Wnt1, and β-catenin protein was significantly reduced in VD group(P<0.01).Compared with VD group, the learning and memory abilities of the mice were improved, the content of MDA decreased(P<0.01), the activities of SOD and GSH-Px increased(P<0.01), and the pathological damage in hippocampus was significantly improved.The expression of Wnt1 and β-catenin protein increased significantly in TSB treatment group(P<0.01).Conclusions TSB can improve the cognitive dysfunction of VD mice, and its mechanism may be related to the activation of the LRP6/Wnt1/β-catenin pathway in hippocampus.
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ABSTRACT: Based on the data of "employment and food demand of urban migrant workers", this paper empirically analyzed the impact of urban pension insurance on the nutritional intake structure of migrant workers. The results showed that participating in urban pension insurance can change the nutritional intake structure of migrant workers. Additionally, fat and protein replace carbohydrate as the main nutrition sources for migrant workers. After controlling the income and labor intensity of migrant workers and other factors, urban pension insurance has a positive effect on the intake of fat and protein of migrant workers for they increase by 13.5% and 8.8% respectively. There is no significant effect on the intake of carbohydrates of migrant workers. The calorie intake of migrant workers increases by 6.8% accounting for the change of nutritional intake structure. Endogenous and robustness tests showed that the above conclusions are robust. Heterogeneity analysis showed that there is no significant difference in the effect of urban pension insurance on calorie intake of migrant workers in different income levels and age groups.
RESUMO: Este artigo usa os dados da pesquisa de "Emprego e demanda alimentar dos trabalhadores migrantes urbanos" para analisar empiricamente o impacto do seguro patrimonial urbano na estrutura de ingestão nutricional dos trabalhadores migrantes. O estudo constatou que: o seguro-pensão urbano mudou a estrutura de ingestão nutricional dos trabalhadores migrantes. Gordura e proteína substituíram os carboidratos e se tornaram a principal fonte de nutrição dos trabalhadores migrantes. Depois de controlar fatores como a renda e a intensidade do trabalho dos trabalhadores migrantes, o seguro de pensão urbana aumentou significativamente a ingestão de gordura e proteína dos trabalhadores migrantes em 13,5% e 8,8%, respectivamente, enquanto a ingestão de carboidratos dos trabalhadores migrantes não foi afetada. Significativamente afetado. A transformação da estrutura de ingestão nutricional dos trabalhadores migrantes aumentou sua ingestão calórica em 6,8%. Os testes de endogenia e robustez mostram que as conclusões acima são robustas. A análise de heterogeneidade mostra que não há diferença significativa no efeito do seguro previdenciário urbano sobre o aumento da ingestão de calorias para trabalhadores migrantes de diferentes níveis de renda e diferentes grupos etários.