Biomedical subjects

Shiwen Wang

Publications and source records attributed to Shiwen Wang.

12 recordsLinked to original sources

PubMed2006

A comparison of elderly and adult multiple organ dysfunction syndrome in the rat model.

Multiple organ dysfunction syndrome (MODS) in the elderly is the most common cause of mortality in critically ill elderly patients, and it is different from MODS in the adult in clinic. Rare studies have been done on its pathogenesis and the comparison between adult and elderly MODS animal models. This work aimed at exploring the mechanisms mediating elderly MODS and compared this with adult MODS. Male Sprague-Dawley aged and adult rats were intraperitoneally injected with zymosan for incitement of MODS. Aged rats receiving zymosan showed severer pulmonary, cardiac and renal dysfunctions than adult rats. Likewise, the tissue lesions under light microscope in major organs of zymosan treated aged rats were much worse than those of zymosan treated adult rats. Moreover, zymosan treated aged rats showed 142% and 64% greater increase in pulmonary alveolar macrophages (AMs) apoptotic rate and serum TNF-alpha level, respectively, whereas 43% smaller increase in serum IL-10 level compared to zymosan treated adult rats. Furthermore, lung injury was much worse than that in other organs in zymosan treated aged rats. Overall, these results suggest that zymosan can be used in aged rats to incite MODS in the elderly. In the animal model of elderly MODS, there are (1) severer injury in lung, heart and kidney vs adult; (2) easier to develop severe systemic inflammatory response syndrome (SIRS) instead of compensatory anti-inflammatory response syndrome (CARS) compared to the adult; and (3) severer inflammation in lung than other organs indicative of the possible roles of lung in triggering MODS in the elderly.

Aging↗

PubMed2006

Nicotine prevents the apoptosis induced by menadione in human lung cancer cells.

Approximately 50% of long-term cigarette smokers die prematurely from the adverse effects of smoking, including on lung cancer and other illnesses. Nicotine is a main component in tobacco and has been implicated as a potential factor in the pathogenesis of human lung cancer. However, the mechanism of nicotine action in the development of lung cancer remains largely unknown. In the present study, we designed a nicotine-apoptosis system, by pre-treatment of nicotine making lung cancer cell A549 to be in a physiological nicotine environment, and observed that nicotine promoted cell proliferation and prevented the menadione-induced apoptosis, and exerts its role of anti-apoptosis by shift of apoptotic stage induced by menadione from late apoptotic stage to early apoptotic stage, in which NF-kappaB was up-regulated. Interference analysis of NF-kappaB in A549 cells showed that knock down of NF-kappaB resulted in apoptosis promotion and counteracted the protective effect of nicotine. The findings suggest that nicotine has potential effect in lung cancer genesis, especially in patients with undetectable early tumor development and development of specific NF-kappaB inhibitors would represent a potentially exciting new pharmacotherapy for tobacco-related lung cancer.

Apoptosis↗

PubMed2006

Serum matrix metalloproteinase 9 as a marker for the assessment of severe acute pancreatitis.

Previous studies have shown that matrix metalloproteinase 9 (MMP-9) degrades basement membrane components in inflammation, but the change of serum MMP-9 level in the progression of acute pancreatitis remains unclear. The aim of our study was to assess the value of MMP-9 as a prognostic marker in acute pancreatitis. The prospective study included 10 patients with severe acute pancreatitis (SAP) and 10 patients with mild acute pancreatitis. The study also enrolled 10 healthy individuals as control. The serum MMP-9 level, serum C-reactive protein (CRP) level, serum tumor necrosis factor alpha (TNF-alpha) level and acute physiology and chronic health evaluation (APACHE) II score were measured at 1 hr and 48 hrs after admission. APACHEII scores and serum MMP-9, TNF-alpha and CRP levels were significantly increased in patients with SAP compared to those with mild acute pancreatitis and control subjects at 1 hr after admission (p < 0.01). When the states of illness were improved, the levels of the above-mentioned markers were decreased in patients with SAP at 48 hrs after admission (1 hr vs 48 hrs, p < 0.01 or p < 0.05). Furthermore, significant positive correlation was found between serum MMP-9 level and serum TNF-alpha level, serum CRP level or APACHEII score in patients at 1 hr after admission (MMP-9/TNF-alpha, r = 0.956; MMP-9/CRP, r = 0.935; MMP-9/APACHE II score, r = 0.957; p < 0.01). These results suggest that MMP-9 is involved in the deterioration of SAP and serum MMP-9 level is a valuable assessment marker for the severity of SAP.

APACHE↗

PubMed2006

Captopril, an Angiotensin-converting enzyme inhibitor, attenuates the severity of acute pancreatitis in rats by reducing expression of matrix metalloproteinase 9.

It has been reported that matrix metalloproteinase 9 (MMP-9) disrupts basement membrane and increases vascular permeability. MMP-9 therefore might participate in the pathogenesis of severe acute pancreatitis (SAP). Captopril, an angiotensin-converting enzyme inhibitor, could reduce MMP-9 expression. However, the effect of captopril on the outcome of SAP is not ascertained. The aim of this study was to determine whether captopril attenuates the severity of SAP by reducing MMP-9 expression. Thirty Sprague-Dawley rats were randomly divided into 3 groups (n = 10 for each). Rats were given intraperitoneal injection of saline (SAP group) or captopril (4 mg/kg) (treated group), and then given retrograde infusion of 5% sodium taurocholate (1.5 ml/kg) into the pancreatic duct under laparotomy to induce SAP. One group of rats, injected with saline, underwent only sham operation (Control). Experimental samples were collected at 24 hrs after the induction of SAP or sham operation. Various markers of severity of SAP, such as serum levels of amylase and trypsinogen activation peptide and the vascular permeability, were increased in rats with SAP, but were significantly decreased in captopril-treated rats (p < 0.01). Likewise, the serum MMP-9 levels and expression levels of pancreatic tissue MMP-9 were significantly higher in rats with SAP than those in captopril-treated rats and control rats (p < 0.01 for both parameters), but showed no difference between captopril-treated and control rats. These results suggest that captopril may attenuate vascular permeability by reducing MMP-9 expression in SAP, thereby ameliorating severity of the disease. The use of captopril might become a new therapeutic agent for SAP.

Amylases↗

PubMed2006

Human Streptococcus suis outbreak, Sichuan, China.

From mid-July to the end of August 2005, a total of 215 cases of human Streptococcus suis infections, 66 of which were laboratory confirmed, were reported in Sichuan, China. All infections occurred in backyard farmers who were directly exposed to infection during the slaughtering process of pigs that had died of unknown causes or been killed for food because they were ill. Sixty-one (28%) of the farmers had streptococcal toxic shock syndrome; 38 (62%) of them died. The other illnesses reported were sepsis (24%) and meningitis (48%) or both. All isolates tested positive for genes for tuf, species-specific 16S rRNA, cps2J, mrp, ef, and sly. A single strain of S. suis caused the outbreak, as shown by the identification of a single ribotype. The high death ratio was of concern; prohibiting backyard slaughtering ended the outbreak.

Adult↗

PubMed2004

Lung, spleen, and kidney are the major places for inducible nitric oxide synthase expression in endotoxic shock: role of p38 mitogen-activated protein kinase in signal transduction of inducible nitric oxide synthase expression.

Bacterial lipopolysaccharide (LPS) is known to induce endotoxic shock with inducible nitric oxide (NO) synthase (iNOS) expression and NO production. However, the major place for NO production in shock remains unclear. Although there is some literature about p38 mitogen-activated protein kinase (MAPK) in regulating LPS-induced iNOS expression, the results are contradictory. To interpret the precise cell mechanism and the role of p38 MAPK in the expression of iNOS during endotoxic shock, we carried out the following investigations. A severe endotoxic shock model was reproduced in mice 6 h after LPS injection. The plasma NO level was increased in a dose- and time-dependent manner after LPS stimulation and was suppressed by administration of SB203580 [4-(4-fluorophenyl)-2-4-methylsulfonylphenyl-5-(4-pyridyl) imidazole], a highly specific inhibitor of p38 MAPK. The iNOS expression was increased in many organs, including heart, liver, spleen, lung, gut, and kidney in endotoxic shock. Among them, the highest expression of iNOS mRNA and protein was in the lung, moderate expression was in the spleen and kidney, and the lowest expression was in the heart, gut, and liver. The level of expression in lung was 5.5 times that of iNOS mRNA and was 3.1 times that of iNOS protein than in heart, and 1.6 and 1.8 times that of iNOS mRNA and 1.7 and 1.4 times that of iNOS protein than in spleen and kidney, respectively. The p38 MAPK activity increased after LPS injection, and SB203580 markedly reduced LPS-induced expressions of iNOS protein and mRNA in the lung. The results indicates that lung, spleen, and kidney are the major places for iNOS expression in endotoxic shock and are important therapeutic target organs for attenuating NO production in shock treatment.

Animals↗

PubMed2002

[Gerontology].

Explore the source record for details and available documents.

Aging↗

PubMed2002

Role of p38 MAPK in ICAM-1 expression of vascular endothelial cells induced by lipopolysaccharide.

Lipopolysaccharide (LPS) stimulation of endothelial cells induces the expression of intercellular adhesion molecule-1 (ICAM-1), a critical adhesion molecule involved in the adhesive interaction between leukocytes and endothelial cells in shock and inflammation. Although there is little literature about role of p38 mitogen-activated protein kinase (MAPK) in ICAM-1 protein expression of LPS-induced endothelial cells, it is still not defined whether gene transcription is regulated by p38 MAPK in ICAM-1 expression of LPS-induced endothelial cells. In this study, the potential role of p38 MAPK in ICAM-1 expression of LPS-induced endothelial cells was studied in vitro and in vivo. In vitro studies, the results showed that compared with basic expression of ICAM-1 protein on cultured human umbilical vein endothelial cells (HUVECs), the ICAM-1 expression was increased initially at 2 h after LPS stimulation, reached peak value at 24 h, and descended at 36 h obviously. A dose-dependent relationship existed between LPS concentration and ICAM-1 expression. The abundance of ICAM-1 mRNA in cytoplasma of endothelial cells was upregulated significantly by LPS stimulation at 2 h and was maintained at a high level from 4 to 36 h. The upregulation of ICAM-1 protein and mRNA expression of LPS-induced HUVECs was markedly inhibited by SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole], a highly specific inhibitor of p38 MAPK. Activity of p38 MAPK in HUVECs was increased at 15 min after LPS stimulation and reached the maximum at 60 min, then descended significantly. Activity of p38 MAPK was inhibited significantly by SB203580 in vitro. In vivo studies, administration of SB203580 (12.5 or 25 mg/kg, per ora) markedly reduced LPS-induced expression of ICAM-1 protein and mRNA of lung tissues of male BALB/c mice. These data highlight that the upregulation of ICAM-1 expression of LPS-induced endothelial cells in vitro and in vivo is mediated by p38 MAPK pathway at the level of gene transcription. The ICAM-1 expression of LPS-induced endothelial cells is characteristic of time dependence and dose dependence, and tolerates to chronic LPS stimulation. Inhibition of the p38 MAPK signal pathway may be used as an approach to attenuate ICAM-1 production in the treatment of septic shock.

Animals↗

PubMed2002

Association of the phosphatidylinositol signal pathway with prolonged myocardial ischemia.

OBJECTIVE: To study the changes in activity of phosphatidylinositol 4 kinase (PI 4 kinase), phosphatidylinositol 4 phosphate 5 kinase (PIP 5 kinase) and protein kinase C (PKC) during myocardial ischemia and elucidate the relationship between phosphatidylinositol signal pathways and prolonged myocardial ischemia. METHODS: In vivo an ischemic rat model was used. Activity of PI 4 kinase, PIP 5 kinase and PKC were measured at different times in postischemic heart cells using isotope analysis. RESULTS: The activity of PI kinase, PIP kinase and PKC in the myocardium increased to peak at 1 hour postischemia, with activities 6.1, 3.0 and 4.0 fold over control levels, respectively. Their activities declined to normal levels with time. CONCLUSION: The phosphatidylinositol signal pathway is involved in prolonged myocardial ischemia, but its mechanism needs further study.

1-Phosphatidylinositol 4-Kinase↗

PubMed2002

[Protective effect of Ginkgo biloba extract on acute lung injury induced by lipopolysaccharide in D-galactose aging rats].

OBJECTIVE: To investigate the effect of Ginkgo biloba extract (GBE) on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in aging rats. METHODS: The rats were randomly divided into two parts: six rats served as normal controls; 18 rats were used for producing the aging animal model ( D-gal 50 mg/kg body weight was injected intraperitoneally, once a day for 6 weeks). The aging rats were then randomly divided into 3 groups: 6 rats as the aging control group; another 6 as the LPS treated aging group (LPS,5 mg/kg body weight intravenous injection); and the third as the GBE+LPS group (6 rats, GBE was started 7 days before the experiment,given once a day via the esophagus, the amount of flavone glycosides administered being 8 mg/kg body weight, and on the day of experiment, one dose of GBE was given 2 hours before LPS administration ). The samples were collected 2 hours after LPS or saline administration. RESULTS: Compared with normal controls, the SOD activity in red cells and the Na(+) -K(+) -ATPase activity in the lung tissue decreased markedly (all P < 0.05), but the LDH activity increased (P < 0.05) in the aging rats. ALI was observed in the aging rats 2 hours after LPS administration. Compared with the aging control, in the LPS treated rats, there were more inflammatory cells in the lung tissue; protein content in bronchial alveolar lavage fluid (BALF) and the pulmonary permeability index (PPI) increased significantly (all P < 0.001); LD, MDA, NO(2) (-)/NO(3)(-), ET-1 and TNF-alpha content and LDH activity in blood, and MPO activity in lung tissue all increased significantly. On the contrary, SOD activity in red cells and Na(+) -K(+) -ATPase activity in lung tissue decreased markedly (P < 0.05, P < 0.01). These changes, except SOD, were markedly attenuated in the GBE+LPS rats. CONCLUSIONS: The anti-oxidant activity was decreased in D-gal-induced aging rats. Intravenous administration of LPS caused acute lung injury in aging rats. GBE had protective effect on ALI induced by LPS.

Aging↗

PubMed2002

[Hepatic injury induced by acute lung injury in aging rats].

OBJECTIVE: To investigate the induction of hepatic function damage by acute lung injury (ALI) in aging rats and the effect of Ginkgo Biloba extract (GBE) on this process. METHODS: Thirty male Wistar rats were used to produce the aging animal model. Aging rats were randomly divided into three groups: the control group, the lipopolysaccharide (LPS, intravenous injection) group, and the GBE + LPS group (GBE given 7 days before experiment, once a day, via the esophagus). Samples from the blood, the lung and the liver were collected 2 and 6 h after LPS or saline administration. RESULTS: ALI was induced by intravenous injection of LPS in aging rats. Compared with the aging control, the total bilirubin content and the glutamic pyruvic transaminase (GPT) activity in serum did not change at 2 h after LPS administration. But at 6 h, they were increased, respectively from (10.9 +/- 0.6) mg/L and (26 +/- 3) U in the control group to (30.1 +/- 2.1) mg/L and (88 +/- 12) U in the LPS group (P < 0.001). MDA content increased in the blood and the lung tissue at 2 has compared to the control group, from (15.9 +/- 1.8) micro mol/L and (18.8 +/- 2.1) nmol/mg protein to (22.1 +/- 1.9) micro mol/L and (28.8 +/- 3.1) nmol/mg protein (all P < 0.001), respectively. SOD activity in the lung tissue was decreased significantly, from (25.5 +/- 2.6) mU/L and (36.1 +/- 2.4) U/mg protein to (20.6 +/- 1.9) mU/L and (32.0 +/- 2.7) U/mg protein, respectively (P < 0.05, P < 0.001). The GSH-P(X) activity and the Na(+)-K(+)-ATPase activity in the lung tissue at 2 hours after LPS administration were decreased markedly, from (28.2 +/- 2.8) U/mg protein and (4.9 +/- 0.5) micromol Pi x mg(-1) protein x h(-1). to (21.1 +/- 2.7) U/mg protein and (3.1 +/- 0.3) micromol Pi x mg(-1) protein x h(-1). These changes lasted 6 h after LPS administration. These parameters did not change significantly in the hepatic tissue at 2 h after LPS administration. But after 6 h, MDA content was increased from (7.9 +/- 0.9) nmol/mg protein to (10.9 +/- 0.7) nmol/mg protein; while the GSH-P(X) and the Na(+)-K(+)-ATPase activities were decreased markedly, from (59.0 +/- 3.9) U/mg protein and (0.87 +/- 0.04) micromol Pi x mg(-1) protein x h(-1) to (49.2 +/- 3.0) U/mg protein and (0.77 +/- 0.04) micromol Pi x mg(-1) protein x h(-1) (P < 0.001, P < 0.01). There was no obvious change in the SOD activity. All the changes were significantly attenuated in the GBE + LPS group (P < 0.05, P < 0.01). CONCLUSION: Hepatic function damage could be induced by ALI in aging rats. GBE showed a protective effect on ALI and hepatic function damage in this animal model.

Aging↗

PubMed2002

[Use of a novel baculovirus vector to express nucleoprotein gene of Crimean-Congo hemorrhagic fever virus in both insect and mammalian cells].

OBJECTIVE: To construct a novel baculovirus vector which is capable of promoting the high-yield expression of foreign gene in mammalian cells and to express by this vector the nucleoprotein (NP) gene of Crimean-Congo hemorrhagic fever virus (CCHFV) Chinese isolate (Xinjiang hemorrhagic fever virus, XHFV) BA88166 in insect and Vero cells. METHODS: Human cytomegalovirus (CMV) immediate early (IE) promoter was ligated to the baculovirus vector pFastBac1 downstream of the polyhedrin promoter to give rise to the novel vector pCB1. XHFV NP gene was cloned to this vector and was well expressed in COS-7 cells and Vero cells by means of recombinant plasmid transfection and baculovirus infection. RESULTS: The XHFV NP gene in vector pCB1 could be well expressed in mammalian cells. Vero cells infected with recombinant baculovirus harboring NP gene could be employed as antigens to detect XHF serum specimens whose results were in good correlation with those of ELISA and in parallel with clinical diagnoses. CONCLUSIONS: This novel baculovirus vector is able to express the foreign gene efficiently in both insect and mammalian cells, which provides not only the convenient diagnostic antigens but also the potential for developing recombinant virus vaccines and gene therapies.

Animals↗