Expression of high mobility group protein B1 in the lungs of rats with sepsis

Qiu, Qiao-meng; Li, Zhong-wang; Tang, Luming; Sun, Qi; Lu, Zhongqiu; Liang, Huan; Hong, Guangliang; Li, Mengfang

doi:10.5847/wjem.j.1920-8642.2011.04.011

Cited by 8 publications

(3 citation statements)

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“…These results indicated that inflammation would induce the activation of the coagulation system as well as down regulation of physiological anticoagulant mechanisms and inhibition of the fibrinolytic system with the development of sepsis. [11] In addition, our data showed that D-dimer, AT-III, PT and APTT were all signifi cantly related with TNF-α and hs-CRP in patients with critical illness. Plessier et al [12] reported the severity of coagulation dysfunction was closely related to the severity of sepsis in patients with infection.…”

Section: Discussionmentioning

confidence: 57%

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Ding¹,

Cao²,

Ma³

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND: Current studies on CD62P have focused mainly on cardiovascular diseases, while only few studies have evaluated the effects of CD62P on the development of sepsis and the association between endothelial cell injury with infl ammation and coagulation. This study attended to explore the association between endothelial cell injury with infl ammation and coagulation by evaluating the expression of soluble CD62P (s-CD62P) in plasma and its mechanism in patients with sepsis, thus to provide the evidence of effective treatment of sepsis with anti-adhesion therapy targeted CD62P. METHODS: A total of 70 critically ill patients with systemic inflammatory response syndrome (SIRS) admitted to intensive care unit (ICU) between September 2009 and February 2010 were enrolled for a prospective and control study. According to the diagnostic criteria of sepsis/SIRS, the patients were divided into two groups: a sepsis group (n=38) and a SIRS group (n=32). Another 20 healthy volunteers served as a control group. Patients in the sepsis group and SIRS group were matched by clinical signs of high blood pressure, diabetes and its complications. The demographics of the patients including age, sex, body mass index (BMI), smoking and alcohol addict were compared among the groups. Six mL peripheral blood samples were collected within 24-hour admission in ICU for enzymelinked immunosorbent assay (ELISA) to detect the plasma levels of s-CD62P, TNF-α, and hs-CRP. And variables of coagulation function such as platelet (PLT), prothrombin (PT), activated partial thromboplastin time (APTT), D-dimer and antithrombin-III (AT-III) were analyzed during 24 hours after admission to ICU. Meanwhile sequential organ failure assessment (SOFA) score of critically ill patients was evaluated. Data were expressed as mean±standard deviation and were statistically analyzed by using SPSS 17.0 statistical software. The differences in plasma levels of s-CD62P of patients in each group were analyzed by ANOVA and the Kruskal-Wallis test. The relations between s-CD62P and infl ammatory cytokines as well as with coagulation were determined by Pearson's product moment correlation coeffi cient analysis. Changes were considered as statistically signifi cant if P value was less than 0.05. RESULTS: Compared with the control group and SIRS group, the sepsis group demonstrated signifi cantly higher levels of s-CD62P, TNF-α and highly sensitive C-reactive protein (hs-CRP) (P<0.05). The plasma levels of D-dimer, PT, and APTT in the sepsis and SIRS groups were signifi cantly higher than those in the control group, while the platelet count and the activity of AT-III were obviously lower (P<0.05). In the sepsis group, the plasma levels of hs-CRP and TNF-α were positively correlated with PT, APTT, and D-dimer, and negatively correlated with AT-III and PLT (P<0.05). The plasma levels of s-CD62P were signifi cantly correlated with the plasma levels of TNF-α, hs-CRP, D-dimer, PT, and APTT, whereas they were correlated negatively well with PLT and AT-III (P<0.05). CONCLUSIONS:...

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Section: Discussionmentioning

confidence: 57%

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Ding¹,

Cao²,

Ma³

et al. 2013

World Journal of Emergency Medicine

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“…Several studies have shown that LPS positively regulates inflammation by triggering the phosphorylation of p65 and IκB to stimulate the NF-κB pathway and promote the release of inflammatory cytokines (Dong & Yuan, 2018;Duan et al, 2012;Fu et al, 2013;Yang et al, 2020). Further, a relationship between Hmgb1expression and ALI was observed in rats suffering from V. vulnificusor LPS-induced sepsis, with significant pathological injuries in the lungs (Lan et al, 2017;Qiu et al, 2011).…”

Section: F I G U R Ementioning

confidence: 99%

Protocatechuic acid attenuates lipopolysaccharide‐induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis

et al. 2021

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Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)-induced septic lung injury. Eighty-two male Balb/c mice were divided into six groups: control, PCA30 (30 mg/kg), LPS (10 mg/kg), PCA10-LPS, PCA20-LPS, and PCA30-LPS treated with 10, 20 and 30 mg/kg PCA, respectively, for seven days before intraperitoneal LPS injection. PCA pre-treatment, especially at higher dose, significantly reduced LPS-induced lung tissue injury as indicated by increased heat shock protein 70 and antioxidant molecules (reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) accompanied by lower oxidative stress indices (malondialdehyde and nitric oxide).PCA administration decreased inflammatory mediators including myeloperoxidase, nuclear factor kappa B (NF-κB p65), and pro-inflammatory cytokines, and prevented the development of apoptotic events in the lung tissue. At the molecular level, PCA downregulated mRNA expression of nitric oxide synthase 2, C/EBP homologous protein, and high mobility group box1 in the lungs of all PCA-LPS treated mice. Thus, PCA-pre-treatment effectively counteracted sepsis-induced acute lung injury in vivo by promoting and antioxidant status, while inhibiting inflammation and apoptosis.Practical implications: Sepsis-mediated organ dysfunction and high mortality is aggravated by acute lung injury (ALI). Therefore, new therapeutic approaches are needed to encounter sepsis-mediated ALI. Protocatechuic acid (PCA) is a naturally occurring phenolic acid with various biological and pharmacological activities. PCA is abundant in edible plants including Allium cepa L., Oryza sativa L., Hibiscus sabdariffa, Prunus domestica L., and Eucommia ulmoides. In this investigation we studied the potential protective role of pure PCA (10, 20 and 30 mg/kg) on LPS-mediated septic lung injury in mice through examining oxidative challenge, inflammatory response, apoptotic events and histopathological changes in addition to evaluating the levels and mRNA expression of heat shock protein 70, C/EBP homologous protein and Funding informationTaif University, Grant/Award Number: TURSP-2020/153 high mobility group box1 in the lung tissue. The recorded results showed that PCA pre-administration was able to significantly abrogate the damages in the lung tissue associated septic response. This protective effect comes from its strong antioxidant, anti-inflammatory, and anti-apoptotic activities, suggesting that PCA may be applied to alleviate ALI associated with the development of sepsis.

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“…[ 15 ] In the present study, the plasma level of uPA in the SIRS group was decreased more significantly than in the non-SIRS group and controls ( P <0.001 and P <0.001; Table 2 , Figure 1 ). Qiu et al[ 22 ] identified that in a clinical situation, frequently characterized by fibrin occlusion of the microcirculation, the ability of polymorphonuclear leukocytes (PMN) to express uPA activity is diminished or absent. Yu et al[ 23 ] demonstrated that dramatically increased plasminogen activator inhibitor type 1 (PAI-1) levels during staphylococcal infection led to a reduction of metabolically active uPA levels.…”

Section: Discussionmentioning

confidence: 99%

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

Ding

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND:Urokinase-type plasminogen activator (uPA) and urokinase-type plasminogen activator receptor (uPAR) are known as important factors, which mediate a variety of functions in terms of vascular homeostasis, inflammation and tissue repair. However, their role in systemic inflammatory response syndrome (SIRS) has been less well studied. This study aimed to test the hypothesis that the abnormalities of fibrinolysis and degradation of extracellular matrix mediated by uPA and uPAR are directly related to the patients with SIRS. We therefore analyzed their role and clinicopathological significance in patients with SIRS.METHODS:A case-control study was conducted with 85 patients who were divided into two groups according to the diagnostic criteria of SIRS: SIRS group (n=50) and non-SIRS group (n=35). The SIRS group was divided into MODS group (n=26) and non-MODS group (n=24) by their severity, and survival group (n=35) and non-survival group (n=15) by their prognosis. Another 30 healthy adults served as normal controls. uPA and uPAR in plasma were detected by commercial enzyme-linked immunosorbent assay (ELISA) kits.RESULTS:The plasma level of uPA was lower in the SIRS group than in the non-SIRS group and controls (P<0.001 and P<0.001). It was lower in sepsis patients and the MODS group than in the non-sepsis patients and the non-MODS patients (all P<0.05). However, there was no difference in uPA level between survivors and non-survivors (P>0.05). The plasma level of uPAR increased in the SIRS group compared with the non-SIRS group and controls (P<0.001 and P<0.001). There was a significant elevation of uPAR in sepsis patients, MODS patients and non-survivors as compared with non-sepsis patients, non-MODS patients and survivors respectively (all P<0.05). Plasma uPAR levels were positively correlated with APACHE II score (r=0.575, P<0.001) and SOFA score (r=0.349, P=0.013). AUCs for the prediction of SIRS mortality were 0.67 and 0.51, respectively, for uPA and uPAR.CONCLUSION:uPAR could be a predictor of poor outcome in patients with SIRS.

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Expression of high mobility group protein B1 in the lungs of rats with sepsis

Cited by 8 publications

References 9 publications

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Protocatechuic acid attenuates lipopolysaccharide‐induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis

Urokinase-type plasminogen activator receptor as a predictor of poor outcome in patients with systemic inflammatory response syndrome

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