|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Effects of Xinfeng capsule on pulmonary function based on treg-mediated notch pathway in a rat model of adjuvant arthritis显示文摘OBJECTIVE:To observe the impact of xinfeng xapsule(XFC) on pulmonary function in a rat model of adjuvant arthritis(AA) and to investigate the mechanism of action.METHODS:Forty rats were randomly divided into four groups of ten:normal control(NC);model control(MC);tripterygium glycosides tablet(TPT);and xinfeng capsule(XFC).Except for the NC group,AA was induced in all rats by intracutaneous injection of 0.1 mL Freund's complete adjuvant in the right paw on the 19th day.NC and MC groups were given(0.9%) physiological saline.The TPT and XFC groups were given TPT(10 mg/kg) and XFC(1.2 g/kg),respectively.Thirty days after administration,changes in paw edema(E),the arthritis index(AI),pulmonary function,levels of regulatory T-cells(Treg),ultrastructure of lung tissue,and expression of Notch receptors and ligands in lung tissue were observed.RESULTS:In the MC group,E and the AI were increased and pulmonary function significantly decreased;the structure of alveolar type-II cells was damaged;ratios of Treg in peripheral blood were reduced;and expression of Notch receptors such as Notch3 and Notch4 and ligands such as Delta1 in lung tissue were significantly increased whereas expression of Notch1,Jagged1 and Jagged2 were significantly decreased.After intervention with XFC,E and the AI were decreased;pulmonary function was enhanced;the structure of alveolar type-II cells was improved;and expression of Treg,Notch1,Jagged1,Jagged2 was elevated,whereas that of Notch3,Notch4 and Delta1 was reduced.CONCLUSION:XFC can not only inhibit E and the AI and improve joint symptoms,it can also improve pulmonary function and reduce inflammation in lung tissue.These actions could be carried out through increases in the expression of Treg,Notch receptors(Notch1) and ligands(Jagged1,Jagged2),and reductions in the expression of Notch3,Notch4 and Delta1.These phenomena would reduce the deposition of immune complexes and the inflammatory response in lung tissue,thereby improving joint symptoms and pulmonary function. | Lei Wan Jian Liu Chuanbing Huang Yuan Wang Xi Shen Wandong Zhang Guizheng Wang Haixia Fan Yao Ge Ruilian Chen Yunxiang Cao Ruikai Zong Li Lei | 2012 | Journal of Traditional Chinese Medicine2012，32，3： | 17 |
| 2 | Use of Xinfeng capsule to treat abarticular pathologic changes in patients with rheumatoid arthritis显示文摘OBJECTIVE: To observe the influence of Xinfengcapsule(XFC) on abarticular pathologic changes(APCs) and other indices of patients with rheumatoid arthritis(RA) and explore the mechanism of action of XFC in improving such changes.METHODS: Three-hundred RA patients were divided randomly into a treatment group(n=150) and control group(n=150). A normal control(NC)group(n=90) was also created. Changes in cardiac function, pulmonary function, anemia indices and platelet parameters of RA patients were measured.Curative effects of the two groups were compared,and comparison carried out with the NC group.RESULTS: In 300 RA patients, late diastolic peak flow velocity(A peak) was much higher(P<0.01)and early diastolic peak flow velocity(E peak), E/A,and left ventricular fraction shortening much lower(P<0.01) than those in the NC group. Vital capacity(VC), forced vital capacity in one second, forced vital capacity(FVC), maximal voluntary ventilation(MVV), maximal expiratory flow in 50% of VC(FEF50) and FEF75 were lowered remarkably(P<0.05 or P<0.01). Platelet count(PLT), plateletcrit(PCT) and mean platelet volume(MPV) increased markedly(P<0.05 or P<0.01), and hemoglobin(Hb)level decreased significantly(P<0.05). After XFC treatment, the A peak and PLT and PCT were much lower(P<0.05), and E/A and the number of red blood cells as well as Hb level were much higher(P<0.05), as were FVC, MVV and FEF50(P<0.05 or P<0.01), in the treatment group than those in the NC group. Total score of pain and swelling in joints,uric-acid level and high-sensitivity C-reactive protein level were much lower, and superoxide dismutase level as well as the number of CD4 +CD25+ regulation T cells(Treg) and CD4+CD25+CD127- Treg were much higher(P<0.05 or P<0.01)in the treatment group than those in the NC group.CONCLUSION: RA patients with pathologic changes in joints also suffer from lower cardiac and pulmonary functions and from parameters of anemia and platelet factors. XFC can improve the symptoms of RA patients, ameliorate their cardiac and pulmonary functions and reduce the parameters of anemia and platelet factors. XFC lowers the immune inflammatory reaction to improve APCs in RA patients. | Jian Liu Yunxiang Cao Chuanbing Huang Yuan Wang Xi Chen Wandong Zhang Guizhen Wang Haixia Fan Yao Ge Ruilian Chen Ruikai Zong Yajun Qi Yue Sun Yifei Liu Fang Wang | 2014 | Journal of Traditional Chinese Medicine2014，34，5： | 10 |
| 3 | IL-17 is associated with poor prognosis and promotes angiogenesis via stimulating VEGF production of cancer cells in colorectal carcinoma显示文摘 | Jiankun Liu Yuzhong Duan Xiaoming Cheng Xi Chen Wei Xie Haixia Long Zhihua Lin Bo Zhu | 2011 | Biochemical and Biophysical Research Communications2011，，2： | 2 |
| 4 | 2021 Chinese consensus on the diagnosis and management of primary immune thrombocytopenia in pregnancy显示文摘Immune thrombocytopenia(ITP)is an acquired disease characterized by isolated thrombocytopenia,which is one of the most common causes of thrombocytopenia during pregnancy.Women with ITP who have severe thrombocytopenia are at an increased risk for life-threatening obstetric complications.Therefore,we established this consensus statement on the diagnosis and management of ITP during pregnancy(detailed information is available in the Supplementary File,http://gffzz16e312a87a7141a5hkxvwxnwfpp5x6qqx.ffgz.tsg.suse.edu.cn/A978). | Zhang Xiaohui Chen Fangping Chen Xiequn Cheng Yunfeng Fang Meiyun Feng Jianming Fu Haixia Gao Hong Han Yue He Aili Hou Ming Hu Yu Huang Ruibin Huang Wenrong Jing Zhicheng Kong Peiyan Liang Aibin Liang Meiying Liu Daihong Liu Junling Liu Lin Liu Xiaowei Ma Liangming Mei Heng Ni Heyu Niu Ting Peng Jun Qiao Jianlin Ren Jinhai Song Yongping Tang Liang V Tong Tong Wang Shaoyuan Wang Xin Wang Zhao Wei Hui Wu Depei Wu Guangsheng Xu Caigang Xu Xue Xu Yajing Yang Linhua Yang Renchi Yang Tonghua Yin Chenghong Yu Li Zhang Guangsen Zhang Lei Zhang Liansheng Zhang Xi Zhao Weili Zhao Yongqiang Zhou Daobin Zhou Hu Zhou Zeping Zhu Tienan Wang Jianliu Huang Xiaojun | 2022 | Chinese Medical Journal2022，，8： | 2 |
| 5 | CUL4B facilitates HBV replication by promoting HBx stabilization显示文摘Objective:Hepatitis B virus(HBV)infection is a major public health problem worldwide.However,the regulatory mechanisms underlying HBV replication remain unclear.Cullin 4 B-RING ubiquitin E3 ligase(CRL4 B)is involved in regulating diverse physiological and pathophysiological processes.In our study,we aimed to explain the role of CUL4 B in HBV infection.Methods:Cul4 b transgenic mice or conditional knockout mice,as well as liver cell lines with CUL4 B overexpression or knockdown,were used to assess the role of CUL4 B in HBV replication.Immunoprecipitation assays and immunofluorescence staining were performed to study the interaction between CUL4 B and HBx.Cycloheximide chase assays and in vivo ubiquitination assays were performed to evaluate the half-life and the ubiquitination status of HBx.Results:The hydrodynamics-based hepatitis B model in Cul4 b transgenic or conditional knockout mice indicated that CUL4 B promoted HBV replication(P<0.05).Moreover,the overexpression or knockdown system in human liver cell lines validated that CUL4 B increased HBV replication in an HBx-dependent manner.Importantly,immunoprecipitation assays and immunofluorescence staining showed an interaction between CUL4 B and HBx.Furthermore,CUL4 B upregulated HBx protein levels by inhibiting HBx ubiquitination and proteasomal degradation(P<0.05).Finally,a positive correlation between CUL4 B expression and HBV pg RNA level was observed in liver tissues from HBV-positive patients and HBV transgenic mice.Conclusions:CUL4 B enhances HBV replication by interacting with HBx and disrupting its ubiquitin-dependent proteasomal degradation.CUL4 B may therefore be a potential target for anti-HBV therapy. | Haixia Shan Bo Wang Xiaodong Zhang Hui Song Xi Li Yongxin Zou Baichun Jiang Huili Hu Hao Dou Changshun Shao Lifen Gao Chunhong Ma Xiaoyun Yang Xiaohong Liang Yaoqin Gong | 2022 | Cancer Biology & Medicine2022，19，1： | 2 |
| 6 | IL-17 is associated with poor prognosis and promotes angiogenesis via stimulating VEGF production of cancer cells in colorectal carcinoma显示文摘 | Jiankun Liu Yuzhong Duan Xiaoming Cheng Xi Chen Wei Xie Haixia Long Zhihua Lin Bo Zhu | 2011 | Biochemical and Biophysical Research Communications2011，，2： | 1 |
| 7 | The development of 4m HTS power cable显示文摘 | Hou Bo Xi Haixia Yuan Feng | 2004 | Superconductivity Science Technology2004，，17： | 1 |
| 8 | CYP2S1 is a synthetic lethal target in BRAFV600E-driven thyroid cancers显示文摘BRAF^(V600E)is the most common genetic alteration and has become a major therapeutic target in thyroid cancers;however,intrinsic feedback mechanism limited clinical use of BRAF^(V600E)specific inhibitors.Synthetic lethal is a kind of interaction between two genes,where only simultaneously perturbing both of the genes can lead to lethality.Here,we identified CYP2S1 as a synthetic lethal partner of BRAF^(V600E)in thyroid cancers.First,we found that CYP2S1 was highly expressed in papillary thyroid cancers(PTCs)compared to normal thyroid tissues,particularly in conventional PTCs(CPTCs)and tall-cell PTCs(TCPTCs),and its expression was positively associated with BRAFV600E mutation.CYP2S1 knockdown selectively inhibited cell proliferation,migration,invasion and tumorigenic potential in nude mice,and promoted cell apoptosis in BRAFV600E mutated thyroid cancer cells,but not in BRAF wildtype ones.Mechanistically,BRAF^(V600E)-mediated MAPK/ERK cascade upregulated CYP2S1 expression by an AHR-dependent pathway,while CYP2S1 in turn enhanced transcriptional activity of AHR through its metabolites.This AHR/CYP2S1 feedback loop strongly amplified oncogenic role of BRAF^(V600E)in thyroid cancer cells,thereby causing synthetic lethal interaction between CYP2S1 and BRA^(FV600E).Finally,we demonstrated CYP2S1 as a potential therapeutic target in both BRAF^(V600E)-drived xenograft and transgenic mouse models by targetedly delivering CYP2S1-specific siRNA.Altogether,our data demonstrate CYP2S1 as a synthetic lethal partner of BRAFV600E in thyroid cancers,and indicate that targeting CYP2S1 will provide a new therapeutic strategy for BRAFV600E mutated thyroid cancers. | Yiqi Li Xi Su Chao Feng Siyu Liu Haixia Guan Yue Sun Nongyue He Meiju Ji Peng Hou | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 0 |
| 9 | ISOLATION AND EXPANSION OF HUMAN EMBRYONIC NEURAL STEM/PROGENITOR CELLS IN VITRO显示文摘Objective:To isolate, culture and identify human embryonic neural stem cells and to establish a practical passaging method.Method:The cerebral cortex cells were isolated from aborted embryos (11~13 weeks) by mechanical dissociation,and cultured in DMEM/F12 culture medium supplemented with N2 and growth factors for proliferation. Upon passaging, the neurospheres were pipetted gentlely to separate them into several cell masses and then grown in growth medium. The cells were grown in DMEM/F12 medium with serum (without growth factors) to induce differentiation. The stem cell, neuron, astrocyte and oligodendrocyte were identified by immunocytochemistry with antibodies to vimentin, MAP 2, GFAP and GalC, respectively. Results:The primary cells grew together and formed neurospheres at 5 th ~7 th day. They were all vimentin positive and could be passaged for at least 8 passages. After passaging, the cell masses grew up and formed new neurospheres rapidly.These cells could differentiated into MAP 2(+),GFAP(+) or GalC(+) cells.Conclusion:The neural stem cells from human embryonic cerebral cortex have the capacity of proliferation and multi-differentiation in vitro. The passaging methods we used in this experiment were practical and convenient. | Lu Haixia,Song Tusheng,Zhai Wei 1,Li Minjie,Kang Qianyan,Liu Yong The Research Center of Neuroscience in Xi’an Jiaotong University Medical School, Xi’an 710061$$$$ | 2002 | 中国现代医学杂志2002，12，23： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员