检索结果-南通市图书馆

TLR4 signaling induced TLR2.expression in the process of mimic cerebral ischemia/reperfusion in vitro

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

中国科学：生命科学英文版 2010年第2期53卷 223-228页

作者： SUN Peng1,ZHANG Qing2.HAN JiYuan1,TIAN Yuan3 & ZHANG JingHui3 1department of Emergency,union hospital,{2.,huazhong university of Science and technology,wuhan 43002..china 2.0} of Anesthesia,union hospital,{2.,huazhong university of Science and technology,wuhan 43002..china 3department of General Surgery,union hospital,{2.,huazhong university of Science and technology,wuhan 43002..china 1. department of Emergency Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China2. Department of Anesthesia Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China3. Department of General Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

Both TLR4 and TLR2.participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia/***,it still remains unclear whether a crosstalk exists between TLR2.and TLR4 in ischemic cerebral *** the present study,we investigated the effect of TLR4 signaling on TLR2.expression during mimic cerebral I/R in ***-2.cells were cultured and treated with ischemia/reperfusion,then transfected with the plasmid pEGFP-H1/TLR4-siRNA,the plasmid pEGFP-H1/control sequence-siRNA and the blank plasmid,***,the expression of TLR2.and TLR4 mRNA and protein,NF-κB p65 mRNA and supernatant TNF-α level were significantly higher in ischemia/reperfusion treated cells than those lack of ischemia/reperfusion treatment,and as compared with those in ischemia/reperfusion treated cells without transfection,no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1/control sequence-siRNA transfected cells respectively,while the expression levels in the plasmid pEGFP-H1/TLR4-siRNA transfected cells were significantly ***,in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC),an NF-κB inhibitor,on the TLR4-induced TLR2.expression in BV-2.cells treated with ischemia/reperfusion,it was found that TLR4 and TLR2.mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated *** data suggested that TLR2.activation,signaled by TLR4 and regulated by NF-κB,might be directly involved play an important role in ischemia/reperfusion induced brain damage.

关键词： Toll-like receptor 4 Toll-like receptor 2 cerebral ischemia/reperfusion microglia

NMDA and AMPA receptors mediate intracellular calcium increase in rat cortical astrocytes

在线全文

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2004年第6期25卷 12-18页

作者： Bo HU, Sheng-gang SUN2. E-tang TONGNeurology department, union hospital, {2. college, huazhong university of Science and technology, wuhan 430022. china Neurology department Union Hospital Tongji College Huazhong University of Science and Technology Wuhan 430022 China

AIM: To study the effect of glutamate on the intracellular calcium signal of pure cultured rat astrocytes and the roleof N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) re-ceptors in the procedure. METHODS: The fluorescence of calcium was measured by Fura-2.AM (F345/F380).RESULTS: L-Glutamate induced [Ca2.]i increase in most of the cells in concentration- and time-dependent *** 50 mmol/L induced the fluorescence increase by almost three to four times, while the effect of AMPA 50mmol/L was just half of that of D-(-)-2.amino-5-phosphonopentanoic acid (D-AP-5; a selective antagonist of theNMDA receptor). 6-Cyano-7-nitroquinoxaline-2.3-dione (CNQX, a selective antagonist of the AMPA receptor)abolished the effects of NMDA and AMPA, respectively. D-AP-5 and CNQX simultaneously or respectively attenu-ated the effect of L-glutamate at different degrees, but could not abolish it entirely. CONCLUSION: Glutamatemodulated intracellular Ca2. of pure cultured rat astrocytes through different pathways. The activation of NMDAand AMPA receptors took part in the complex mechanisms.

关键词： glutamate astrocytes NMDA receptors AMPA receptors calcium

Hyaluronic acid fragments evoke Kupffer cells via TLR4 signaling pathway

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Science china(Life Sciences) 2009年第2期52卷 147-154页

Kupffer cells, expressing toll-like receptor 4 (TLR4), play a central role in hepatic ischemia/reperfusion (I/R) injury. Hyaluronic acid (HA) fragments, degradative products of high-molecular-weight HA (HMW-HA), acquire the ability to activate immune cells under inflammatory conditions. Here we inves- tigated whether HA fragments could activate Kupffer cells and analyzed the underlying mechanism. Kupffer cells were isolated from wild-type mice (WT, C3H/HeN) and TLR4 mutant mice (C3H/HeJ) and HA fragments were produced by the methods of enzyme digestion and chromatography. Then Kupffer cells were stimulated by HA fragments or other control stimuli. The activation of Kupffer cells was estimated as the release of pro-inflammatory cytokines. The activation of p38 MAPK pathway of Kupffer cells was checked and blocking experiments were done as well. The results indicated that HA fragments acquired the ability to activate Kupffer cells in vitro, which was TLR4 dependent and not due to contamination of lipopolysaccharide. Experiments of p38 MAPK kinase inhibition by SB-2.3580 verified p38 MAPK was required in HA fragments induced Kupffer cells activation. This suggests that HA fragments, degradative products of one of the major glycosaminoglycans of the extracellular matrix, play critical roles in Kupffer cell activation mediated by TLR4 signaling pathway, which is, at least partially, de- pendent on p38 MAPK activation.

关键词： Kupffer cells hyaluronic acid fragments toll-like receptor 4 p38 MAPK lipoplysaccharide reperfusion injury liver

Expression and signifi cance of TLR4 and HIF-1α in pancreatic ductal adenocarcinoma

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2010年第23期16卷 2881-2888页

作者： Jian-Jun Zhang,He-Shui Wu,Lin Wang,Yuan Tian,Jing-Hui Zhang,Hai-Long Wu department of Pancreatic Surgery,union hospital,{2.,huazhong university of Science and technology,wuhan 430022.Hubei Province,china department of Pediatrics,union hospital,{2.,huazhong university of Science and technology,wuhan 430022.Hubei Province,china Laboratory of General Surgery,union hospital,{2.,huazhong university of Science and technology,wuhan 430022.Hubei Province,china department of Pancreatic Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 Hubei Province China. heshuiwu@***

AIM:To investigate the expression of toll-like receptor(TLR) 4,nuclear factor-κB(NF-κB) p65 and hypoxiainducible transcription factor 1α(HIF-1α) in pancreatic ductal adenocarcinoma and their clinical ***:The mRNA of TLR4 and HIF-1α were investigated by real-time polymerase chain reaction in 30 cases of pancreatic ductal adenocarcinoma and its adjacent tissues,and expression of TLR4,NF-κB p65 and HIF-1α protein were detected by immunohistochemistry in 65 cases of pancreatic ductal adenocarcinoma tissues and 38 cases of corresponding adjacent *** relationship between TLR4 or HIF-1α and pathologic features,as well as the association between TLR4 and HIF-1α,were also ***-Meier method was used to assess the impact of expression of TLR4 and HIF-1α on survival of patients with pancreatic ***:The relative quantif ication of TLR4 and HIF-1α mRNA in tumor tissues was 0.81±0.10 and 0.87±0.11,respectively,signif icantly higher than that in adjacent tissues(0.81±0.10 vs 0.70±0.16,P=0.002.0.87±0.11 vs 0.68±0.13,P=0.000).The protein expression of TLR4,NF-κB p65 and HIF-1α in tumor tissues was 69.2.%,66.15% and 70.80%,respectively,being signif icantly higher than that in adjacent normal tissues(69.2.% vs 39.50%,P=0.003;66.15% vs 31.58%,P=0.001;70.80% vs 36.80%,P=0.001).There was no signif icant correlation between TLR4 or HIF-1α expression and the age,gender,tumor location,the degree of tumor differentiation in the patients(P>0.05).However,there was signif icant correlation between the expression of TLR4 or HIF-1α and tumor size,lymph node metastasis,venous invasion and clinical staging(P4 and HIF-1α had a signif icant impact on survival of patients with pancreatic ***:TLR4,NF-κB p65 and HIF-1α are overexpressed in pancreatic adenocarcinoma,TLR4 may be partly involved in up-regulating HIF-1α,and both synergestically promote development of pancreatic adenocarcinoma.

关键词： Pancreatic ductal adenocarcinoma Toll-like receptor 4 Nuclear factor-κB p65 Hypoxia-inducible factor 1

Antioxidative effect of propofol during cardiopulmonary bypass in adults

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Acta Pharmacologica Sinica 2004年第3期25卷 80-86页

作者： Shi-hai ZHANG2.Shou-yong WANG,Shang-long YAO department of anesthesiology,{2.,tongji medicalcollege,huazhong universityof Science & technology,wuhan 43002..china department of anesthesiology Union Hospital Tongji Medical College Huazhong University of Science & Technology Wuhan 430022 China

AIM: To investigate the antioxidative potential of propofol (an intravenous anesthetic with a chemical structure similarto phenol-basedfree radicalscavengers suchas vitaminE) during cardiopulmonary bypass(CPB). METHODS: Thirty adult patients referred for elective cardiac procedure with CPB were included and randomly allocated to a propofol group or a control group. Patients in the propofol group received propofol (0.1 mg·kg-1·min-1) intrave- nously for anesthesia maintenance, whereas those allocated to the control group received fentanyl 10 μg/kg intrave- nously and inhaled enflurane (1 %-1.5 %). Blood samples were collected at 7 time points: before the start of CPB, at 30 and 60 min of CPB, at the conclusion of CPB, 10 min after the administration of protamine, and 12.and 2. h after the cessation of CPB. Plasma levels of free F2.isoprostanes (sensitive markers of free radicals production) and complement C5a were determined by mass-spectrometricassay and enzyme immunoassay, respectively. Neu- trophil adhesion to endothelial cells was observed at ×2.0 magnificationunder a light microscope. RESULTS: Levels of F2.isoprostanes, complement C5a and neutrophil adhesion rate increased significantly during and after CPB in both groups. There were significantly higher levels of F2.isoprostanes, C5a, and more neutrophils adhering to endothelial cells in the control group than those in the propofol group, respectively. CONCLUSION: Cardio- pulmonary bypass is associated with a great production of damaging free radicals. Propofol may be beneficial both as an anesthetic and as a potent free radical scavenger in patients presenting pathologies associated with free radical reactions during CPB.

关键词： propofol cardiopulmonary bypass free radicals F2.isoprostanes complement 5a

Growth-inhibitory Effects of Curcumin on Ovary Cancer Cells and Its Mechanisms

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Journal of huazhong university of Science and {2.(medical Sciences) 2004年第1期24卷 55-58页

作者：郑丽端童强松吴翠环 department of Pathology department of Pediatric Surgery

To study the growth inhibitory effects of curcumin on human ovary cancer A2.80 cells in vitro and its molecular mechanisms, the growth inhibition rates of A2.80 cancer cells, after being treated with 10 μmol/L-50 μmol/L curcumin for 6-2. h, were examined by MTT method. The morphological changes of cancer cells were observed under inversion microscopy. Cellular apoptotic rates were determined by using TUNEL. The protein expression levels of bcl 2. p53 and MDM2.in cancer cells were examined by SP immunohistochemistry. After being treated by various concentrations of curcumin, the growth of cancer cells was inhibited significantly. Some cancer cells presented characteristic morphological changes of apoptosis. The rates of apoptosis were 6.41 % -2..48 % ( P 2.and p53 was decreased, which depended on the action time ( P 2.expression. It was concluded that curcumin could significantly inhibit the growth of ovary cancer cells. The induction of apoptosis by down re gulating the expression of bcl 2.and p53 was probably one of its molecular mechanisms.

关键词： curcumin ovary cancer gene expression apoptosis

Intercellular Adhension Molecule-1 in the Pathogenesis of Heroin-induced Acute Lung Injury in Rats

在线全文

学校读者我要写书评

暂无评论

Journal of huazhong university of Science and {2.(medical Sciences) 2004年第5期24卷 430-432页

作者：周琼白明邹世清 department of Respiratory Diseases Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China department of Withdrawal Liyuan Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430072 China

The expression of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of heroin-induced acute lung injury (ALI) in rats was investigated. The model of ALI was established by intravenous injection of heroin into tail vein in rats. Thirty-six rats were randomly divided into heroin-treated groups (1 h, 2.h, 4 h, 6 h and 2. h) and normal control group. Changes in histopathologic morphology and biological markers of ALI were measured. The expression of ICAM-1 in lung tissue was detected by using immunohistochemistry and RT-PCR. The results showed that the W/D ratio and protein contents in BALF of the heroin-treated groups were significantly higher than that of the control group (P<0.01). The histopathological changes in the lung tissue were more obvious in heroin-treated groups. The ICAM-1 protein and mRNA expression in the lung tissue of heroin-treated groups were significantly increased as compared with that of the control group (P<0.01), and correlated with the ALI parameters in a time-dependent manner. Increasing of ICAM-1 expression was involved in the formation of heroin-induced lung injury. Furthermore, the level of expression was positively correlated with the severity of lung injury.

关键词： heroin acute lung injury intercellular adhesion molecule-1

Effect of Inhalational Anesthetics on Cytotoxicity and Intracellular Calcium Differently in Rat Pheochromocytoma Cells (PC12.

在线全文

学校读者我要写书评

暂无评论

Journal of huazhong university of Science and {2.(medical Sciences) 2008年第1期28卷 104-109页

作者：王秋筠李克忠姚尚龙 department of anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology

Isoflurane, a commonly used inhaled anesthetic, induces apoptosis in rat pheochromocytoma cells （PC12. in a concentration- and time-dependent manner with unknown mechanism. We hypothesized that isoflurane induced apoptosis by causing abnormal calcium release from the endoplasmic reticulum （ER） via activation of inositol 1,4,5-trisphosphate （IP3） receptors. Alzheimer＇s presenilin-1 （PS 1） mutation increased activity of IP3 receptors and therefore rendered cells vulnerable to isoflurane-induced cytotoxicity. Sevoflurane and desflurane had less ability to disrupt intracellular calcium homeostasis and thus being less potent pared the cytotoxic effects of various inhaled to cause cytotoxicity. This study examined and com-anesthetics on PC12.cells transfected with the Alzheimer＇s mutated PS 1 （L2.6V） and the disruption of intracellular calcium homeostasis. PC 12.cells transfected with wild type （WT） and mutated PS 1 （L2.6V） were treated with equivalent of 1 MAC of isoflurane, sevoflurane and desflurane for 12.h. MTT reduction and LDH release assays were performed to evaluate cell viability. Changes of calcium concentration in cytosolic space （[Ca^2.]c） were determined after exposing different types of cells to various inhalational anesthetics. The effects of IP3 receptor antagonist xestospongin C on isoflurane-induced cytotoxicity and calcium release from the ER in L2.6V PC12.cells were also determined. The results showed that isoflurane at 1 MAC for 12.h induced cytoxicity in L2.6V but not WT PC12.cells, which was also associated with greater and faster elevation of peak [Ca^2.]c in L2.6V than in the WT cells. Xestospongin C significantly ameliorated isoflurane cytotoxicity in L2.6V cells, as well as inhibited the calcium release from the ER in L2.6V cells. Sevoflurane and desflurane at equivalent exposure to isoflurane did not induce similar cytotoxicity or elevation of peak [Ca^2.]c in L2.6V PC 12.cells. These results suggested that isoflurane induced cytoxicity by par

关键词： inhalational anesthetics cytotoxicity calcium

Synthesis of cystine C_(60) derivative and its protective effects on hydrogen peroxide-induced apoptosis in PC12.cells

在线全文

学校读者我要写书评

暂无评论

Chinese Chemical Letters 2007年第2期18卷 145-148页

作者： Zhen Hu, Hai Ping Xing, Zhou Zhu, Wei Wang, Wen Chao Guan department of Chemistry, huazhong {2. of Science and technology, wuhan 430074, china department of Neurology, tongji hospital, tongji medical college, wuhan 430030, china [a]department of Chemistry Huazhong University of Science and Technology Wuhan 430074 China [b]department of Neurology Tongji Hospital Tongji Medical College Wuhan 430030 China

Oxidative stress has been considered as a major cause of cellular injuries in a variety of clinical abnormalities, especially prominent in neural diseases. One of the usable ways to prevent the reactive oxygen species (ROS)-mediated cellular injury is dietary or pharmaceutical augmentation of some free radical scavenger. Water-soluble amino-fullerene is a novel compound that behaves as a free radical scavenger with excellent biology consistent. In the present study, we have synthesized and characterized a novel cystine C60 derivative for the first time, and investigated the effects on hydrogen peroxide-induced oxidative stress and apoptotic death in cultured rat pheochromocytoma (PC12. cells. PC12.cells treated with hydrogen peroxide underwent apoptotic death as determined by MTT, PI/Hoechst 33342.staining and flow cytometry analysis. These results suggested that cystine C60 derivative has the potential to prevent oxidative stress-induced cell death and has no evident toxicity.

关键词： Cystine C_(60) derivative Reactive oxygen species H_2._2 Apoptosis PC 12.cells