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Objective:To explore the efficacy and safety of sivelestat, a neutrophil elastase (NE) inhibitor, in the treatment of acute lung injury (ALI) in the intensive care unit (ICU).Methods:A retrospective analysis was performed on 171 patients with ALI in the ICU of the First Affiliated Hospital of Zhengzhou University from June 2020 to June 2021, including 77 patients in the sivelestat group and 94 patients in the conventional treatment group. Acute physiology and chronic health evaluation (APACHE) Ⅱ score, Murray lung injury score, oxygenation index (PaO 2/FiO 2 ratio), inflammatory cytokines (IL-6, IL-10, TNF-α), ventilator-free days (VFD), the length of ICU stay, and the 28-day mortality were collected to assess the efficacy of sivelestat. At the same time, adverse reactions and laboratory test results within 30 days after the use of sivelestat were recorded to assess the safety. Results:Compared with conventional treatment, oxygenation index, Murray lung injury scores, IL-6, IL-10, and TNF-α were significantly improved after 7 days of sivelestat treatment. Compared with the conventional treatment group, the VFD was significantly longer ( P = 0.0119) and the length of ICU stay was significantly shorter ( P = 0.0269) in the sivelestat group. The mortality was 14.29% in the sivelestat group and 22.34% in the conventional treatment group and, with no statistically significant. In the meantime, sivelestat did not increase adverse reactions within 30 days after treatment. Conclusions:Sivelestat treatment is safe and more effective than conventional treatment for ALI patients in the ICU.
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Clinical data of 93 patients with severe craniocerebral injury admitted in the Emergency Intensive Care Unit (EICU) of the First Affiliated Hospital of Zhengzhou University from September 2016 to September 2018 were retrospectively analyzed. Forty six patients received 10% hypertonic salt solution 60 ml (hypertonic salt group) and 47 patients received 20% mannitol 125 ml (mannitol group) for relieving early postoperation cerebral edema. The changes of intracranial pressure, central venous pressure, heart rate, mean arterial pressure (MAP), urine volume and serum sodium level at 2, 4 and 6 h after dehydrating agents were compared between two groups. There were no significant differences in the intracranial pressure, central venous pressure, heart rate and urine volume between two groups at 2, 4 and 6 h after the first dehydration treatment (all P>0.05). The MAP values of the two groups were (88±11) and (80±10), (85±10) and (78±9), (79±12) and (73±13) mmHg (1 mmHg=0.133 kPa) at 2, 4 and 6 h after the first dehydration treatment; and the serum sodium levels were (145±5) and (136±4), (144±6) and (133±5), (140±5) and (135±4) mmol/L, respectively. There were significant differences between two groups (all P<0.05). It is suggested that hypertonic salt can reduce intracranial pressure and increase cerebral perfusion better than mannitol in severe craniocerebral injury.
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Objective:To explore the effect of Hsp22 on the activation of cardiac fibroblasts stimulated by TGFβ1 and its possible molecular mechanism.Methods:Cardiac fibroblasts of adult mice were isolated and cultured, and stimulated with TGFβ1 to induce fibroblast activation. Fibroblasts were incubated with Hsp22 of different concentrations (1, 2, 4, 8, 10 μg/mL) for 24 h, and their activation, proliferation and secretion were observed. CCK8 kit was used to detect cell proliferation. RT-PCR was used to detect the transcription of fibrogenic factor. Immunofluorescence was used to detect the expression of α-SMA protein. Immunoblotting was used to detect the possible signal protein.Results:CCK8 results showed that fibroblast increased significantly after TGFβ1 stimulation ( P<0.05). The expression of α-SMA in fibroblasts and the transcription of fibrosis-related genes increased significantly after TGFβ1 stimulation ( P<0.05). Different concentrations (1, 2, 4, 8, and 10 μg/mL) of Hsp22 all inhibited the proliferation of fibroblasts significantly (( P<0.05). Eight μg/mL and 10 μg/mL Hsp22 inhibited the expression of α-SMA ( P<0.05). and reduced the transcription of fibrosis-related genes ( P<0.05). Immunoblotting results indicated that after induced by TGFβ1, the expression of WNT and β-catenin, the phosphorylation level of GSK3β, and the nuclear translocation of β-catenin increased ( P<0.05). Ten μg/mL Hsp22 inhibited the expression of WNT and β-catenin, and reduced the phosphorylation of GSK3β the nuclear translocation of β-catenin and the phosphorylation of smad2 and smad3( P<0.05). Conclusions:Hsp22 could block TGFβ1-induced fibroblast activation, proliferation and secretion via inhibiting the WNT/β-catenin signaling pathway.
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Clinical data of 93 patients with severe craniocerebral injury admitted in the Emergency Intensive Care Unit (EICU) of the First Affiliated Hospital of Zhengzhou University from September 2016 to September 2018 were retrospectively analyzed. Forty six patients received 10% hypertonic salt solution 60 ml (hypertonic salt group) and 47 patients received 20% mannitol 125 ml (mannitol group) for relieving early postoperation cerebral edema. The changes of intracranial pressure, central venous pressure, heart rate, mean arterial pressure (MAP), urine volume and serum sodium level at 2, 4 and 6 h after dehydrating agents were compared between two groups. There were no significant differences in the intracranial pressure, central venous pressure, heart rate and urine volume between two groups at 2, 4 and 6 h after the first dehydration treatment (all P>0.05). The MAP values of the two groups were (88±11) and (80±10), (85±10) and (78±9), (79±12) and (73±13) mmHg (1 mmHg=0.133 kPa) at 2, 4 and 6 h after the first dehydration treatment; and the serum sodium levels were (145±5) and (136±4), (144±6) and (133±5), (140±5) and (135±4) mmol/L, respectively. There were significant differences between two groups (all P<0.05). It is suggested that hypertonic salt can reduce intracranial pressure and increase cerebral perfusion better than mannitol in severe craniocerebral injury.
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Objective To compare the clinical efficacy of high-flow nasal cannula oxygen therapy (HFNC) with non-invasive positive pressure ventilation (NPPV) in patients with traumatic cervical spinal cord injury complicated with acute respiratory failure (ARF).Methods A prospective randomized controlled trial was performed in EICU of the First Affiliated Hospital of Zhengzhou University from May 2016 to January 2018.One hundred sixty-eight consecutive patients with traumatic cervical spinal cord injury complicated with ARF,who did not respond to conventional oxygen therapy,were assigned to the HFNC or NPPV treatment group sequenced by the random number table.The baseline clinical characteristics of randomized participants and respiratory frequency (RR),PaCO2,mean arterial pressure (MAP) at 1,12,24,48 h after treatment were evaluated.Comfortable scale,tracheal intubation rate within 28 d,duration of mechanical ventilation,length of stay in ICU and mortality rate were compared as well.Results There was no significant differences in baseline clinical characteristics,such as sex,age.between the two groups (P＞0.05).RR and PaCO2 were lower in the HFNC group at all time point.In addition,the HFNC group had significantly lower PaCO2 than the NPPV group at 24 and 48 h after treatment (P＜0.01);Oxygenation index (PaO2/FiO2) was improved in both groups,and the HFNC group had superior oxygenation index than the NPPV group at 12,24,48 h after treatment (P＜0.01).Furthermore,the HFNC group had better comfort scale (6.93±0.71 vs 4.29±0.93,P＜0.01),shorter length of stay in ICU and duration of mechanical ventilation compared to the NPPV group (P＜0.01).There was no significant differences in tracheal intubation rate and mortality rate between the two groups (P＞0.05).Conclusions In addition to the superior efficacy in improving respiratory function and shortening length of stay in ICU,HFNC was well tolerated by patients with traumatic cervical spinal cord injury complicated with ARF,and could be recommended in clinical practice.
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Objective To investigate the effect of Hsp22 on phenylephrine-induced cardiomyocytes hypertrophy.Methods Primary rat myocardial cells were isolated and cultured in Department of Cardiology,the First Affiliated Hospital of Zhengzhou University.Cells were divided into four groups randomly:Control group,model group,treatment group with 1 μg/mL Hsp22,and treatment group with 10 μg/mL Hsp22.Phenylephrine stimuli was used to induce cardiomyocytes hypertrophy model.Cell viability was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.Cardiomyocytes surface area was evaluated by α-actin immunofluorescence staining.Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the transcription level of hypertrophic markers.Reactive oxygen species level was detected by 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe.Apoptosis was detected by TUNEL staining.Signal pathway protein expression was detected by Western blot.SPSS 13.0 was used for statistical analysis.Data were expressed as mean + standard deviation.All data were analyzed by one-way ANOVA between groups.Comparisons between two groups were performed using LSD-t test.A P＜0.05 was considered statistically significant.Results Different concentrations of Hsp22 had no effect on cardiomyocytes viability (F=6.622;P＞0.05).Phenylephrine stimulation significantly increased cardiomyocytes area (t=10.80;P＜0.05),increased the transcription level of hypertrophy markers atrial natriuretic peptide (t=37.72;P＜0.05),type B natriuretic peptide (t=16.85;P＜0.05),and myosin heavy chain beta (t=41.53;P＜0.05).Different concentrations of Hsp22 significantly reduced cardiomyocytes area (PE+ 1 μg/mL Hsp22 t=4.018;P＜0.05;PE+10 μg/mL Hsp22 t=10.80;P＜0.05),reduced the transcription level of hypertrophic markers atrial natriuretic peptide (PE+1 μg/mL Hsp22 t=27.12,P＜0.05;PE+10 μg/mL Hsp22 t=37.72,P＜0.05),type B natriuretic peptide (PE+1 μg/mL Hsp22 t=4.82,P＜0.05;PE+10 μg/mL Hsp22 t=12.74,P＜0.05),and myosin heavy chain beta (PE+1 μg/mL Hsp22 t=23.68,P＜0.05;PE+10 μg/mL Hsp22 t=30.54,P＜0.05).Westem blot showed that Hsp22 increased the activation of AMP-activated protein kinase α (PE+1 μg/mL Hsp22 t=5.89,P＜0.05;PE+10 μg/mL Hsp22 t=5.88,P＜0.05),reduced mTOR phosphorylation level (PE+1 μg/mL Hsp22 t=16.80,P＜0.05;PE+10.μg/mL Hsp22 t=20.46,P＜0.05).Conclusions Hsp22 inhibits cardiomyocytes hypertrophy by activating AMP-activated protein kinase α.Hsp22 may become a potential anti-hypertrophic drug.