Shanxi Da Yi Hospital

Taiyuan, China

Shanxi Da Yi Hospital

Taiyuan, China
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Liao H.,Shanxi Provincial Peoples Hospital | Banbury L.,Southern Cross University of Australia | Liang H.,Shanxi Provincial Peoples Hospital | Wang X.,Shanxi Da Yi Hospital | And 3 more authors.
Journal of Traditional Chinese Medicine | Year: 2014

OBJECTIVE: To study the effects of extracts from Honghua (Flos Carthami) on lipopolysaccharide induced nitric oxide (NO) production in RAW 264.7 cells and the influence of the extracts on yeast α-glucosidase activity. The total flavonoid content of the extracts was also determined. METHODS: Cytotoxicity of the extracts to RAW 264.7 cells was evaluated by the ATPlite™ method. Inhibitory effects of the extracts on NO production were evaluated by Griess assay. Curcumin was used as a positive control. Screening of extracts for potential α-glucosidase inhibitors was done by a fluorometric assay. The assay was based on the hydrolysis of 4-methylumbelliferyl-a-D-glucopyranoside to form the fluorescent product, 4-methylumbelliferone. Acarbose was used as a positive control. The total flavonoid content was tested using kaempferol as the standard. RESULTS: There were significant inhibitory effects on NO production when the extracts were 25-100 μg/ mL (P<0.05) and curcumin was 2-4 μg/mL (P< 0.001). The extracts showed an inhibitory effect on α-glucosidase activity at the concentrations of 15.6-125 μg/mL with a half maximal (50%) inhibitory concentration (IC50) of (32.8 ± 5.7) μg/mL, compared with the IC50 of acarbose at (1.8±0.4) μg/mL. There was a significant difference between the two IC50 values (P<0.001). The total content of flavonoids per gram of dried herb was 1.14 mg. CONCLUSION: Honghua (Flos Carthami) showed inhibitory effects on NO production in activated RAW 264.7 macrophage cells and an inhibitory effect on yeast α-glucosidase. There might be a relationship between these pharmacological effects and its flavonoid content. © 2014 JTCM. All rights reserved.


Ren Y.,Shanxi Da Yi Hospital | Jia J.,Shanxi Da Yi Hospital | Sa J.,Shanxi Medical University | Qiu L.-X.,Shanxi Medical University | And 5 more authors.
Chinese Medical Journal | Year: 2017

Background: While depression and certain cardiac biomarkers are associated with acute myocardial infarction (AMI), the relationship between them remains largely unexplored. We examined the association between depressive symptoms and biomarkers in patients with AMI. Methods: We performed a cross-sectional study using data from 103 patients with AMI between March 2013 and September 2014. The levels of depression, N-terminal proB-type natriuretic peptide (NT-proBNP), and troponin I (TnI) were measured at baseline. The patients were divided into two groups: those with depressive symptoms and those without depressive symptoms according to Zung Self-rating Depression Scale (SDS) score. Baseline comparisons between two groups were made using Student’s t-test for continuous variables, Chi-square or Fisher’s exact test for categorical variables, and Wilcoxon test for variables in skewed distribution. Binomial logistic regression and multivariate linear regression were performed to assess the association between depressive symptoms and biomarkers while adjusting for demographic and clinical variables. Results: Patients with depressive symptoms had significantly higher NT-proBNP levels as compared to patients without depressive symptoms (1135.0 [131.5, 2474.0] vs. 384.0 [133.0, 990.0], Z = −2.470, P = 0.013). Depressive symptoms were associated with higher NT-proBNP levels (odds ratio [OR] = 2.348, 95% CI: 1.344 to 4.103, P = 0.003) and higher body mass index (OR = 1.169, 95% confidence interval [CI]: 1.016 to 1.345, P = 0.029). The total SDS score was associated with the NT-proBNP level (β = 0.327, 95% CI: 1.674 to 6.119, P = 0.001) after multivariable adjustment. In particular, NT-proBNP was associated with three of the depressive dimensions, including core depression (β = 0.299, 95% CI: 0.551 to 2.428, P = 0.002), cognitive depression (β = 0.320, 95% CI: 0.476 to 1.811, P = 0.001), and somatic depression (β = 0.333, 95% CI: 0.240 to 0.847, P = 0.001). Neither the overall depressive symptomatology nor the individual depressive dimensions were associated with TnI levels. Conclusions: Depressive symptoms, especially core depression, cognitive depression, and somatic depression, were related to high NT-proBNP levels in patients with AMI. © 2017 Chinese Medical Journal.


Pang M.,Shanxi Medical University | Wang H.,Shanxi Medical University | Bai J.-Z.,University of Auckland | Cao D.,Shanxi Medical University | And 7 more authors.
Experimental Biology and Medicine | Year: 2015

Clara cell protein (CC16) is a well-known anti-inflammatory protein secreted by the epithelial Clara cells of the airways. It is involved in the development of airway inflammatory diseases such as chronic obstructive pulmonary disease and asthma. Previous studies suggest that CC16 gene transfer suppresses expression of interleukin (IL)-8 in bronchial epithelial cells. However, its role in the function of these cells during inflammation is not well understood. In this study, we evaluated the effect of CC16 on the expression of matrix metalloproteinase (MMP)-9 in lipopolysaccharide (LPS)-stimulated rat tracheal epithelial cells and its underlying molecular mechanisms. We generated recombinant rat CC16 protein (rCC16) which was bioactive in inhibiting the activity of phospholipase A2. rCC16 inhibited LPS-induced MMP-9 expression at both mRNA and protein levels in a concentration-dependent (0–2 µg/mL) manner, as demonstrated by real time RT-PCR, ELISA, and zymography assays. Gene transcription and DNA binding studies demonstrated that rCC16 suppressed LPS-induced NF-κB activation and its binding of gene promoters as identified by luciferase reporter and gel mobility shift assays, respectively. Western blotting and immunofluorescence staining analyses further revealed that rCC16 concentration dependently inhibited the effects of LPS on nuclear increase and cytosol reduction of NF-κB, on the phosphorylation and reduction of NF-κB inhibitory IκBα, and on p38 MAPK-dependent NF-κB activation by phosphorylation at Ser276 of its p65 subunit. These data indicate that inhibition of LPS-mediated NF-κB activation by rCC16 involves both translocation- and phosphorylation-dependent signaling pathways. When the tracheal epithelial cells were pretreated with chlorpromazine, an inhibitor of clathrin-mediated endocytosis, cellular uptake of rCC16 and its inhibition of LPS-induced NF-κB nuclear translocation and also MMP-9 production were significantly abolished. Taken together, our data suggest that clathrin-mediated uptake of rCC16 suppresses LPS-mediated inflammatory MMP-9 production through inactivation of NF-κB and p38 MAPK pathways in tracheal epithelial cells. © 2015, by the Society for Experimental Biology and Medicine.


PubMed | University of Auckland, Shanxi Medical University and Shanxi Da Yi Hospital
Type: Journal Article | Journal: Experimental biology and medicine (Maywood, N.J.) | Year: 2015

Clara cell protein (CC16) is a well-known anti-inflammatory protein secreted by the epithelial Clara cells of the airways. It is involved in the development of airway inflammatory diseases such as chronic obstructive pulmonary disease and asthma. Previous studies suggest that CC16 gene transfer suppresses expression of interleukin (IL)-8 in bronchial epithelial cells. However, its role in the function of these cells during inflammation is not well understood. In this study, we evaluated the effect of CC16 on the expression of matrix metalloproteinase (MMP)-9 in lipopolysaccharide (LPS)-stimulated rat tracheal epithelial cells and its underlying molecular mechanisms. We generated recombinant rat CC16 protein (rCC16) which was bioactive in inhibiting the activity of phospholipase A2. rCC16 inhibited LPS-induced MMP-9 expression at both mRNA and protein levels in a concentration-dependent (0-2g/mL) manner, as demonstrated by real time RT-PCR, ELISA, and zymography assays. Gene transcription and DNA binding studies demonstrated that rCC16 suppressed LPS-induced NF-B activation and its binding of gene promoters as identified by luciferase reporter and gel mobility shift assays, respectively. Western blotting and immunofluorescence staining analyses further revealed that rCC16 concentration dependently inhibited the effects of LPS on nuclear increase and cytosol reduction of NF-B, on the phosphorylation and reduction of NF-B inhibitory IB, and on p38 MAPK-dependent NF-B activation by phosphorylation at Ser276 of its p65 subunit. These data indicate that inhibition of LPS-mediated NF-B activation by rCC16 involves both translocation- and phosphorylation-dependent signaling pathways. When the tracheal epithelial cells were pretreated with chlorpromazine, an inhibitor of clathrin-mediated endocytosis, cellular uptake of rCC16 and its inhibition of LPS-induced NF-B nuclear translocation and also MMP-9 production were significantly abolished. Taken together, our data suggest that clathrin-mediated uptake of rCC16 suppresses LPS-mediated inflammatory MMP-9 production through inactivation of NF-B and p38 MAPK pathways in tracheal epithelial cells.


Chen L.,Shanxi Da Yi Hospital | Tong H.,Shanxi Da Yi Hospital | Yang Z.,Shanxi Da Yi Hospital
Journal of Bionanoscience | Year: 2013

Fourth ventricular dystopia tumor is an extremely rare tumor. We are reporting a case of fourth ventricular dystopia tumor in a girl, where total extirpation of the lesion was performed, pertinent literature, regarding on the lesions located in the posterior fossa midline, has been reviewed. The differential diagnosis of Fourth ventricular lesions is discussed. Copyright © 2013 American Scientific Publishers.

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