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Effects of anisodamine on the expressions of vascular endothelial growth factor and intercellular adhesion molecule 1 in experimental infusion phlebitis

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Chinese Medical Journal 2012年第2期125卷 300-305页

作者： Zhang Zhen-xiang Wang Peng Zhang Qiu-shi Pan Xue Zhao Qing-xia Wang Xiao-kai Zhengzhou Univ Coll Nursing Zhengzhou 450052 Henan Peoples R China

Background Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis.This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor （VEGF） and intercellular adhesion molecule 1 （ICAM-1） in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.Methods Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group,the model group,the magnesium sulfate group and the anisodamine group.The rabbit model of infusion phlebitis,induced by intravenous administration,was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline.We evaluated expression by histopathology,immunohistochemistry,reverse transcription-polymerase chain reaction,and Western blotting assay.Results Pathohistological changes of the model group were observed,such as loss of venous endothelial cells,inflammatory cell infiltration,edema and thrombus.The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion,inflammatory cell infiltration,proliferation,swelling of endothelium and perivascular hemorrhage.The model group showed the highest expressions of VEGF and ICAM-1 of the four groups （P〈0.01）.On the contrary,anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group （P 〈0.01）.There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group （P 〉0.05）.Conclusion Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1,and shows significant protective effects

关键词： anisodamine infusion phlebitis vascular endothelial growth factor intercellular adhesion molecule 1

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Inhibiting phosphatase and actin regulator 1 expression is neuroprotective in the context of traumatic brain injury

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Neural Regeneration Research 2023年第7期18卷 1578-1583页

作者： Yao Jing Lin Zhang Shi-Wen Chen Yan Guo Shi-Ming Ju Fang Yuan Hao Chen Dian-Xu Yang Heng-Li Tian Zhi-Ming Xu Jun Ding Department of Neurosurgery Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina

Studies have found that the phosphatase actin regulatory factor 1 expression can be related to stroke,but it remains unclear whether changes in phosphatase actin regulatory factor 1 expression also play a role in traumatic brain injury.In this study we found that,in a mouse model of traumatic brain injury induced by controlled cortical impact,phosphatase actin regulatory factor 1 expression is increased in endothelial cells,neurons,astrocytes,and microglia.When we overexpressed phosphatase actin regulatory factor 1 by injection an adeno-associated virus vector into the contused area in the traumatic brain injury mice,the water content of the brain tissue increased.However,when phosphatase actin regulatory factor 1 was knocked down,the water content decreased.We also found that inhibiting phosphatase actin regulatory factor 1 expression regulated the nuclear factor kappa B signaling pathway,decreased blood-brain barrier permeability,reduced aquaporin 4 and intercellular adhesion molecule 1 expression,inhibited neuroinflammation,and neuronal apoptosis,thereby improving neurological function.The findings from this study indicate that phosphatase actin regulatory factor 1 may be a potential therapeutic target for traumatic brain injury.

关键词： apoptosis aquaporin 4 blood brain barrier intercellular adhesion molecule 1 neuroinflammation nuclear factor kappa B occludin phosphatase and actin regulator-1 traumatic brain injury zonula occludens 1

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Effect of Methyl-CpG Binding Domain Protein 2(MBD2) on AMD-like Lesions in ApoE-Deficient Mice

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2014年第3期34卷 408-414页

作者：潘俊如王琛余其林张述李斌胡军 Department of Ophthalmology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China The Center for Biomedical Research Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

Summary： The role of methyl-CpG binding domain protein 2 （MBD2） in an ApoE-deficient mouse model of age-related macular degeneration （AMD） was investigated. Eight-week-old Mbd2/ApoE double deficient （Mbd2^-/- ApoE^-/-） mice （n=12, 24 eyes, experimental group） and MBD2 （wt） ApoE^-/- mice （n=12, 24 eyes, control group） were fed on Western-type diet for 4 months. The mice were sacrificed, and total serum cholesterol levels were analyzed and Bruch＇s membrane （BM） of the eyes was removed for ultrastructural observation by transmission electron microscopy. Moreover, intercellular adhesion molecule 1 （ICAM-1） immunoreactivities were evaluated by fluorescence microscopy in sections of the eyes in both groups for further understanding the function mechanism of MBD2. There was no significant difference in the total serum cholesterol levels between control group and experimental group （P〉0.05）. Transmission electron microscopy revealed that AMD-like lesions, various vacuoles accumulated on BM, notable outer collagenous layer deposits and dilated basal infoldings of retinal pigment epithelium （RPE） were seen in both groups, and the BM in control group was significantly thickened as compared with experimental group （P〈0.05）. Fluorescence micrographs exhibited the expression of ICAM-1 in choroid was higher in control group than in experimental group. We are led to conclude that MBD2 gene knockout may lead to accumulation of more deposits on the BM and influence the pathogenesis of AMD via triggering endothelial activation and inflammatory response in choroid, improving microcirculation, and reducing lipid deposition so as to inhibit the development of AMD-like lesions. Our study helps to provide a new therapeutic approach for the clinical treatment of AMD.

关键词： methyl-CpG binding domain protein 2 aged-related macular degeneration endothelial dysfunction intercellular adhesion molecule 1

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Orosomucoid-like protein 3,rhinovirus and asthma

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World Journal of Critical Care Medicine 2021年第5期10卷 170-182页

作者： You-Ming Zhang Section of Genomic and Environmental Medicine National Heart and Lung InstituteMolecular Genetics GroupDivision of Respiratory SciencesImperial College LondonLondon SW36LYUnited Kingdom

The genetic variants of orosomucoid-like protein 3(ORMDL3)gene are associated with highly significant increases in the number of human rhinovirus(HRV)-induced wheezing episodes in children.Recent investigations have been focused on the mechanisms of ORMDL3 in rhinovirus infection for asthma and asthma exacerbations.ORMDL3 not only regulates major human rhinovirus receptor intercellular adhesion molecule 1 expression,but also plays pivotal roles in viral infection through metabolisms of ceramide and sphingosine-1-phosphate,endoplasmic reticulum(ER)stress,ER-Golgi interface and glycolysis.Research on the roles of ORMDL3 in HRV infection will lead us to identify new biomarkers and novel therapeutic targets in childhood asthma and viral induced asthma exacerbations.

关键词： Asthma intercellular adhesion molecule 1 Orosomucoid-like protein 3 Rhinovirus infection Sphingolipids

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