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| 1 | Hippocampal overexpression of TREM2 ameliorates high fat diet induced cognitive impairment and modulates phenotypic polarization of the microglia显示文摘Type 2 diabetes mellitus(T2DM)and Alzheimer's disease(AD)share several common pathophysiological features.Rare variants of triggering receptor expressed on myeloid cells 2(TREM2)increase the risk of developing AD,suggesting the involvement of TREM2 and innate immunity in AD development.It is still unknown whether TREM2 is related to cognitive impairment in T2DM.Here,we investigated the effects of the hippocampal overexpression of TREM2 on cognitive in long-term high-fat diet(HFD)-fed mice.Male C57BL/6J mice were maintained on HFD for 50 weeks.TREM2 was overexpressed in the hippocampus 36 weeks after HFD feeding using adeno-associated virus vector(AAV)-mediated gene delivery.The results showed that the HFD feeding induced rapid and persistent weight gain,glucose intolerance and significant impairments in learning and memory.Compared with AAV-con,AAV-TREM2 significantly ameliorated cognitive impairment without altering body weight and glucose homeostasis in HFD mice.The overexpression of TREM2 upregulated the synaptic proteins spinophilin,PSD95 and synaptophysin,suggesting the improvement in synaptic transmission.Dendritic complexity and spine density in the CA1 region were rescued after TREM2 overexpression.Furthermore,TREM2 markedly increased the number of iba-1/Arg-1-positive microglia in the hippocampus,suppressed neuroinflammation and microglial activation.In sum,hippocampal TREM2 plays an important role in improving HFD-induced cognitive dysfunction and promoting microglial polarization towards the M2 anti-inflammatory phenotype.Our study also suggests that TREM2 might be a novel target for the intervention of obesity/diabetes-associated cognitive decline. | Min Wu Maolin Liao Rongfeng Huang Chunxiu Chen Tian Tian Hongying Wang Jiayu Li Jibin Li Yuxiang Sun Chaodong Wu Qifu Li Xiaoqiu Xiao | 2022 | Genes & Diseases2022，9，2： | 4 |
| 2 | 茶多酚对人膀胱癌BIU-87细胞间隙连接蛋白43表达和细胞间隙连接通讯功能的影响(英文)显示文摘Objective:The aim of our study was to investigate the effects of(-)-epigallocatechin-3-gallate(EGCG,the major phytochemistry component in green tea)on the expression of connexin43(Cx43)gene and detect the intercellular communication of the human bladder cancer cell lines BIU-87,and explore its possible mechanisms of prevention and cure for the bladder tumor.Methods:The methyl thiazolyl tetrazolium and Annexin-V/PI double-labeled flow cytometry methods were used to observe the growth inhibitory rate(IR)and apoptosis rate(AR)of BIU-87 cells treated by EGCG at different concentrations(0, 5,10 and 20 mg/L),respectively.The reverse transcription-polymerase chain reaction(RT-PCR)and Western Blotting analy- sis were employed to detect the relative expression levels of the Cx43 mRNA and its protein.The scrape-loading fluorescence dye transfer method was used to assess the gap junction intercellular communication(GJIC)under fluorescence microscope. Results:EGCG at concentrations(10 and 20 mg/L)both could significantly inhibit the proliferation and induce the apoptosis of BIU-87 cells.The IR and AR were(15.67±1.15)%,(18.33±1.53)%and(42.00±4.34)%,(27.33±3.21)%,respectively. And compared with the control groups of 0 mg/L and 5 mg/L(P﹤0.05),EGCG could significantly up-regulate the expression of Cx43 mRNA and its protein and enhance the function of BIU-87 cells.The effects had the significant correlation with the dose-dependent of EGCG.Conclusion:EGCG(10,20 mg/L)could effectively up-regulate Cx43 expression and enhance the GJIC of BIU-87 cells.The results may indicate the effects of EGCG inducing bladder tumor cells apoptosis and inhibiting its growth which provides the experimental evidence for further demonstrating the mechanism of chemical prevention and cure for the bladder tumor by EGCG. | Zhengguo Cao Chao Tian Maolin Jiang Kui Wu Xiaojian Zhong Jianxin Li Yuefu Han | 2011 | The Chinese-German Journal of Clinical Oncology2011，10，12： | 0 |
| 3 | Development and application of novel high‐efficiency composite ultrafine cement grouts for roadway in fractured surrounding rocks显示文摘The fractured surrounding rocks of roadways pose major challenges to safe mining.Grouting has often been used to reinforce the surrounding rocks to mitigate the safety risks associated with fractured rocks.The aim of this study is to develop highly efficient composite ultrafine cement(CUC)grouts to reinforce the roadway in fractured surrounding rocks.The materials used are ultrafine cement(UC),ultrafine fly ash(UF),ultrafine slag(US),and additives(superplasticizer[SUP],aluminate ultrafine expansion agent[AUA],gypsum,and retarder).The fluidity,bleeding,shrinkage,setting time,chemical composition,microstructure,degree of hydration,and mechanical property of grouting materials were evaluated in this study.Also,a suitable and effective CUC grout mixture was used to reinforce the roadway in the fractured surrounding rock.The results have shown that the addition of UF and US reduces the plastic viscosity of CUC,and the best fluidity can be obtained by adding 40%UF and 10%US.Since UC and UF particles are small,the pozzolanic effect of UF promotes the hydration reaction,which is conductive to the stability of CUC grouts.In addition,fine particles of UC,UF,and US can effectively fill the pores,while the volumetric expansion of AUA and gypsum decreases the pores and thus affects the microstructure of the solidified grout.The compressive test results have shown that the addition of specific amounts of UF and US can ameliorate the mechanical properties of CUC grouts.Finally,the CUC22‐8 grout was used to reinforce the No.20322 belt roadway.The results of numerical simulation and field monitoring have indicated that grouting can efficaciously reinforce the surrounding rock of the roadway.In this research,high‐performance CUC grouts were developed for surrounding rock reinforcement of underground engineering by utilizing UC and some additives. | Maolin Tian Shaojie Chen Lijun Han Hongtian Xiao | 2024 | Deep Underground Science and Engineering2024，3，1： | 0 |
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