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    26 June 2016, Volume 6 Issue 3 Previous Issue    Next Issue

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    Study of Teratogenicity and Inhibition of Motor Function of Histamine in Development of Zebrafish Larvae
    HUANG Shu-bing,WANG Lin-fang,XU Yi-da,CUI Chun,SHEN Yan-qin
    2016, 6 (3):  1-7.  DOI: 10.3969/j.issn.2095-1396.2016.03.001
    Abstract ( 1210 )   PDF (5480KB) ( 513 )  
    Objective: To investigate the effects of histamine in water environment on the development of zebrafish larvae and its locomotor function. Methods: Newborn fertilized embryos of zebrafish were incubated and fed in gradient concentration of histamine solution (histamine concentrations were 0, 1.25, 2.5, 5, 10 and 20 mmol•L-1, respectively, 0 mmol•L-1 group as blank group). The hatching rate of zebrafish embryos and deformity rate of zebrafish larvae were calculated on the 3 day post-fertiliaztion (dpf) and 4 dpf respectively. The photos of deformed morphology of zebrafish larvae were collected at 4 dpf. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of histamine H1R, H2R and H3R type receptors. Swimming tracing was used to detect the motor function of non-deformed zebrafish larvae in 0, 5 and 20 mmol•L-1 group. Results:The aberration rate of zebrafish larvae increased with the higher concentration of histamine in water while the hatching rate was not affected in each group. Histamine treatment in water induced abnormal development of heart as well as body abnormalities of curving and short tail during the development of zebrafish larvae. Compared to the blank group, the motor function of zebrafish larvae in 5 and 20 mmol•L-1 group was significantly inhibited (P <0.01). The expression of H2R and H3R receptors in 5 and 20 mmol•L-1 was significantly decreased (P < 0.01 or P < 0.001). Conclusion: Histamine treatment in water environment leads to deformation of zebrafish larvae during development and inhibits motor function of larvae.
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    Maternal High Fat Diet Facilitation The Pressor Effect Of Male Offsprings To Angiotensin II
    FANG Zhi-qin, WANG Ya-ling, PENG Wei
    2016, 6 (3):  8-16.  DOI: 10.3969/j.issn.2095-1396.2016.03.002
    Abstract ( 637 )   PDF (1305KB) ( 279 )  
    Objective: To verify maternal rat high fat diet by up-regulating brain renin-angiotensin-system (RAS) to add the sensitivity of adult offspring to angiotensin II (Ang II), facilitation of Ang II induced hypertension. Methods: Adult female SD rats were randomly divided into high fat diet group and standard group, and healthy adult male mating, high fat diet group at 4 weeks before pregnancy, pregnancy and lactation were high fat diet, normal diet group were fed with normal diet in each period, all offspring were divided into two groups: high-fat diet group offspring (OHH) and normal diet group (OCC), the offspring of all offspring were the standard diet after weaning. Measure birth weight of offspring, 3 weeks of age to detect brain the RAS components in lamina terminalise (LT) and paraventricular nucleus (PVN). At 10 weeks of age, the sensitivity of the central nervous system to Ang II was detected in the cerebral ventricle, and the pressor response was observed in Ang II. Results: High fat diet increased the expression of RAS in the brain than the normal diet group, more sensitive pressor effection to intraventricular injection Ang II, and more obvious pressor response to the chronic perfusion Ang II, and the expression of RAS was significantly increased after perfusion. Conclusion: Maternal high fat diet increased the sensitivity of the central nervous system to angiotensin II (Ang II), and facilitated the hypertension induced by Ang II, by means of raising the expression of the ranin-angiotensin-aldosterone-system (RAAS).
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    Chronic Ulcerative Colitis Model Induced by Oxazolone and 2,4,6-Trinitrobenzene Sulfonic Acid in Mice
    SONG Xiao-min, ZHUANG Zhong-bao, ZHANG Hai-wei, SU Xiao-mei, ZHAO Kai-yan, ZHANG Li
    2016, 6 (3):  17-23.  DOI: 10.3969/j.issn.2095-1396.2016.03.003
    Abstract ( 663 )   PDF (6168KB) ( 337 )  
    Objective: To establish the chronic ulcerative colitis model induced by oxazolone and 2,4,6-trinitrobenzene sulfonic acid together in mice. Methods: 24 healthy male Kunming (KM) mice were randomly divided into two groups: normal control group (N group, n=12), model group (group M, n=12). The mice were treated with OXZ and TNBS according to a certain cycle induction method by rectally administration, and the mental state, and the condition of the fur color, eating and defecation were recorded every day, and the disease activity index (disease activity index, DAI) was detected every day as well. Three mice were killed in N group and M group respectively every week, which was recorded N1, N2, N3, N4, M1, M2, M3 and M4 group after the modeling cycle. Meanwhile the colon was separated out, and the CMDI and the CI was determined. The level of the IL-4 and TNF-α detected in Immunohistochemical technique was confirmed. Results: The scores of normal mice were stable, and the scores of M1, M2, M3 and M4 model group were significantly higher than those of normal group. Conclusion: The chronic ulcerative colitis model induced by oxazolone and 2,4,6-trinitrobenzene sulfonic acid together in mice was established successfully. Its pathological characteristics are closer to the human chronic ulcerative colitis and can be kept for a month at least.
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    Advances of Nrf 2/ARE Signaling Pathway in the Major Depression Disorder
    WANG Sha-sha,ZHANG Zhao,ZHANG Mei-jin,HU Jin-feng,CHEN Nai-hong
    2016, 6 (3):  32-37.  DOI: 10.3969/j.issn.2095-1396.2016.03.005
    Abstract ( 746 )   PDF (6438KB) ( 359 )  
    Major depression disorder is a seriously psychological disease,which was characterized by oxidative stress and inflammation in pathogenesis. Oxidative stress and inflammatory response can be induced by excessive activation of the sympathetic nerve and hypothalamic pituitary adrenal axis,which would increase the level of glucocorticoid significantly in depression individuals. Nrf2/ARE signaling pathway is the main antioxidant signaling pathway,Nrf2 as a transcription factor,can be combined with ARE in the nuclear and induce antioxidant enzymes expression. Previous studies showed that Nrf2 -/-  mice with typical symptoms of depression,while treated with anti-infl ammatory drugs alleviate it signifi cantly,suggesting that the immune infl ammatory was involved in depression caused by Nrf2 deletion. This article will review the role of Nrf2 mediated oxidative stress and immune inflammation in depression,and provided the theoretical basis for Nrf2/ARE signaling pathway as a novel target for antidepressant development.
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    The Progress of Transient Receptor Potential Channels in Metabolic Syndrome
    GAO Yuan-yuan, GUO Chun-yan
    2016, 6 (3):  38-43.  DOI: 10.3969/j.issn.2095-1396.2016.03.006
    Abstract ( 579 )   PDF (936KB) ( 346 )  
    The transient receptor potential (TRP) channel superfamily is composed of more than 30 nonselective cation channels. TRP channels are grouped into 7 subfamilies. TRP channel subunits contain six hydrophobic stretches and a putative amino and carboxyl terminal pore area on the cytoplasmic side. Various subtypes play an important role in the metabolic syndrome. Protein,fat,carbohydrates-related metabolic disorders can cause a series of disease,such as obesity, hypertension, diabetes, atherosclerosis, bone and mineral disorders, electrolyte disturbances, inflammatory reaction and cancer. This paper reviews the development and the role of TRP channels in the metabolic syndrome.
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    Advances in Research Methods of Blood—Brain Barrier Transporters
    CHEN Jian,HOU Hong-wei,LIU Yong,WANG An,HU Qing-yuan
    2016, 6 (3):  44-55.  DOI: 10.3969/j.issn.2095-1396.2016.03.007
    Abstract ( 606 )   PDF (13537KB) ( 256 )  
    Blood—brain barrier (BBB) has been acknowledged as junction with dynamic and highly organized feature between brain and blood. It plays an important role in preventing free passage of solutes and protecting the central nervous system (CNS) by isolating it from the periphery. The abnormal function of it may speed up the deterioration of several neurological diseases. Its function abnormality precedes or accelerates the deterioration of some nervous system diseases. The study of transporters of blood brain barrier is intended to provide a theoretical evidence for analyzing the function of BBB, exploring the pathogenesis of nervous system disease and promoting the development of brain targeted drug. In this article, the blood brain barrier transporter classification and function, blood brain barrier model and transporter research methods are summarized to provide references for drug development, improving target activity and drug interaction.
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    A Review on the Role of Microglia in Diabetic Neuropathic Pain
    HONG Li-mian, JIN Gui-lin, CHU Mei-mei, YU Chang-xi
    2016, 6 (3):  56-64.  DOI: 10.3969/j.issn.2095-1396.2016.03.008
    Abstract ( 699 )   PDF (964KB) ( 259 )  
    Diabetic neuropathic pain (DNP) is one of the common chronic complications in patients with diabetes mellitus. Because of the complexity of its pathogenesis,the e xact causes of DNP are still unclear. In recent years,the role of microglia in DNP is concerned by researchers. In this review,we discussed the physiological and pathological characteristics of microglia. In addition,the related receptors and signaling pathways of microglia under DNP
    condition were also reviewed. These insights provide a basis for new therapeutic approaches.
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