General Hospital of Chengdu Military Area Command

Chengdu, China

General Hospital of Chengdu Military Area Command

Chengdu, China
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Gong G.,General Hospital of Chengdu Military Area Command | Yuan L.,General Hospital of Chengdu Military Area Command | Cai L.,General Hospital of Chengdu Military Area Command | Ran M.,General Hospital of Chengdu Military Area Command | And 5 more authors.
PLoS ONE | Year: 2014

Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways. Copyright: © 2014 Gong et al.


PubMed | Xijing University and General Hospital of Chengdu Military Area Command
Type: Journal Article | Journal: PloS one | Year: 2014

Tetramethylpyrazine (TMP) has been widely used in China as a drug for the treatment of various diseases. Recent studies have suggested that TMP has a protective effect on ischemic neuronal damage. However, the exact mechanism is still unclear. This study aims to investigate the mechanism of TMP mediated ischemic hippocampal neurons injury induced by oxygen-glucose deprivation (OGD). The effect of TMP on hippocampal neurons viability was detected by MTT assay, LDH release assay and apoptosis rate was measured by flow cytometry. TMP significantly suppressed neuron apoptosis in a concentration-dependent manner. TMP could significantly reduce the elevated levels of connexin32 (Cx32) induced by OGD. Knockdown of Cx32 by siRNA attenuated OGD injury. Moreover, our study showed that viability was increased in siRNA-Cx32-treated-neurons, and neuron apoptosis was suppressed by activating Bcl-2 expression and inhibiting Bax expression. Over expression of Cx32 could decrease neurons viability and increase LDH release. Furthermore, OGD increased phosphorylation of ERK1/2 and p38, whose inhibitors relieved the neuron injury and Cx32 up-regulation. Taken together, TMP can reverse the OGD-induced Cx32 expression and cell apoptosis via the ERK1/2 and p38 MAPK pathways.


Liu D.,General Hospital of Chengdu Military Area Command | Guo M.,General Hospital of Chengdu Military Area Command | Yun M.,General Hospital of Chengdu Military Area Command | Jiao Y.,General Hospital of Chengdu Military Area Command | And 5 more authors.
Scientific Research and Essays | Year: 2011

To investigate the diagnostic sensitivity and specificity of serum and joint fluid citrulline-containing peptide (CCP), variant antibody (anti-CCP antibody) for active rheumatoid arthritis (RA) and to explore their relationship with other clinical inflammatory indicators, the levels of serum and joint fluid anti-CCP antibodies, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and rheumatoid factors (RF) were detected in 104 active RA patients including 68 with knee joint effusion. The sensitivity of serum anti-CCP antibody to RA was 92.3% (96/104) and that of joint fluid anti-CCP antibody was 82.4% (56/68) (P>0.05). The specificity of serum and joint fluid anti-CCP antibody was 100%. There was no significant correlation between anti-CCP antibody and ESR, CRP, score of DAS28, and RF in RA patients positive for serum anti-CCP antibody (P>0.05). After treatment for half month with integrated traditional Chinese and Western medicine, all indicators were improved. The levels of ESR, CRP, RF, score of DAS28 and serum anti-CCP antibody were decreased significantly after treatment when compared with those before treatment (P<0.05). In our study, two patients with early RA (course<2 months) were negative for serum anti-CCP antibody but positive for joint fluid anti-CCP antibody, and seroconversion was noted with the prolongation of disease duration. Combination of serum anti-CCP antibody and joint fluid anti-CCP antibody is helpful for the "early diagnosis" of RA and evaluation of the severity of RA, thus providing basis for the early treatment. The negativity and positivity of anti-CCP antibody are interchangeable under certain conditions. © 2011 Academic Journals.


Gong G.,General Hospital of Chengdu Military Area Command | Bai S.,General Hospital of Chengdu Military Area Command | Wu W.,General Hospital of Chengdu Military Area Command | Hu L.,General Hospital of Chengdu Military Area Command | And 5 more authors.
Journal of Molecular Neuroscience | Year: 2014

Lipopolysaccharide (LPS) preconditioning is a powerful neuroprotective phenomenon by which an injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. The LPS response gene (Lrg) is a recently identified gene in human dental pulp cells treated with LPS. However, the role and mechanism of Lrg in brain ischemia injury have not yet been demonstrated. Here, we sought to determine whether Lrg participates in LPS preconditioning-induced brain ischemia injury. The Lrg protein accumulates in brain tissue after middle cerebral artery occlusion (MCAO). Furthermore, knockdown of Lrg by small interfering RNA (siRNA) significantly increased the infarct size of brain injury. In addition, we investigated the mechanism of Lrg in brain ischemia injury. Lrg-siRNA could regulate inflammatory cytokine expression. Moreover, interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor Kappa B (NF-κB) p65 protein levels were significantly increased by Lrg-siRNA in mice after MCAO. Conversely, interferon regulatory factor 3 (IRF3) protein level was decreased by Lrg-siRNA. Taken together, these results suggest that Lrg regulates the expression of inflammatory cytokines in LPS preconditioning-induced brain ischemia injury via the toll-like receptor 4 (TLR4) signaling pathway. Lrg may therefore serve as a novel therapeutic target for brain ischemia injury. © 2014 Springer Science+Business Media.


Wang R.-J.,Chongqing Medical University | Shen W.-W.,Chongqing Medical University | Huang C.,General Hospital of Chengdu Military Area Command | Liu F.-Z.,Chongqing Medical University | And 4 more authors.
Tumor | Year: 2014

Objective: To investigate the effects of conditioned medium (CM) of lung cancer cell line A549 on the proliferation and oseoclast differentiation of human peripheral blood CD14-positive monocytes, and explore the role of Notch signaling in this process. Methods: CD14-positive monocytes obtained from human peripheral blood were incubated with a-MEM containing macrophage colony-stimulating factor (M-CSF) as the control group. The conditioned medium (CM) of lung cancer cell line A549 was used to incubate CD14-positive monocytes with M-CSF, named as A549 CM group. The Notch pathway blocking agent N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) was used to treat monocytes with A549 CM and M-CSF, named as DAPT group. Receptor activator for nuclear factor-?B ligand (RANKL) was supplied to all groups after 6 d. The expression levels of osteoclast marker genes tartrate-resistant acid phosphatase (TRAP), cathepsin K (CK), calcitonin receptor (CTR) and Notch key target genes hairy and enhancer of split-1 (HES-1) and HES-related with YRPF motif-1 (HEY-1) were measured by real-time fluorescence quantitative PCR. The TRAP staining was used to detect the formation of osteoclast, and the bone resorption was evaluated by scanning electron microscopy. The fluorescent expression of active fragment NICD was determined by immunofluorescence. The proliferation of CD14-positive monocytes was detected by cell counting kit-8 (CCK-8) method. Results: The mRNA expression levels of TRAP, CK and CTR, the number of TRAP+ multinuclear cells and the area of bone resorption, as well as the nuclear fluorescence intensity of NICD in A549 CM group were upregulated as compared with the control group (P < 0.05), and these indexes in DAPT group were down-regulated as compared with A549 CM group, but still higher than those in the control group (P < 0.05). The mRNA expression levels of HES-1 and HEY-1 in A549 CM group were higher than those in DAPT group and the control group (P < 0.05), and no significant difference was found in the latter two groups. The cell proliferation rate of CD14-positive monocytes in A549 CM group was higher than that in the control group (P < 0.05), and which in DAPT group was highest (P < 0.05). Conclusion: The CM of lung cancer A549 cells can promote osteoclast differentiation by activating Notch signaling. Meanwhile, Notch signaling activation can inhibit the proliferation of CD14-positive monocytes. Copyright © 2014 by TUMOR.


Gong G.,General Hospital of Chengdu Military Area Command | Hu L.,General Hospital of Chengdu Military Area Command | Qin F.,General Hospital of Chengdu Military Area Command | Yin L.,General Hospital of Chengdu Military Area Command | And 3 more authors.
Neuroscience Letters | Year: 2016

Background Tremendous experimental and clinical studies identify that remifentanil anesthesia might elicit postoperative opioid-induced hyperalgesia (OIH) and aggravate nociceptive hypersensitivity, whereas definite mechanisms remain equivocal. WNT signaling and fractalkine pathway have been manifested to participate in varieties of pain pathogenesis, respectively, but no report is on whether they could lead to OIH. This study intended to investigate the effect of WNT3a/β-catenin on fractalkine and its receptor CX3CR1 in OIH in rats model of incision pain. Methods A WNT scavenger Fz-8/Fc and a neutralizing antibody against CX3CR1 (anti-CX3CR1) were injected intrathecally after remifentanil infusion. Exogenous WNT agonist delivery was utilized in naïve rats. PWT and PWL were documented for postsurgical 48 h to assess mechanical and thermal hyperalgesia. Also, expressions of WNT3a, FZ1, FZ8, β-catenin, fractalkine and CX3CR1 in spinal dorsal horn were measured by Western blot and RT-qPCR after nociceptive testing. Results We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, β-catenin, fractalkine and CX3CR1 levels. Moreover, OIH was attenuated by intrathecal application of Fz-8/Fc and anti-CX3CR1. Up-regulation of spinal fractalkine and CX3CR1 expression after remifentanil anesthesia was reversed by Fz-8/Fc. Also, WNT agonist administration could directly generate hypernociception and elevate fractalkine/CX3CR1 level in naïve rats, which was prevented by anti-CX3CR1. Conclusion These present findings demonstrated that the involvement of spinal WNT3a/FZ8/β-catenin in OIH through modulating fractalkine/CX3CR1 in rats. © 2016 Elsevier Ireland Ltd


Sun Z.-X.,General Hospital of Chengdu Military Area Command | Zeng W.-Z.,General Hospital of Chengdu Military Area Command
Chinese Journal of Biologicals | Year: 2016

Viral hepatitis C is a globally distributed infectious diseases caused by hepatitis C virus (HCV), most of which is likely to be developed chronic hepatitis C (CHC), cirrhosis and hepatocellular carcinoma (HCC). Nonalcoholic fatty 1 lver disease is a kind of comprehensive chronic liver disease which is not due to alcohol or definite factors but is associated with obesity and insulin resistance. Hepatitis C complicated with NAFLD may accelerate the onset and progress of liver diseases, which is more likely to be develop to chronic hepatitis, cirrhosis and hepatocellular carcinoma. This paper reviews the epidemiology of CHC and NAFLD as well as the interaction, action mechanism, diagnosis and therapy of the two diseases.


PubMed | General Hospital of Chengdu Military Area Command
Type: Journal Article | Journal: Journal of molecular neuroscience : MN | Year: 2014

Lipopolysaccharide (LPS) preconditioning is a powerful neuroprotective phenomenon by which an injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. The LPS response gene (Lrg) is a recently identified gene in human dental pulp cells treated with LPS. However, the role and mechanism of Lrg in brain ischemia injury have not yet been demonstrated. Here, we sought to determine whether Lrg participates in LPS preconditioning-induced brain ischemia injury. The Lrg protein accumulates in brain tissue after middle cerebral artery occlusion (MCAO). Furthermore, knockdown of Lrg by small interfering RNA (siRNA) significantly increased the infarct size of brain injury. In addition, we investigated the mechanism of Lrg in brain ischemia injury. Lrg-siRNA could regulate inflammatory cytokine expression. Moreover, interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor Kappa B (NF-B) p65 protein levels were significantly increased by Lrg-siRNA in mice after MCAO. Conversely, interferon regulatory factor 3 (IRF3) protein level was decreased by Lrg-siRNA. Taken together, these results suggest that Lrg regulates the expression of inflammatory cytokines in LPS preconditioning-induced brain ischemia injury via the toll-like receptor 4 (TLR4) signaling pathway. Lrg may therefore serve as a novel therapeutic target for brain ischemia injury.


To investigate the therapeutic effect of carbon monoxide (CO) on high-altitude hypoxia-induced cardiac damage.Forty male C57BL/6 mice were randomly divided into 4 groups. The mice were exposed to normoxia or simulated 5,500-meter high-altitude hypoxia in a hypobaric chamber for 7 days. During the first 3 days, the mice were pretreated with CO-saturated hemoglobin (Hb)-based oxygen carrier (CO-HBOC), oxygen-saturated hemoglobin-based oxygen carrier (O2-HBOC) at a dose of 0.3 g Hb/kg/day or an equivalent volume of saline. The in vivo left ventricle function, cardiac enzyme release, histopathological changes, apoptosis and inflammation were also measured.High-altitude hypoxia induced significant cardiac damage, as demonstrated by impaired cardiac function and increased proapoptotic, proinflammatory and pro-oxidant markers. Pretreatment with CO-HBOC significantly improved cardiac performance, reduced cardiac enzyme release and limited myocardial apoptosis. The increased inflammatory response was also suppressed. In addition to the preserved mitochondrial structure, hypobaric hypoxia-induced mitochondrial oxidative damage was remarkably attenuated. Moreover, these antiapoptotic and antioxidative effects were accompanied by an upregulated phosphorylation of Akt, ERK and STAT3.This study demonstrated that CO-HBOC provides a promising protective effect on high-altitude hypoxia-induced myocardial injury, which is mediated by the inhibition of inflammation and mitochondrial oxidative damage.

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