Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

Sui, Bo; Li, Yongwang; Ma, Li

doi:10.3892/etm.2014.1876

Cited by 8 publications

(9 citation statements)

References 28 publications

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“…Those specific brain regions were selected in our study because expression of PICs and their receptors is upregulated in those regions following CA in rats and in general they are also more related to neurological deficits after cerebral ischemia than other brain regions [18, 20]. Our results showed that CA amplifies the levels of IL-6 and TNF-α in addition to IL-1β, which is consistent with the previous report [11]. Notably, we further found that the protein expression of PIC receptors such as IL-1R, IL-6R and TNFR1 were also increased in the cortex and hippocampus CA1 regions.…”

Section: Discussionsupporting

confidence: 90%

“…In an important prior study [11], UTI has been shown to play a protective role in CA induced-cerebral ischemia by attenuating brain edema and inflammatory responses (i.e., central IL-6 and TNF-α) and thereby improving survival and neurological function. In contrast, in the present study, we further studied the effects of UTI on the protein expression levels of PIC receptors in CA rats.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, an important prior study [11] suggests that UTI can attenuate the levels of central IL-6 and TNF-α and improve brain edema, neurological function and survival in CA rats. Nevertheless, the underlying mechanisms leading to the effects of UTI on ischemic insults still need to be determined.…”

Section: Introductionmentioning

confidence: 99%

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Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Jiang

Wang

et al. 2016

Translational Neuroscience

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Ulinastatin [urinary trypsin inhibitor (UTI)] plays an important role in the protection of organs against ischemic injury during severe inflammation. The purposes of this study were to examine the effects of UTI on the levels of pro-inflammatory cytokines (PICs) and protein expression of PIC receptors in the neocortex and hippocampus CA1 region of rats after transient global ischemia induced via cardiac arrest (CA). Specifcally, interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were analyzed. CA was induced by asphyxia followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were employed to determine PICs and their receptors in the neocortex and hippocampus. Our results show that IL-1β, IL-6 and TNF-α were significantly elevated in the neocortex and hippocampal CA1 field after CA. This was accompanied with an increase in PIC receptors, namely IL-1R, IL-6R and TNFR1. Systemic injection of UTI attenuated the amplification of PIC signal pathways in these brain regions. UTI also improved the modified Neurological Severity Score and brain tissue edema in CA rats. Notably, UTI resulted in an increase in survival of CA rats as compared to CA rats without treatment. In conclusion, UTI plays a beneficial role in modulating transient global ischemia induced by CA by altering PIC signal mechanisms, but further studies are needed to draw more firm conclusions.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Jiang

Wang

et al. 2016

Translational Neuroscience

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“…The anti‐inflammatory activities, organ protective effect, and clinical effectiveness of ulinastatin in several SIRS conditions have been investigated in many animal studies14, 15, 16 and clinical studies 5, 10, 13, 17, 18, 19. Based on these results, we hypothesized that ulinastatin would have beneficial effects on MOF patients.…”

Section: Discussionmentioning

confidence: 98%

Ulinastatin did not reduce mortality in elderly multiple organ failure patients: a retrospective observational study in a single center ICU

Uchida

Abe

Ono

et al. 2017

Acute Medicine & Surgery

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AimOur aim was to evaluate the effect of ulinastatin on 28‐day mortality in patients who developed multiple organ failure (MOF) related to their acute illness and were admitted to the intensive care unit (ICU).MethodsWe carried out a retrospective observational study of MOF patients in a general ICU of a tertiary care hospital in Japan from January 2009 to December 2012. The primary outcome was 28‐day all‐cause mortality. Secondary outcomes were ventilator‐free days, ICU‐free days, and vasopressor‐free days at day 28. We investigated the association between ulinastatin treatment and outcomes using multivariable regression analysis.ResultsA total of 212 MOF patients were included, 79 (37%) of whom received ulinastatin. The median age was 70 years (interquartile range, 60–77) and median APACHE II score was 25 (interquartile range, 19–29). Overall 28‐day mortality was 20%. There were no significant differences between the ulinastatin group and the control group in age, gender, or APACHE II score. The ulinastatin group had higher prevalence of sepsis (44% versus 22%, P = 0.001). Multivariable logistic regression analysis showed that ulinastatin was not associated with 28‐day mortality (odds ratio = 1.22; 95% confidence interval, 0.54–2.79). Moreover, ulinastatin did not reduce the mortality in patients with sepsis (odds ratio = 1.92; 95% confidence interval, 0.52–7.13). However, ICU‐free days and ventilator‐free days was significantly fewer in the ulinastatin group than control group.ConclusionsIn this retrospective observational study, ulinastatin was not associated with mortality in elderly patients with established MOF, although it might be related to patient's utility.

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“…Recombinant human activated protein C (APC), an anti-inflammatory agent, benefits severe sepsis patients via rearrangement of actin-phosphomyosin light chain (20). Ulinastatin (UTI), another inhibitor of inflammation, inhibits the production of TNF-␣ and interleukin-6 (IL-6) by suppressing toll-like receptor 4 (TLR4) and the downstream signal pathway (14,28,48,50). Such therapies, including APC and UTI, fail to decrease the morbidity and mortality associated with sepsis, likely because the pathogenesis of sepsis is not completely understood.…”

mentioning

confidence: 99%

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

Zhang

Yang

Zhu

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC20 pathway in septic rats. Am J Physiol Lung Cell Mol Physiol 309: L1323-L1332, 2015. First published September 4, 2015 doi:10.1152/ajplung.00016.201543 has been shown to participate in several cardiovascular diseases. Increased vascular permeability is a common and severe complication in sepsis or septic shock. Whether or not Cx43 takes part in the regulation of vascular permeability in severe sepsis is not known, and the underlying mechanism has not been described. With cecal ligation and puncture-induced sepsis in rats and lipopolysaccharide (LPS)-treated vascular endothelial cells (VECs) from pulmonary veins, the role of Cx43 in increased vascular permeability and its relationship to the RhoA/Rock1 pathway were studied. It was shown that vascular permeability in the lungs, kidneys, and mesentery in sepsis rats and LPS-stimulated monolayer pulmonary vein VECs was significantly increased and positively correlated with the increased expression of Cx43 and Rock1 in these organs and cultured pulmonary vein VECs. The connexin inhibitor carbenoxolone (10 mg/kg iv) and the Rock1 inhibitor Y-27632 (2 mg/kg iv) alleviated the vascular leakage of lung, mesentery, and kidney in sepsis rats. Overexpressed Cx43 increased the phosphorylation of 20-kDa myosin light chain (MLC 20) and the expression of Rock1 and increased the vascular permeability and decreased the transendothelial electrical resistance of pulmonary vein VECs. Cx43 RNA interference decreased the phosphorylation of MLC20 and the expression of Rock1 and decreased LPS-stimulated hyperpermeability of cultured pulmonary vein VECs. The Rock1 inhibitor Y-27632 alleviated LPS-and overexpressed Cx43-induced hyperpermeability of monolayer pulmonary vein VECs. This report shows that Cx43 participates in the regulation of vascular permeability in sepsis and that the mechanism is related to the Rock1-MLC20 phosphorylation pathway. connexin 43; vascular permeability; sepsis; RhoA/Rock1 pathway; MLC 20

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Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

Cited by 8 publications

References 28 publications

Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Ulinastatin did not reduce mortality in elderly multiple organ failure patients: a retrospective observational study in a single center ICU

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats

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Postconditioning improvement effects of ulinastatin on brain injury following cardiopulmonary resuscitation

Cited by 8 publications

References 28 publications

Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Effects of ulinastatin on global ischemia via brain pro-inflammation signal

Ulinastatin did not reduce mortality in elderly multiple organ failure patients: a retrospective observational study in a single center ICU

Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC20pathway in septic rats

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Role of connexin 43 in vascular hyperpermeability and relationship to Rock1-MLC₂₀pathway in septic rats