摘要：
Since Ashford and Porter first discovered that cells ＂eat themselves＂ in 1962, the process known as autophagy has generated intense interest in both biomedical research and clinical medicine. Autophagy is a regulated cellular pathway that transports damaged, modified or aging organelles and proteins to lysosomes/vacuoles for degradation.
摘要：
Recently, widespread interest has grown regarding melatonin treatment of hypertension including its cardioprotective effects. Studies in rodents indicate that melatonin plays a role in the pathogenesis of hypertension in rats with metabolic syndrome. Piromelatine, a melatonin agonist, serotonin 5-HT-1A and 5-HT-1D agonist and serotonin 5-HT2B antagonist is a multimodal agent with sleep promoting, anti-diabetic, analgesic, anti-neurodegenerative, anxiolytic and antidepressant potential, currently in development for the treatment of insomnia. In this report we assessed the effects of piromelatine and melatonin treatment on blood pressure in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Five groups of 12-wk-old rats (10/group) were treated for 5 weeks with a vehicle, piromelatine (5, 15 and 50 mg/kg BW) and melatonin (10 mg/kg BW) and an age-matched WKY control group. Systolic blood pressure (tail-cuff method) was measured weekly at 9:00 a.m. and at 9:00 p.m. The rats body weight, plasma glucose, insulin, triglyceride, adiponectin, total cholesterol, HDL and LDL/VLDL cholesterol were also measured. Our results showed that both piromelatine and melatonin reduced SHR blood pressure significantly both during the morning and the evening. Piromelatine, but not melatonin, also reduced SHR body weight gain and both significantly decreased plasma glucose and insulin levels and increased adiponectin levels. Piromelatine, similar to melatonin, has an antihypertensive effect and also attenuates body weight, improves metabolic profiles and might be useful in the treatment of hypertension and the metabolic syndrome.
摘要：
OBJECTIVE: This study was to investigate the molecular mechanisms underlying the 27nt-miRNA-mediated regulation of expression of the endothelial nitric oxide synthase (eNOS) gene. METHODS: Cell lines overexpressing 27nt-miRNA or its mutant were established by transfecting the miRNA expression vector into the endothelial cells. eNOS mRNA and protein expression were examined by RT-PCR and Western Blotting, respectively. Luciferase activity reporter system was used to study the target of 27nt-miRNA. RESULTS: The results showed that overexpression of 27nt-miRNA significantly inhibited eNOS mRNA level and protein expression, and reduced the eNOS transcriptional efficiency. Such inhibitory effects of 27nt-miRNA were attenuated by the sequence mutations in 27nt-miRNA. Interestingly, the transcription factor SP-1 expression was reduced by 27nt-miRNA. Meanwhile, overxpression of SP-1 protein partially restored eNOS expression, and rescued the 27nt-miRNA-mediated reduction of endothelial cell proliferation. Moreover, certain sites in the SP-1 mRNA were found to be the direct target of 27nt-miRNA by a luciferase reporter system. CONCLUSIONS: These results demonstrate that the 27nt-miRNA suppresses eNOS gene expression and SP-1 expression in vascular endothelial cells. The 27nt-miRNA directly target to SP-1 mRNA, thereby contributing to proliferation of endothelial cells.
作者：
Song Yin;Xing Zheng;Xu Yao;Yuhong Wang;Duanfang Liao;...
期刊：
癌症治疗(英文),2013年4(1):113-123 ISSN：2151-1934
作者机构：
Division of Stem Cell Regulation and Application, State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (Incubation), Hunan University of Chinese Medicine, Changsha, China;Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China
摘要：
Curcumin has been reported to possess multifunctional bioactivities with low toxicity. However, the clinical application of curcumin has been significantly limited by its instability and poor metabolic property. Up to now, multiple approaches are being sought to overcome these limitations to obtaining “super curcumin”, and many analogues of curcumin have been designed and synthesized. In all of those analogues, a series of mono-carbonyl curcumin analogues deleting the β-diketone draw our attention. Since the seven-carbon β-diketone linker in curcumin may be responsible for its instability, the series of mono-carbonyl curcumin analogues deleting the β-diketone may be potential prodrug with improved pharmacokinetic and pharmacodynamic properties. This review just focuses on these more stable mono-carbonyl analogues of curcumin, and shows the new class of active structure by introducing the synthesis and anticancer activity of them.
作者机构：
[Wang Chang-Bo; Li Bin-Yuan; Qin Ling-Xue; Dong Xiao; He Shu-Ya; Wang San-Hu; Ma Yun] Univ South China, Dept Biol & Biochem, Hengyang 421001, Peoples R China.;[Xu Can] Univ South China, Affiliated Hosp 1, Dept Cardiol, Hengyang 421001, Peoples R China.
通讯机构：
[He Shu-Ya] U;Univ South China, Dept Biol & Biochem, Hengyang 421001, Peoples R China.
关键词：
FXR1P;CMAS;GM1;biological effect;PC12;VSMC
摘要：
Fragile X syndrome (FXS) is a genetic mental retardation disease, with incidence second only to trisomy 21 syndrome. Fragile X mental retardation protein(FMRP), is the causative factor of FXS and encoded by the Fragile X mental retardation1(FMR1)gene, which is widely expressed in cells of the nerve, muscle, and testes. Fragile X related protein 1 (FXR1P) is encoded by a homologous gene to FMR1——Fragile X related gene 1 (FXR1) and can interact with proteins and RNAs. Many illnesses were involved in the altered expression of FXR1. To understand the biological effect of the interaction between FXR1P and CMAS, we constructed a FXR1 overexpression vector and investigated its expression in PC12 (the rat pheochromocytoma) cells and VSMC (vascular smooth muscle cell) and the effect of the overexpression on cell morphology and several cell processes related to CMP-N-acetylneuraminic acid synthetase (CMAS) activity. We demonstrate that the overexpression of FXR1 gene can increase activity of CMAS in PC12 cells and provide a certain degree growth protection for that cells. Thus, it suggests FXR1P is a tissue-specific regulator to alter the concentration of GM1 in PC12 cells, but not in VSMC.
作者机构：
[Guo, Zi-fen; Xuan, Gui-ping] Univ South China, Inst Pharm & Pharmacol, Hengyang 421001, Peoples R China.;[Wu, Hong-bin; Lai, Chun-hua] Guilin Med Univ, Dept Tradit Chinese Med, Guilin 541004, Peoples R China.
会议名称：
The 12th Meeting of the Asia Pacific Federation of Pharmacologists(第十二届亚洲太平洋地区药理学家联盟会议暨中国药理学会第十二次全国学术会议)
会议时间：
2013-7-9
会议地点：
上海
会议主办单位：
中国药理学会
会议论文集名称：
The 12th Meeting of the Asia Pacific Federation of Pharmacologists(第十二届亚洲太平洋地区药理学家联盟会议暨中国药理学会第十二次全国学术会议)论文集
关键词：
Yang Ren Tiao Chong Soup;fever due to yin-deficiency;climacteric syndrome;hormone
摘要：
<正>Aim:To observe the effect of Yang Ren Tiao Chong Soup on model rats of fever due to yin-deficiency climacteric syndrome.Methods:The specific pathogen free（SPF） SD female rats were used as the experimental animal.Rat models of fever due to yin-deficiency climacteric syndrome were induced by removal of bilateral ovaries combination with perfusion of hot Chinese medicine.The changes of model rats’ water intake,the temperature of anus,the rate of keratinocytes vaginal epithelial cells,the uterine coefficient and a variety of serum hormone level were all observed.
作者：
Jinhong Liu;GuoZuo Xiong;DuanFang Liao;Qinhui Tuo
期刊：
African Journal of Pharmacy and Pharmacology,2013年7(19):1144-1147 ISSN：1996-0816
作者机构：
[Jinhong Liu; GuoZuo Xiong; DuanFang Liao; Qinhui Tuo] Learning Key Laboratory for Pharmacoproteomics,School of Life Science and Technology,University of South China;[Jinhong Liu; GuoZuo Xiong; DuanFang Liao; Qinhui Tuo] Department of General Surgery,The Second Affiliated Hospital in University of South China;[Jinhong Liu; GuoZuo Xiong; DuanFang Liao; Qinhui Tuo] Department of Traditional Chinese Diagnotics,School of Pharmacy,Hunan University of Chinese Medicine
会议名称：
第11届全国脂质与脂蛋白学术会议
会议时间：
2012-09-21
会议地点：
太原
会议论文集名称：
第11届全国脂质与脂蛋白学术会议论文集
摘要：
Death domain-associated protein (Daxx) was originally identiï¬ed as a protein that speciï¬cally binds to the death domain of the transmembrane death receptor Fas (also called CD95) in the cytoplasm and potentiates Fas-induced apoptosis. Over expression of Daxx enhances Fas-mediated apoptosis and activates the Jun N-terminal kinase (JNK) pathway. Daxx was found in the nuclears where it localizes to promyelocytic leukaemia (PML) oncogenic domains (PODs). As a highly conserved nuclear protein, Daxx plays an important role in proapoptosis, antiapoptosis and transcriptional regulation. This article reviews the latest advances in the study of the biological function of Daxx.
