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	1. Caspase-3 involved in aluminum-induced impairment of long-term potentiation in rats in vivo through Akt/GSK-3β pathway
	Zhang Huifang,Yang Xiaojuan,Qin Xiujun,Niu Qiao
	Preventive Medicine and Hygienics 15 September 2015
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	Abstract:Amount of studies have indicated that aluminum exposure could impair learning and memory function in human population and animal models. The ability of Al to inhibit hippocampal long-term potentiation (LTP) ,which is one of phenomena underlying synaptic plasticity, hints possibility of Al impairing synaptic plasticity. LTP is dependent on the insertion (exocytosis) of AMPA receptors to synaptic membrane, Akt/GSK-3β signaling pathway has been demonstrated to mediate AMPAR delivery in the hippocampus and LTP, and a mechanism that caspase-3 can cleave Akt is involved in synaptic plasticity, but the underlying molecular mechanism among them is still not elucidated. To investigate the mechanism of LTP impairment and related signal pathway variations induced by Al exposure, SD rats were randomly distributed into 6 groups and treated intracerebroventricularly injection with Al(mal)3 and caspase-3 inhibitor z-DEVD-fmk at different doses, protein levels of active caspase-3, Akt and GSK-3β were also detected. Al treatment produced dose-dependent suppression of LTP and dose-dependent decreases of AMPAR subunits GluR1 and GluR2 in the membrane extracts and the total extracts. The AMPA receptor proteins were degraded and trafficking of AMPA receptor subunits to synaptic membrane sites during HFS-induced LTP was suppressed. Al administration caused a increased accumulation of active caspase-3 and a gradual decrease of Akt and p-GSK-3β. Interestingly, at the same time z-DEVD-fmk significantly reversed both the Al induced increase of active caspase-3 and suppression of LTP. Furthermore, z-DEVD-fmk also reversed the decrease of the protein content of GluR1 and GluR2 in both the total and membrane- enriched extracts. More importantly, z-DEVD- fmk effectively reversed Al induced decrease of Akt and p-GSK-3β. Taken all the results together, Al depressed LTP and AMPAR contents, while z-DEVD-fmk reversed Al-induced LTP depression, increase of active caspase-3, decrese of AMPAR contents, and decrease of Akt and p-GSK-3β. Our findings clarified the underlying mechanism between Al-induced LTP impairment and related signal pathways, ie. activation of casapse-3 - cleavage of Akt -reduction of phosphorylation of GSK-3β- activation of GSK-3β- internalization of AMPAR - inhibiton of externalization of AMPAR, and finally impairment of LTP.
	TO cite this article:Zhang Huifang,Yang Xiaojuan,Qin Xiujun, et al. Caspase-3 involved in aluminum-induced impairment of long-term potentiation in rats in vivo through Akt/GSK-3β pathway[OL].[15 September 2015] http://en.paper.edu.cn/en_releasepaper/content/4654938


	2. Effects of Atrazine on the Proliferation and Cytotoxicity of Murine Lymphocytes with the use of Carboxyfluorescein Succinimidyl Ester-based Flow Cytometric Approaches
	Chen Jinyao,Huo Jiao,Jia Zhenchao,Song yang,Li Yan,Zhang Lishi
	Preventive Medicine and Hygienics 14 November 2014
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	Abstract:Atrazine (ATZ) is one of the most commonly applied herbicides worldwide. ATZ has been associated with adverse effects on the immune system; however, the mechanism of its immunotoxicity has not been completely elucidated. In this study, the immunotoxic effects of ATZ on murine splenic lymphocytes and magnetic bead-enriched NK cells were investigated in vitro with the use of carboxyfluorescein succinimidyl ester (CFDA-SE)-based flow cytometric approaches. Proliferation responses, NK cell activity, and T-cell early activation were determined with CFDA-SE loading, CFDA-SE/propidium iodide (PI) staining, and CD69+ expression, respectively. Cell apoptosis/cycle, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were evaluated using PI, 2',7'-dichlorodihydrofluorescein diacetate, and rhodamine 123, respectively. The intracellular expressions of apoptosis-related Bcl-2 and caspase-3 were analyzed through intracellular staining and flow cytometry. Results showed that proliferation and NK cell activity were suppressed by ATZ treatment. Such suppression might be associated with the cell apoptosis induced by increased ROS and declined MMP. The underlying mechanism might be the induced caspase-3 expression and decreased Bcl-2 expression. ATZ could elicit immunotoxic effects on murine lymphocytes; its presence in the environment might compromise immune function in organisms. The flow cytometric methods presented in this study should be further investigated in immunotoxicology.
	TO cite this article:Chen Jinyao,Huo Jiao,Jia Zhenchao, et al. Effects of Atrazine on the Proliferation and Cytotoxicity of Murine Lymphocytes with the use of Carboxyfluorescein Succinimidyl Ester-based Flow Cytometric Approaches[OL].[14 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4617659


	3. Effect of Monobutyl phthalate on the expression of GPR30 gene in Sertoli cells
	HU Yang,LU Yuqiu,LI Dongmei,HAN Xiaodong
	Preventive Medicine and Hygienics 26 December 2011
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	Abstract:Recent studies indicated that the rapid and nongenomic action of xenoestrogen may be mediated through the membrane estrogen receptor-G protein-coupled receptor (GPR30). In this study we aimed to explore whether GPR30 is expressed in rat testicular Sertoli cells and the possible effect of monobutyl phthalate (MBP) on the expression of GPR30 in Sertoli cells. By using Rt-PCR, Western-Blot and immunocytochemistry, we assessed the expression of GPR30 in both gene and protein level. Then we examined the change of gene level of GPR30 in Sertoli cells exposed to MBP (0.01-1mM) for24h. The results indicated that GPR30 was expressed in rat testicular Sertoli cells and increased in gene level in Sertoli cells following administration with MBP even at a relative low concentration. We suppose that change of GPR30 expression may play an important role in effect of xenoestrogen MBP on Sertoli cells.
	TO cite this article:HU Yang,LU Yuqiu,LI Dongmei, et al. Effect of Monobutyl phthalate on the expression of GPR30 gene in Sertoli cells[OL].[26 December 2011] http://en.paper.edu.cn/en_releasepaper/content/4457665


	4. Effects of BmKNJX11, a bioactive polypeptide purified from Buthus martensi Karsch, on TTX-R sodium channels in rat dorsal root ganglion neurons
	Xijie Wang,Peng Xu,Shanshan An,Qin Sun,Jie Cheng,Rong Gao,Hang Xiao
	Preventive Medicine and Hygienics 28 July 2009
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	Abstract:BmKNJX11is a 7036.85 Da polypeptide purified from the venom of Asian scorpion Buthus martensi Karsch (BmK). With whole cell recording, BmKNJX11 inhibited tetrodotoxin- resistant voltage-gated sodium channels (TTX-R VGSC) in freshly isolated rat dorsal root ganglion (DRG) neurons in a concentration- and voltage-dependent manner. At a concentration of 40 μg/ml BmKNJX11 increased the activation threshold and produced positive shifting of TTX-R sodium current (INa) activation curve. In addition, BmKNJX11 induced shifting of the steady-state inactivation curve to left, delayed the recovery of TTX-R INa from inactivation, and also reduced the fraction of available sodium channels. These results suggested that BmKNJX11 might exert effects on VGSC by binding to a specific site. Considering that TTX-R VGSC expressed in DRG neurons play a critical role in nociceptive transmission, the interaction of BmKNJX11 with TTX-R VGSC might lead to a change in excitability of nociceptive afferent fibers which may be involved in the observed peripheral pain expression.
	TO cite this article:Xijie Wang,Peng Xu,Shanshan An, et al. Effects of BmKNJX11, a bioactive polypeptide purified from Buthus martensi Karsch, on TTX-R sodium channels in rat dorsal root ganglion neurons[OL].[28 July 2009] http://en.paper.edu.cn/en_releasepaper/content/34118


	5. Up-regulation of RAGE and S100A6 in rats exposed to cigarette smoke
	Zhang Su-ping,Wu Yan-wen,Wu Zhao-zhao,Hai-Yun Liu,Ji-Hua Nie,Tong Jian
	Preventive Medicine and Hygienics 08 January 2009
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	Abstract:Cigarette smoke has been widely investigated in terms of epidemiological and pathological observation in relation to human lung diseases. In this study, we established an animal model exposed to cigarette smoke and looked for the potential molecular mechanisms at the protein level. Wistar rats were exposed to cigarette smoke at concentrations of 20% and 60% as the low and high concentration group. The exposure was conducted twice a day、5 days a week for 43 weeks. As a major metabolite of nicotine in cigarette, cotinine in rat urine was determined by LC-MS. A time-and dose-dependent analysis indicated that the cotinine level may be used as a biomarker of smoke exposure. Expression of receptor for advanced glycation endproducts(RAGE), an immunoglobulin superfamily that triggers the intracellular signal cascade reaction leading to inflammation and its ligand S100A6(calgranulin) in bronchial epithelial cells and lung tissues of rats exposed to cigarette smoke, were found to be correlated with the cotinine level, indicating that RAGE and S100A6 may attribute to the inflammation and oxidative damage caused by cigarette smoke.
	TO cite this article:Zhang Su-ping,Wu Yan-wen,Wu Zhao-zhao, et al. Up-regulation of RAGE and S100A6 in rats exposed to cigarette smoke[OL].[ 8 January 2009] http://en.paper.edu.cn/en_releasepaper/content/27495

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