摘要：
目的 观察橘皮素对PC-12细胞β淀粉样蛋白（Aβ）水平的影响并探讨其可能的机制。方法不同浓度（0.1、1、10、100μmol/L）的橘皮素,作用不同时间（0 h、6 h、12 h、24 h、48 h）处理PC-12细胞后,采用ELISA检测细胞培养液Aβ40和Aβ42水平,Western blot检测PC-12细胞三磷酸腺苷结合盒转运体A1（ABCA1）蛋白水平,RT-PCR检测PC-12细胞ABCA1 m RNA水平。ABCA1 Si RNA抑制ABCA1蛋白表达。结果 10μmol/L及100μmol/L橘皮素组Aβ40和Aβ42水平显著下降,ABCA1蛋白水平明显增加,而所有组ABCA1 m RNA水平没有改变。使用100μmol/L橘皮素处理PC-12细胞,处理后ABCA1 m RNA表达与对照组比较差异无显著性,24 h及48 h组ABCA1水平显著增加,Aβ40和Aβ42水平显著下降。使用ABCA1 Si RNA抑制PC-12细胞ABCA1蛋白表达后,ABCA1 si RNA处理组与对照组比较,Aβ40和Aβ42水平显著增加。结论 橘皮素可通过增加ABCA1蛋白来降低PC-12细胞Aβ40和Aβ42水平。
摘要：
Recent studies have suggested that miR-590 may play critical roles in cardiovascular disease. This study was designed to determine the effects of miR-590 on lipoprotein lipase (LPL) expression and development of atherosclerosis in apolipoprotein E knockout (apoE(-/-)) mice and explore the potential mechanisms. En face analysis of the whole aorta revealed that miR-590 significantly decreased aortic atherosclerotic plaque size and lipid content in apoE (-/-) mice. Double immunofluorescence staining in cross-sections of the proximal aorta showed that miR-590 agomir reduced CD68 and LPL expression in macrophages in atherosclerotic lesions. MiR-590 agomir down-regulated LPL mRNA and protein expression as analyzed by RT-qPCR and western blotting analyses, respectively. Consistently, miR-590 decreased the expression of CD36 and scavenger receptor A1 (SRA1) mRNA and protein. High-performance liquid chromatography (HPLC) analysis confirmed that treatment with miR-590 agomir reduced lipid levels either in plasma orinabdominal cavity macrophages of apoE(-/-) mice. ELISA analysis showed that miR-590 agomir decreased plasma levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6). In contrast, treatment with miR-590 antagomir prevented or reversed these effects. Taken together, these results reveal a novel mechanism of miR-590 effects, and may provide new insights into the development of strategies for attenuating lipid accumulation and pro-inflammatory cytokine secretion.
作者机构：
[Chen, Xin] Hunan Tradit Chinese Med Coll, Zhuzhou, Peoples R China.;[Huang, Lei] Hunan Prov Hosp Tradit Chinese Med, Zhuzhou, Peoples R China.;[Ouyang, Xinping; He, Pingping] Univ South China, Inst Cardiovascular Res, Dept Physiol, Coll Med, Hengyang, Peoples R China.;[He, Pingping] Univ South China, Sch Nursing, Hengyang, Peoples R China.;[Wang, Bo; Liao, Huiying] Univ South China, First Affiliated Hosp, Hengyang, Peoples R China.
会议名称：
International Conference on Biological Engineering and Biomedical (BEAB)
会议时间：
JAN 10-12, 2014
会议地点：
Yichang, PEOPLES R CHINA
会议主办单位：
[Huang, Lei] Hunan Prov Hosp Tradit Chinese Med, Zhuzhou, Peoples R China.^[Chen, Xin] Hunan Tradit Chinese Med Coll, Zhuzhou, Peoples R China.^[Ouyang, Xinping;He, Pingping] Univ South China, Inst Cardiovascular Res, Dept Physiol, Coll Med, Hengyang, Peoples R China.^[He, Pingping] Univ South China, Sch Nursing, Hengyang, Peoples R China.^[Wang, Bo;Liao, Huiying] Univ South China, First Affiliated Hosp, Hengyang, Peoples R China.^[Lu, Suqing] Univ Guilin Med, Affiliated Hosp, Dept Urol, Guilin, Peoples R China.^[Su, Qi] Univ South China, Dept Pathol, Hengyang, Peoples R China.
摘要：
In this study, we down-regulate the expression of calreticulin (CRT) in differentiation of human leukemic HL-60 cells induced by diallyl disulfide (DADS) so as to find out the molecular mechanism of differentiation in HL-60 cells induced by DADS. By using several methods like Giemsa's staining, siRNA, MTT, qPCR, Westenbloting, flow cytometry etc., we tested the morphology changes of HL-60 cells, detected the expression of CRT before and after the use of siRNA and DADS, also we measured the proliferation of HL-60 cells. The results showed that DADS can apparently change the morphology of HL-60, furthermore both DADS and siRNA can decrease the expression of CRT. Once CRT was silenced, the proliferation of HL-60 was inhibited in the meantime the expression of CD33 and CD11b was significantly decreased. Therefore, DADS can down-regulates CRT-induced HL-60 differentiation meanwhile the silent CRT can induce the differentiation of HL-60 cells and enhance DADS-induced HL-60 cells differentiation.
作者机构：
[Ouyang, Xinping; Li, Jin-Feng; He, Pingping; Li, Yuanhui] Univ South China, Inst Cardiovasc Dis, Coll Med, Dept Physiol, Hengyang, Peoples R China.;[Wang, Bo; Liao, Huiying; Fu, Wan] Univ South China, First Affiliated Hosp, Hengyang, Peoples R China.;[Zhang, Tao] Univ South China, Second Affiliated Hosp, Hengyang, Peoples R China.;[He, Pingping] Univ South China, Sch Nursing, Hengyang, Peoples R China.
会议名称：
International Conference on Biological Engineering and Biomedical (BEAB)
会议时间：
JAN 10-12, 2014
会议地点：
Yichang, PEOPLES R CHINA
会议主办单位：
[Ouyang, Xinping;Li, Jin-Feng;Li, Yuanhui;He, Pingping] Univ South China, Inst Cardiovasc Dis, Coll Med, Dept Physiol, Hengyang, Peoples R China.^[Wang, Bo;Liao, Huiying;Fu, Wan] Univ South China, First Affiliated Hosp, Hengyang, Peoples R China.^[Zhang, Tao] Univ South China, Second Affiliated Hosp, Hengyang, Peoples R China.^[He, Pingping] Univ South China, Sch Nursing, Hengyang, Peoples R China.
摘要：
Objective: To test the effects of capsaicin on learning and memory ability in Alzheimer's disease (AD) mice. Results: Capsaicin (CAP) has no effect on spontaneous activity in APP/PS1 transgenic mice. CAP reduces the average escape latency and average swimming distance of Morris water maze in APP/PS1 transgenic mice. CAP adds academic record of Y maze in APP/PS1 transgenic mice. Conclusion: Capsaicin improves the function of learning and memory in AD mice.
摘要：
Background: Accumulating evidence suggests that microRNA-590 (miR-590) has protective effects on cardiovascular diseases, but the mechanism is unknown. Interestingly, previous studies from our laboratory and others have shown that macrophage-derived lipoprotein lipase (LPL) might accelerate atherosclerosis by promoting lipid accumulation and inflammatory response. However, the regulation of LPL at the post-transcriptional level by microRNAs has not been fully understood. In this study, we explored whether miR-590 affects the expression of LPL and its potential subsequent effects on lipid accumulation and pro-inflammatory cytokine secretion in human THP-1 macrophages. Methods and results: Using bioinformatics analyses and dual-luciferase reporter assays, we found that miR-590 directly inhibited LPL protein and mRNA expression by targeting LPL 3'UTR. LPL Activity Assays showed that miR-590 reduced LPL activity in the culture media. Oil Red 0 staining and high-performance liquid chromatography assays showed that miR-590 had inhibitory effects on the lipid accumulation in human THP-1 macrophages. We also illustrated that miR-590 alleviated pro-inflammatory cytokine secretion in human THP-1 macrophages as measured by ELISA. With the method of small interfering RNA, we found that LPL siRNA can inhibit the miR-590 inhibitor-induced increase in lipid accumulation and secretion of pro-inflammatory cytokines in oxLDL-treated human THP-1 macrophages. Conclusions: MiR-590 attenuates lipid accumulation and pro-inflammatory cytokine secretion by targeting LPL gene in human THP-1 macrophages. Therefore, targeting miR-590 may offer a promising strategy to treat atherosclerotic cardiovascular diseases. (C) 2014 Elsevier B.V. and Societe francaise de biochimie et biologie Moleculaire (SFBBM). All rights reserved.
