Shanglong Yao

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (29)49.73 Total impact

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    ABSTRACT: A variety of inflammatory mediators and effector cells participate together in acute lung injury, and lead to secondary injury that is due to an inflammatory cascade and secondary diffuse lung parenchyma injury. Inflammation is associated with an oxidative stress reaction, which is produced in the development of airway inflammation, and which has positive feedback on inflammation itself. Resolvin D1 can reduce the infiltration of neutrophils, regulate cytokine levels and reduce the inflammation reaction, and thereby promote the resolution of inflammation. The purpose of this study is to investigate the effects of resolvin D1 on an inflammatory response and oxidative stress during lipopolysaccharide (LPS)-induced acute lung injury. LPS (3 mg/kg) was used to induce the acute lung injury model. Pretreatment resolvin D1 (100 ng/mouse) was given to mice 30 minutes before inducing acute lung injury. Mice were observed at 6 hours, 12 hours, 1 day, 2 days, 3 days, 4 days and 7 days after LPS was administrated, then they were humanely sacrificed. We collected bronchoalveolar lavage fluid (BALF) and the lung tissues for further analysis. Paraffin section and HE staining of the lung tissues were made for histopathology observations. Parts of the lung tissues were evaluated for wet-to-dry (W/D) weight ratio. tumor necrosis factor (TNF)-α, inter leukin (IL)-1β, IL-10 and myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA). A lipid peroxidation malondialdehyde (MDA) assay kit was used to detect MDA. A total superoxide dismutase assay kit with WST-1 was used to analyze superoxide dismutase (SOD). We determined the apoptosis of neutrophils by Flow Cytometry. A real-time quantitative PCR Detecting System detected the expression of mRNA for heme oxygenase (HO)-1. Pretreatment with resolvin D1 reduced the pathological damage in the lung, decreased the recruitment of neutrophils and stimulated their apoptosis. It markedly decreased the expressions of TNF-α, IL-1β and increased the expressions of IL-10, and decreased the production of MDA and increased the expressions of SOD. The mRNA expression of HO-1 was also significantly increased. Resolvin D1 displays potent anti-inflammatory actions by regulating cytokines, inhibiting aberrant neutrophil recruitment and stimulating apoptosis of neutrophils. Resolvin D1 can also relieve the injury due to oxidative stress. The mechanisms might be related to increase HO-1 expression.
    Chinese medical journal 03/2014; 127(5):803-9. · 0.90 Impact Factor
  • You Shang, Shanglong Yao
    Chinese medical journal 03/2014; 127(5):801-2. · 0.90 Impact Factor
  • Chinese medical journal 03/2014; 127(5):968-70. · 0.90 Impact Factor
  • Lin Chen, You Shang, Shanglong Yao
    Zhonghua wei zhong bing ji jiu yi xue. 02/2014; 26(2):126-8.
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    ABSTRACT: The varicella zoster virus (VZV) ORF4 protein, one of immediate-early genes protein, is associated with the tegument in purified virions. ORF4 protein functions at both transcriptional and post-transcriptional levels, present during different phase of whole VZV life cycle. ORF4 protein acts as a nucleocytoplasm shuttle protein, the precise nuclear location signals (NLS) and molecular mechanisms of nucleocytoplasm transport are not elucidated. At this study, we constructed a series of mutants, used fluorescence microscopy and Co-IP analysis to identify an unconventional bipartite NLS ((130)RKHRDRSLSNRRRRP(144)) in VZV ORF4. This study also demonstrates that nuclear import of VZV ORF4 occurs via a Ran-dependent pathway with importin-α5 and importin-β1. Additionally, NLS function of ORF4 is independent from VZV ORF62 protein. ORF62 protein cannot influence the intracellular distribution of ORF4 protein without NLS. So interaction between ORF4 and ORF62 protein is speculated to occur in nucleus. Thus, NLS is indispensable for the post-transcriptional function of ORF4.
    Virus Genes 01/2014; · 1.77 Impact Factor
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    ABSTRACT: The activation of astrocytes contributes to inflammatory responses underlying brain injury and neurodegenerative diseases. Lipoxins have emerged as mediators of endogenous anti-inflammatory events. However, the involvement of aspirin-triggered-lipoxin A4 (ATL) in astrocyte-induced neuroinflammatory responses has not been investigated. Here, we examined the anti-inflammatory effects of ATL in the central nervous system using rat astrocyte cultures stimulated with lipopolysaccharide (LPS). We found that pretreatment with ATL exerted potent anti-inflammatory effects by inhibiting LPS-induced production of nitric oxide and prostaglandin E2. ATL also reduced the expression of cyclooxygenase 2 and inducible nitric oxide synthase mRNA and protein. Furthermore, ATL suppressed the LPS-induced translocation of the NF-κB p65 subunit to the nucleus and prevented LPS-induced IκBα phosphorylation in a dose-dependent manner. These findings suggest that ATL attenuates neuroinflammation by inhibiting the NF-κB signal transducer pathway in cultured cortical astrocytes.
    International immunopharmacology 01/2014; 18(1):85–89. · 2.21 Impact Factor
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    ABSTRACT: Mechanical ventilation can cause structural and functional disturbances in the lung termed ventilator-induced lung injury (VILI). The aim of this study was to evaluate whether BML-111, a lipoxin receptor agonist, could attenuate VILI. Following induction of anesthesia and tracheostomy, Sprague-Dawley rats were ventilated with low tidal volume (6ml/kg, LVT) or high tidal volume (20ml/kg, HVT) for 4 hr. Some rats subjected to HVT ventilation received BML-111 or vehicle (saline) by intraperitoneally injection. Some rats subjected to HVT and BML-111(1mg/kg) received BOC-2 (a FPR2/ALX antagonist) by intraperitoneally 30 min before BML-111. Sham rats were tracheotomized without ventilation. Treatment with BML-111 attenuated VILI, as evidenced by improved oxygenation and reduced histological injury compared to HVT induced lung injury. BML-111 decreased indices of inflammation such as interleukin (IL)-1β, IL-6, tumor necrosis factor-α and bronchoalveolar lavage neutrophil infiltration. Administration with BML-111 suppressed the decrement of the NF-κB inhibitor IκB-α, diminished NF-κB activation, and reduced activation of MAPK in VILI. This study indicates that BML-111 attenuated VILI via a NF-κB and MAPK dependent mechanism. BML-111 may be a promising strategy for alleviation of VILI in patients subjected to mechanical ventilation.
    Shock (Augusta, Ga.) 12/2013; · 2.87 Impact Factor
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    ABSTRACT: Trigeminal neuralgia is the worst pain that human beings have ever experienced. Few researches have illustrated perioperative pain in patients with trigeminal neuralgia undergoing radiofrequency thermocoagulation (RFT) of the gasserian ganglion under local anesthesia. Because there are some undeniable drawbacks of using intravenous short-term anesthesia during the intervention repeatedly, some physicians keep patients awake throughout the puncture procedure, using local anesthesia. The purpose of this investigation was to examine perioperative pain in patients with trigeminal neuralgia undergoing RFT of the gasserian ganglion. Participants were 104 patients with classic trigeminal neuralgia. Worst pain intensity, mean pain intensity, quality of sleep, and analgesia satisfaction were evaluated for 24 hours before admission, 24 hours before operation, and 24 hours after operation. Intraoperative worst pain intensity was determined. Preoperative pain was serious, and preoperative sleep quality significantly and positively correlated with preoperative mean pain (r = 0.52; P = 0.00) and worst pain (r = 0.49; P = 0.00). Few patients (1.9%) responded to preoperative treatment, and the preoperative treatment obtained low analgesia satisfaction scores (3.9 [1.3]). Most patients experienced severe pain during cannulation under local anesthesia. No patients complained of pain during radiofrequency lesioning. The RFT of the gasserian ganglion alleviated pain obviously. Most patients (94.2%) responded to the operation, and the operation got high analgesia satisfaction scores (8.9 [0.7]). The results demonstrate that preoperative pain in patients with trigeminal neuralgia undergoing RFT of the gasserian ganglion is prevalent and undertreated and that intraoperative pain is severe under local anesthesia during cannulation.
    The Journal of craniofacial surgery 07/2013; 24(4):1298-1302. · 0.81 Impact Factor
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    ABSTRACT: Prolonged exposure to an opioid induces hyperalgesia and tolerance, which negatively affect pain management in turn and significantly hamper the application of opioids. A growing body of evidence has demonstrated that glial activation contributes to the development of these two side effects. Recent studies have demonstrated that morphine, binding to an accessory protein of Toll-like receptor 4 (TLR4), activates microglia and produces neuroinflammation in a manner parallel to lipopolysaccharide. Meanwhile, lipopolysaccharide activates microglia through TLR4/caspase signalling. Therefore, we hypothesise that morphine may activate microglia through TLR4/caspase signalling and that caspase inhibitors may attenuate opioid-induced hyperalgesia and tolerance via inhibiting microglial activation and neuroinflammation.
    Iranian Journal of Medical Hypotheses and Ideas 07/2013; 7(2):31–34.
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    Ping Gui, Qingping Wu, Jing Wu, Shanglong Yao
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    ABSTRACT: To investigate the efficacy of esmolol in protecting the myocardium from ischemia during pediatric cardiac surgery. Esmolol, an ultra-short acting beta 1-adrenoceptor blocker, reduces myocardial injury in adult cardiac operations. However, this technique is rarely used in pediatric cardiac surgery. Thirty children with ventricular septal defect were randomly allocated to the esmolol group and the control group. Patients received intravenous esmolol (0.05 mg·kg(-1) ·min(-1) after tracheal intubation, 0.3 mg·kg(-1) ·min(-1) during cardiopulmonary bypass (CPB) and 0.03-0.05 mg·kg(-1) ·min(-1) until the end of surgery) or placebo, respectively. Plasma levels of creatine kinase-MB, cardiac troponin I in the esmolol group 2 min after completion of CPB, at the end of surgery, 4 h after surgery, and the first postoperative day were significantly lower than those in the control group. Values of heart rate 10 min after induction, 2 min before institution of CPB, 2 min after completion of CPB, and at the end of surgery were significantly lower in the esmolol group; however, mean arterial pressure, CPB time, cross-clamp time, and the rate of heart spontaneous rebeating were not statistically different between two groups. Cumulative postoperative dosage of dopamine in the esmolol group (100.1 ± 53.1 mg) was significantly less than that in the control group (171.4 ± 92.1 mg). Esmolol can protect the myocardium from ischemic injury during CPB in children and significantly reduce the use of inotropic drug.
    Pediatric Anesthesia 03/2013; 23(3):217-21. · 2.44 Impact Factor
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    ABSTRACT: Trigeminal neuralgia is the worst pain that human beings have ever experienced. Surgery might be the only solution for some patients because no other way can relieve their severe pain. They experience intolerable pain before operation and during radiofrequency thermocoagulation of the gasserian ganglion. The aim of the current study was to prospectively evaluate the preoperative and perioperative analgesic effects of preoperative single peripheral nerve block. Sixty patients with classic trigeminal neuralgia who were scheduled to undergo radiofrequency thermocoagulation of the gasserian ganglion were randomly divided into a control group (n = 30) and a nerve block group (n = 30). Patients in the nerve block group were treated with single peripheral nerve block using 1% lidocaine and betamethasone on the day of admission. Average pain, worst pain, quality of sleep, and analgesia satisfaction were evaluated before surgery. The incidence and intensity of perioperative episodic pain were determined before the needle reached the gasserian ganglion. Compared with the control group, a single peripheral nerve block significantly attenuated average pain (P < 0.01) and worst pain (P < 0.01), ameliorated the quality of sleep (P < 0.01), and increased analgesia satisfaction (P < 0.01). Moreover, patients in the nerve block group experienced a decrease in incidence (P < 0.01) and intensity (P < 0.01) of episodic pain during surgery as compared with the participants in the control group. These results demonstrate that a single peripheral nerve block may be an effective way to relieve preoperative and perioperative intolerable pain of trigeminal neuralgia.
    The Journal of craniofacial surgery 03/2013; 24(2):479-82. · 0.81 Impact Factor
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    ABSTRACT: Tight Junctions (TJ) are important components of paracellular pathways, and their destruction enhances vascular permeability. Resolvin D1 (RvD1) is a novel lipid mediator that has treatment effects on inflammatory diseases, but its effect on inflammation induced increase in vascular permeability is unclear. To understand whether RvD1 counteracts the lipopolysaccharide (LPS) induced increase in vascular cell permeability, we investigated the effects of RvD1 on endothelial barrier permeability and tight junction reorganization and expression in the presence or absence of LPS stimulation in cultured Human Vascular Endothelial Cells (HUVECs). Our results showed that RvD1 decreased LPS-induced increased in cellular permeability and inhibited the LPS-induced redistribution of zo-1, occludin, and F-actin in HUVECs. Moreover, RvD1 attenuated the expression of I κ B α in LPS-induced HUVECs. The NF- κ B inhibitor PDTC enhanced the protective effects of RvD1 on restoration of occludin rather than zo-1 expression in LPS-stimulated HUVECs. By contrast, the ERK1/2 inhibitor PD98059 had no effect on LPS-induced alterations in zo-1 and occludin protein expressions in HUVECs. Our data indicate that RvD1 protects against impairment of endothelial barrier function induced by LPS through upregulating the expression of TJ proteins in HUVECs, which involves the I κ B α pathway but not the ERK1/2 signaling.
    Oxidative Medicine and Cellular Longevity 01/2013; 2013:185715.
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    ABSTRACT: BACKGROUND: This prospective study compared the safety, recovery time and side effects of six distinct general anesthesia regimens for first-trimester surgical abortion. STUDY DESIGN: Two hundred forty women scheduled for surgical abortion at 6 to 8 weeks of gestation were randomized into three groups (n=40) of propofol: group P (2 mg/kg propofol alone), group PF (2 mg/kg propofol+1 mcg/kg fentanyl), group PMF (2 mg/kg propofol+1 mcg/kg fentanyl+0.02 mg/kg midazolam) and three groups (n=40) of etomidate: group E (0.2 mg/kg etomidate alone), group EF (0.2 mg/kg etomidate+1 mcg/kg fentanyl) and group EMF (0.2 mg/kg etomidate+1 mcg/kg fentanyl+0.02 mg/kg midazolam). Vital signs including pulse oxygen saturation (SpO(2)), mean arterial pressure (MAP) and heart rate were recorded as the primary outcomes. The recovery time and side effects were recorded as secondary outcomes. RESULTS: During induction, SpO(2) and MAP decreased significantly in all the three groups of propofol and were significantly lower than those in the groups of etomidate. Mean recovery times to both eye opening and to obeying commands were significantly shorter in group PF than those in groups P and PMF, while there were no significant differences among the three groups of etomidate. Compared with the etomidate groups, the incidence of injection-induced pain was significantly higher, while the scores of myoclonus and postoperative nausea and vomiting were lower, in the three propofol groups. Moreover, myoclonus scores as well as nausea and vomiting scores were lower in group EMF than in groups E and EF. CONCLUSIONS: The results of this study suggest that (a) etomidate is much safer than propofol for first-trimester surgical abortions and (b) using a lower dose of etomidate, supplemented with fentanyl and midazolam, is more beneficial than the use of etomidate with or without fentanyl in reducing adverse effects like myoclonus and postoperative nausea and vomiting.
    Contraception 09/2012; · 3.09 Impact Factor
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    ABSTRACT: Lipoxins have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on neuroinflammation has not been investigated. Microglia is the major cells involved in brain tissue damage during infection and neurodegenerative diseases. One of the major features shared by neuroinflammation conditions is the increased production of reactive oxygen species (ROS) generated by NADPH oxidase activation. In this study, we have examined whether aspirin-triggered lipoxin A(4) (ATL) modulates ROS generation in BV2 cells. Pre-treatment of BV2 cells with ATL blocked ROS production triggered by LPS in the time-dependent and concentration-dependent manner. ATL inhibited the translocation of the cytoplasmic NADPH oxidase subunit p47(phox) to the cell membrane as well as NADPH oxidase activity. Taken together, these results demonstrate that ATL suppresses NADPH oxidase-mediated ROS generation in BV2 microglia cells, strongly indicating that ATL may play an important role against the development and progression of neuroinflammtion.
    Neurochemical Research 05/2012; 37(8):1690-6. · 2.13 Impact Factor
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    Yizhong Huang, Wuyunerdeni, Shanglong Yao
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    ABSTRACT: The US11 protein of herpes simplex virus type 1 (HSV-1) is a small, highly basic phosphoprotein expressed at late times during infection. To date, the function of US11 protein in cell culture and animal models is poorly understood. To further investigate the function of the US11 protein, this study was undertaken to express the US11 protein and raise a polyclonal antibody. The US11 gene was cloned into the prokaryotic expression vector pET-32a (+) to express His-tagged US11 protein in Escherichia coli. After purification by nickel affinity chromatography and refolding, the recombinant protein was used to raise the anti-US11 polyclonal antibody. Western blot analysis demonstrated that the US11 protein was specifically recognized by the polyclonal antibody, and immunofluorescent assay also showed that the antibody was able to probe the US11 protein in the cells infected with HSV-1. In the present study, we obtained a high-level expression of the recombinant US11 protein as well as high titers of rabbit polyclonal antibody specially against US11 protein in HSV-1 infected cells. This special polyclonal antibody provides a good tool for further studying structural and functional characterization of HSV-1 US11 protein.
    Virology Journal 10/2011; 8:490. · 2.09 Impact Factor
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    ABSTRACT: Despite the rising incidence and high rate of treatment failure of ventilator-associated pneumonia (VAP) due to methicillin-resistant Staphylococcus aureus (MRSA), to date there has been no rat model specifically designed for antimicrobial evaluation. β-Defensin-3 Acronym for β-defensin-3 is correct as (BD-3) is an antimicrobial peptide and mainly expresses in the gastrointestinal and respiratory tract. It demonstrates a broad spectrum of potent antimicrobial activity against many potentially pathogenic microbes, including multi-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus faecium. Therefore, the authors hypothesized that the expression of BD-3 might change in lungs of rats with MRSA VAP, and this change might play an important role in the pathogenesis of VAP. Eighty specific pathogen-free male Sprague-Dawley rats were randomly assigned to the following experimental groups: (1) N (nonventilated pneumonia) group (n=34): rats were infected intrabronchially with 0.2 mL of 10(10) cfu/mL MRSA inoculum; (2)V (ventilator-associated pneumonia) group (n=34): rats were ventilated for 4 h using the protective ventilation settings: 6 mL/kg tidal volume, 5 cm H(2)O of positive end-expiratory pressure (PEEP), 88 breaths/min, and F(i)O(2)=0.21. After ventilation, rats were inoculated intrabronchially with the same amount of MRSA as in N group; (3) P (protective mechanical ventilation) group (n=6): 0.2 mL of normal saline was instilled into lungs of rats after 4 h of ventilation as in V group; (4) C (control) group (n=6): only 0.2 mL of normal saline were instilled into lungs of rats. Rats from both P and C groups were killed 48 h after instillation of normal saline. Rats from other two groups were killed 3, 6, 12, 24, 48 h after inoculation. Pneumonia evaluation was performed by macroscopic, histopathologic, and microbiologic criteria. The expression of BD-3 in lungs was determined by immunohistochemistry staining and Western blot analysis. Rats inoculated after 4 h of protective mechanical ventilation rapidly developed progressive pneumonia with heterogeneous distribution of lesions and different degrees of histologic evolution predominating in lower lobes. Lung bacterial concentrations in V group at each time point were significantly higher than those of N group. It was 12.2±0.9log(10) cfu/g of tissue at h 48 in V group, and 8.7±0.4 in N group. Bacteremia occurred in nine of 10 rats at h 48 in V group, while two of 10 rats in N group. Both C and P groups showed a very low level of BD-3. Compared with C group, the expression of BD-3 at h 48 in both N and V groups significantly increased. However, the latter was significantly lower than the former. Rat model of MRSA VAP was obtained by intrabronchially inoculating rats with 2×10(9) cfu MRSA after 4h of protective mechanical ventilation. VAP was more severe than nonventilated pneumonia in terms of histopathologic and microbiologic criteria, especially systemic spread. This may be associated with the inhibited up-regulation of BD-3 expression by mechanical ventilation.
    Journal of Surgical Research 08/2011; 169(2):277-83. · 2.02 Impact Factor
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    ABSTRACT: Whether limb ischemic preconditioning (LIPC) is beneficial for patients undergoing mitral valve replacement (MVR) surgery is unknown. Seventy-five adult patients undergoing MVR surgery were randomly assigned to 3 groups: control group (n=25), LIPC group I (3 × 5-min cycles of right upper arm ischemia and 5-min reperfusion; n=25) and LIPC group II (3 × 5-min cycles of right upper arm ischemia and 5-min reperfusion combined with 2 × 10-min cycles of right upper leg ischemia and 10-min reperfusion; n=25). Cardiopulmonary bypass (CPB) time, cross-clamp time, cardiac index, cumulative postoperative dosage of dobutamine, intensive care stay, postoperative hospital stay were not statistically different. Although the cumulative postoperative dosage of dobutamine was not different, there was a significantly lower inotropic requirement in LIPC II compared with the control group at 4 and 8h after surgery. Plasma levels of cardiac troponin-I in the 3 groups significantly increased during CPB and peaked at 4h after surgery. Levels of cTnI in LIPC II were significantly lower than in the control group at each time point after surgery. Myocardial injury is obvious after MVR surgery. LIPC can protect the myocardium from ischemia-reperfusion injury and decrease the inotropic requirement after surgery. The data also confirmed the requirement for the preconditioning stimulus to cross a threshold.
    Circulation Journal 06/2011; 75(8):1885-9. · 3.58 Impact Factor
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    ABSTRACT: Inflammation and pulmonary injury caused by mechanical ventilation is a complex process in which long pentraxin 3 (PTX3) is suggested to play an important role. The effect of mechanical stretch on PTX3 mRNA and protein expression in human alveolar epithelial cells (A549) was investigated. Immortalized A549 cells were exposed to tightly controlled and physiologically relevant cyclic mechanical stretch. A549 cells grown on collagen I BioFlex plates were exposed to square cyclic stretch at 0.3 Hz using the Flexercell system with 6% or 20% elongation of cells. In another group, cells were pretreated with small interfering RNA directed against PTX3 before stretch. After stretching, conditioned media and cells were collected and analyzed by Western blotting. Real-time PCR of cDNA generated from the stretched cells was performed. Apoptosis and viability of the cells following treatment were assessed using standard procedures. Mechanical cyclic stretch of 20% elongation led to increased PTX3 gene expression, increased release of PTX3 protein, and induced apoptosis and necrosis in A549 cells. Expression of PTX3 highly correlated with the severity of apoptosis. However, the results suggest that PTX3 expression was significantly reduced by pretreatment of the A549 cells with small interfering RNA of PTX3. PTX3 may be an important mediator of lung tissue damage associated with mechanical stretch. Determining the production and regulation of PTX3 during mechanical ventilation may be critical in preventing or reducing ventilator-induced lung injury.
    Medical science monitor: international medical journal of experimental and clinical research 05/2009; 15(5):BR135-40. · 1.22 Impact Factor
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    ABSTRACT: Erythropoietin (EPO) elicits protective effects in lung ischemia-reperfusion, hyperoxia, acute necrotizing pancreatitis, and some other tissues. In the present study, we investigated the possible protective roles of EPO in the lipopolysaccharide (LPS) induced lung injury. Male Sprague-Dawley rats were treated with EPO (3000 U/kg, i.p.) or vehicle (saline), 30 min prior to LPS administration (6 mg/kg, i.v.). Four h following LPS injection, samples of pulmonary tissue were collected. Optical microscopy was performed to examine pathological changes in lungs. Validated methods were used to measure wet/dry ratios (W/D), myeloperoxidase (MPO) activity, malondialdehyde (MDA) concentrations, and nitrite/nitrate (NO(2)(-)/NO(3)(-)) levels in lungs. Western blotting was performed to study the pulmonary expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine protein. Pretreatment with EPO led to (1) significant attenuation of endotoxemia induced evident lung histologic injury and edema; (2) inhibition of LPS mediated induction in MPO activity and MDA concentration; (3) inhibition of LPS mediated overproduction of pulmonary NO(2)(-)/NO(3)(-) levels; and (4) marked suppression in endotoxin induced expression of iNOS and nitrotyrosine. This study provides considerable evidence that EPO has an ability to significantly attenuate endotoxin-induced acute lung injury in rats.
    Journal of Surgical Research 12/2008; 155(1):104-10. · 2.02 Impact Factor
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    ABSTRACT: Accumulating evidence shows that angiotensin II (ANG II) can be generated locally in the lung tissue and may have autocrine and/or paracrine actions on the cellular level. In addition, ANG II precursor, angiotensinogen, as well as ANG II type 1 receptor (AT(1)), are also expressed in the lung tissue. Recent studies revealed that ANG II promoted acute lung injury induced by acid aspiration or sepsis, and that ANG II receptor blockade had a protective effect against acute lung injury. Therefore, the authors hypothesized that ventilator-induced lung injury might also be exacerbated by local ANG II action, and that ANG II receptor blockade would protect the lung from ventilator-induced lung injury. Forty Sprague Dawley rats weighing 300-350 g were randomly divided into the following experimental groups (10 rats in each group): (1) control group: rats were unventilated; (2) LVT (low volume ventilation) group: rats were ventilated with 8 mL/kg tidal volume room air for 2 h; (3) HVT (high volume ventilation) group: rats were ventilated with 40 mL/kg tidal volume room air for 2 h; (4) HVT + Losartan group: rats were pretreated with Losartan (30 mg/kg, i.p.) prior to high volume ventilation. The samples of pulmonary tissue and lung lavage fluid were collected after experiments. The expression of angiotensinogen and AT(1) receptor mRNA in lung tissue was measured by reverse transcriptase-polymerase chain reaction. Apoptosis of the lung cells was assayed with terminal deoxynucleodityl transferase-mediated nick-end labeling method. Lung pathological changes were examined with optical microscopy. Total protein, wet/dry ratios (W/D), myeloperoxidase (MPO) activity, and neutrophil counts of the lung tissue or lavage fluid were measured with corresponding methods. Compared with control or LVT, HVT caused significant ventilator-induced lung injury and increased the expression of angiotensinogen and AT(1) receptor mRNA in the lung. Total protein, the number of apoptotic cells, W/D ratio, MPO activity, and neutrophil counts were significantly higher in the HVT group than in the LVT or control group. Pretreatment with Losartan attenuated ventilator-induced lung injury and prevented the increase in total protein, the number of apoptotic cells, W/D ratio, MPO, and neutrophil counts caused by high volume ventilation. Our study indicates that HVT causes remarkable lung injury and up-regulates angiotensinogen and AT(1) receptor expression of in the lung, and that Losartan, a selective inhibitor of subtype AT(1) receptors for angiotensin II, can relieve acute lung injury caused by high volume ventilation.
    Journal of Surgical Research 04/2008; 145(1):25-32. · 2.02 Impact Factor

Publication Stats

159 Citations
49.73 Total Impact Points


  • 2004–2014
    • Huazhong University of Science and Technology
      • Department of Anesthesiology
      Wu-han-shih, Hubei, China
  • 2008
    • Wuhan Union Hospital
      Wu-han-shih, Hubei, China
  • 2006
    • Southeast University (China)
      Nan-ching-hsü, Jiangxi Sheng, China