Objective To investigate the role of angiotensin-converting enzyme 2 (ACE2) in hyperoxic lung injury. Methods Adult mice were exposed to 95% O2 for 72 h to induce hyperoxic lung injury, and simultaneously treated with ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760. ACE2 expression/activity in lung tissue and angiotensin (Ang)-(1-7)/Ang II in bronchoalveolar lavage fluid (BALF), and the severity of hyperoxic lung injury were evaluated. The levels of inflammatory factors in BALF and lung tissue and the expression levels of phospho-p65, p65 and IkBα were measured. Oxidative parameter and antioxidant enzyme levels in lung tissue were measured to assess oxidative stress. Finally, the expression levels of nuclear factor-erythroid-2-related factor (Nrf2), NAD(P)H quinine oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were measured using Western blotting. Results Hyperoxia treatment significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1-7) ratio, while co-treatment with hyperoxia and DIZE significantly increased lung ACE2 expression/activity and decreased the Ang II/Ang-(1-7) ratio. By contrast, co-treatment with hyperoxia and MLN-4760 significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1-7) ratio. Hyperoxia treatment induced significant lung injury, inflammatory response and oxidative stress, which were attenuated by DIZE but aggravated by MLN-4760. The NF-κB pathways were activated by hyperoxia and MLN-4760 but inhibited by DIZE. The Nrf2 pathway and its downstream proteins NQO1 and HO-1 were activated by DIZE but inhibited by MLN-4760. Conclusion Activation of ACE2 can reduce the severity of hyperoxic lung injury by inhibiting inflammatory response and oxidative stress. ACE2 can inhibit the NF-κB pathway and activate the Nrf2/HO-1/NQO1 pathway, which may be involved in the underlying mechanism.

/pdf/angiotensin-converting-enzyme-2-attenuates-inflammatory-29cc9golpo.pdf

Angiotensin-converting enzyme 2 attenuates inflammatory response and oxidative stress in hyperoxic lung injury by regulating NF-κB and Nrf2 pathways

Stroke is one of the leading causes of mortality worldwide. Protective agents that can diminish injuries caused by cerebral ischemia-reperfusion (I/R) are important in alleviating the harmful outcomes of stroke. The aim of the present study was to investigate the protective role of sanguinarine in cerebral I/R injury. A rat middle cerebral artery occlusion model was used to assess the clinical effect of sanguinarine, and inflammatory cytokines in the serum were detected by ELISA. Western blotting was performed to examine the change in levels of apoptosis-associated proteins in the injured brains. The results suggested that sanguinarine, an anti-inflammatory agent derived from the roots of Sanguinaria canadensis, improved the state of cerebral ischemia in a rat model. The data demonstrated that when rats were treated with sanguinarine prior to middle cerebral artery occlusion, the infarct volume was reduced significantly. The inflammatory factors tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured in sanguinarine and vehicle-treated groups using an enzyme-linked immunosorbent assay, and the expression levels of the three factors were significantly reduced following treatment with sanguinarine (P<0.05). In addition, western blot analysis demonstrated that the ratio of B-cell lymphoma 2/Bcl-2-associated X protein was significantly increased following treatment with sanguinarine (P<0.05). The study demonstrated that sanguinarine exerts a protective effect in cerebral ischemia, and that this effect is associated with the anti-inflammatory and anti-apoptotic properties of sanguinarine.

pdf/anti-inflammatory-and-neuroprotective-effects-of-3k3uitet0i.pdf

Anti-inflammatory and neuroprotective effects of sanguinarine following cerebral ischemia in rats.

Critically ill patients frequently suffer from vitamin C deficiency. Previous studies showed that high doses of vitamin C administration had conflicting results on clinical outcomes in patients with severe sepsis, burns, and trauma. Because of the high incidence and morbidity/mortality with severe pneumonia, we aimed to investigate the effect of administration of high dose vitamin C in critically ill patients with severe pneumonia. Eighty critically ill patients with pneumonia were enrolled in this randomized double-blinded clinical trial. Patients with a CURB-65 score > 3, one major criterion, or ≥ 3 minor criteria were considered as severe pneumonia. Patients were randomly assigned to intervention or placebo groups receiving standard treatment plus 60 mg/kg/day vitamin C as a continuous infusion or normal saline in the same volume correspondingly for 96 h. Serum levels of vitamin C were noted at baseline and 48 h after vitamin C administration. Duration of mechanical ventilation, ICU length of stay, PaO2/FiO2, and mortality rate were noted for all patients till the 28th day. Any complications related to the vitamin C administration were recorded. Duration of mechanical ventilation and vasopressor use were significantly lower in the intervention group (p: < 0.001 and 0.003, respectively). Baseline levels of vitamin C in both groups did not have a significant difference but its levels increased in the intervention group and decreased in the control group during the study period. Mortality rate insignificantly decreased in the intervention group (p = 0.17). Three patients showed hypotension and tachycardia during the administration of vitamin C which was self-limited with decreasing the dose of vitamin C. Our results showed that the intravenous administration of a relatively high dose of vitamin C to critically ill patients with severe pneumonia was safe and could decrease the inflammation, duration of mechanical ventilation, and vasopressor use without any significant effect on mortality. Trial registration: IRCT registration number: IRCT20190312043030N1, Registration date: 2019-08-26, Seied Hadi Saghaleini.

/pdf/effect-of-vitamin-c-on-mortality-of-critically-ill-patients-2mskfwqzwy.pdf

Effect of Vitamin C on mortality of critically ill patients with severe pneumonia in intensive care unit: a preliminary study.

Background: Impairment of intestinal barrier function and increased translocation of bacteria to the systemic blood flow contribute to the emergence of sepsis. Probiotics might be of beneficial effects on critically ill‑patients, modulating intestinal barrier function and reducing inflammation. The aim of this trial was to determine the effect of probiotics on inflammatory markers in critically ill‑patients in Intensive Care Unit (ICU). Materials and Methods: This trial was conducted on 40 critically ill‑patients admitted to the ICU. Patients were randomly assigned to receive placebo or probiotic containing Lactobacillus, Bifidobacterium and Streptococcus thermophilus (VSL#3) for 7 days. Acute Physiology and Chronic Health Evaluation (APACHE II) score Sequential Organ Failure Assessment (SOFA) and systemic concentrations of interleukin‑6 (IL‑6), procalcitonin (PCT) and protein C were measured before initiation of the study and on days 4 and 7. Results: A significant difference in IL‑6 ( P = 0.003), PCT (P = 0.014) and protein C (P < 0.001) levels, and also APACHE II and SOFA scores (P < 0.001) was seen over the treatment period between two groups. Moreover, there was a significant decrease in serum IL‑6 levels (from 211.85 ± 112.76 to 71.80 ± 28.41) ( P < 0.001) and PCT levels (from 1.67 ± 1.27 to 0.47 ± 0.41) (P < 0.001) and a significant increase in serum protein C levels (from 7.47 ± 3.61 to 12.87 ± 3.63) ( P < 0.001) in probiotic group during the study. Conclusion: Probiotics could reduce inflammation in critically ill‑patients and might be considered as an adjunctive therapy in the treatment of critically ill‑patients.

/pdf/effect-of-a-multispecies-probiotic-on-inflammatory-markers-4rlnjc3848.pdf

Effect of a multispecies probiotic on inflammatory markers in critically ill patients: A randomized, double?blind, placebo?controlled trial

Proinflammatory cytokines levels in sepsis and healthy volunteers, and tumor necrosis factor-alpha associated sepsis mortality: A systematic review and meta-analysis.

sepsis is one of the most widespread and lethal disease in Intensive Care Units (ICU). Based on pathophisyology of sepsis, it seems that routine laboratory tests combined with analysis of pro-inflammatory cytokines plasma levels, help clinicians to have more information about disease progress and its correct management.This was a prospective observational study to determine the predictive role of Tumor Necrosis Factor alpha (TNF-α), Interleukin (IL)-1β and IL-6 as three main pro-inflammatory cytokines and Acute Physiology and Chronic Health Evaluation (APACHE II) and Sequential Organ Failure Assessment (SOFA) as two scoring systems in mortality of critically ill patients with severe sepsis. Fifty and five patients with criteria of severe sepsis were included in this study. An exclusion criterion was post Cardiopulmonary Resuscitation (CPR) status. Cytokines (TNF-α, IL-1β and IL-6) were assayed in the first, third and seventh days in blood of patients.Among three measured cytokines, sequential levels of TNF-α and IL-6 showed significant differences between survivors and nonsurvivors. IL-6 had a good correlation with outcome and scoring systems during the period of this study. The areas under the receiver operating characteristic (AUROC) curve indicated that APACHE II (0.858, 0.848, 0.861) and IL-6 (0.797, 0.799, 0.899) had discriminative power in prediction of mortality during sequental measured days. Multiple logestic regression analysis identified that evaluation of APACHE II and TNF-α in the first day and APACHE II and IL-6 in the third and seventh days of severe septic patients are independent outcome predictors. Results of this study suggest that IL-6 and APACHE II are useful cytokine and scoring systems respectively in prediction of mortality and clinical evaluation of severe septic patients.

Identification of enhanced cytokine generation following sepsis. dream of magic bullet for mortality prediction and therapeutic evaluation

Background and purpose of the study: The acute respiratory distress syndrome (ARDS) is a common clinical disorder caused by injury to the alveolar epithelial and endothelial barriers of lung. In ARDS patients, oxidative stress is increased and plasma antioxidant levels are reduced. Vitamin E has an important role in antioxidant defense mechanisms. In this study the effect of vitamin E on decrease of APACHE II score in ARDS patients was investigated. Materials and methods: Twenty patients [mean (SE): age = 51.2 ± 6.41 years] with ARDS were enrolled. After diagnosis based on inclusion and exclusion criteria, ten patients as treatment group received 600 IU vitamin E daily intramuscularly. Control group received normal saline as placebo. Plasma samples and Acute Physiology and Chronic Health Evaluation (APACHE) II score were obtained before administration, 4hrs and 12hrs after each intervention and repeated three days for each patient. Results were analyzed by use of an SPSS software package with a repeated-measures analysis of variance (ANOVA). Results: Significant changes were observed in APACHE II score from first to seventh measurement (p=0.0001) in treatment group, but vitamin E concentration altered significantly in only first to seventh measurement (p= 0.019). Conclusion: From the results of this study, it seems that the use of vitamin E as a lipidsoluble antioxidant along with other supportive measures is beneficial in decreasing APACHE II score in ARDS patients.

/pdf/effects-of-vitamin-e-administration-on-apache-ii-score-in-2enly7pgj1.pdf

Effects of vitamin E administration on APACHE II Score in ARDS patients

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Identification of enhanced cytokine generation following sepsis. dream of magic bullet for mortality prediction and therapeutic evaluation

Effects of vitamin E administration on APACHE II Score in ARDS patients