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Sepsis, a series of pathophysiological abnormalities caused by infection, is also one of the most important factors of death and disability in infected patients all over the world, so it has always been the focus of the medical community. Cytokines are small molecule proteins secreted by cells with biological activity, involved in the immune and inflammatory regulation of sepsis. Many studies using cytokine targeting to treat sepsis have achieved beneficial effects, and the level of cytokines is also believed to be related to the development, severity of sepsis, so they are reliable biomarkers of sepsis. Among them, pro-inflammatory cytokines such as interferon-β (IFN-β) and interleukins (IL-1β, IL-3, IL-6, and IL-7) are the focus of the discussion in this review. IFN-β and IL-1β are double-sided in the treatment of sepsis, namely early low-dose treatment can reduce sepsis by restoring the function of immune cells and play a protective effect, but they are also related to severe inflammatory response of sepsis and can aggravate the mortality of sepsis patients. IL-3 and IL-6 focus more on enhancing inflammatory factors and play a damage role. IL-7 mainly participates in immune regulation, promoting lymphocyte activation and protecting sepsis.
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Objective:To study the effect of oropharyngeal colostrum administration on salivary secretory IgA (sIgA) levels in extremely/very low birth weight preterm infants fed by gastric tube.Methods:Preterm infants with birth weight <1 500 g ( n=90) hospitalized in neonatal intensive care unit of the Affiliated Shenzhen Maternity & Child Healthcare Hospital of Southern Medical University from August 2020 to January 2021 were enrolled as research subjects. They were assigned into observation group and control group. The observation group accepted oropharyngeal administration of colostrum before being fed by gastric tube once every 3 hours for 7 days. The control group was given normal saline before each feeding. Other nursing interventions were consistent with the observation group. Saliva samples were collected at the 2 hour and 7 day after birth and the levels of slgA were tested. SPSS 26.0 statistical software was applied to analyse the data. Results:A total of 81 preterm infants completed this study. The content of salivary sIgA in observation group (42 cases) on 7 day after birth were significantly higher than those on the 2 hour after birth [15.4 (0.6, 106.7) μg/ml vs. 0.6 (0.0, 5.3) μg/ml] ( P<0.05). There was no statistically significant difference between the sIgA levels in the saliva of the control group (39 cases) at the 7 postnatal day and 2 hour after birth [0.0 (0.0, 1.4) μg/ml vs. 0.0 (0.0, 5.2) μg/ml] ( P>0.05). The content of salivary sIgA in observation group were significantly higher than those in control group on the 7 day after birth, the difference was statistically significant ( P<0.05). The salivary sIgA levels in the observation group were negatively correlated with the starting time of oropharyngeal administration of colostrum ( r=-0.330, P<0.05), and positively correlated with the total number of oropharyngeal administration of colostrum ( r=0.388, P<0.05). Conclusions:Oropharyngeal colostrum administration can improve the levels of salivary sIgA of extremely/very low birth weight preterm infants fed by gastric tube.
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Objective:To study the trends and ranges of blood pressure in extremely premature infants (EPIs) during the first 7 days after birth.Methods:From January 2016 to December 2020, EPIs born in our hospital were retrospectively analyzed. Their blood pressure were monitored using umbilical arterial catheters and no patients needed anti-hypotension treatment. The clinical data of the infants and their mothers, blood pressure data during the first 7 days after birth, clinical outcomes and complications were collected. The trends of blood pressure in untreated EPIs were analyzed and the blood pressure ranges of EPIs of different gestational ages (GA) were established.Results:A total of 145 cases of EPIs were included and their systolic pressure, diastolic pressure and mean blood pressure showed upward trends during 2~168 h after birth ( P<0.001). The diastolic pressure increased significantly within 24 h after birth ( P<0.05), systolic pressure and mean blood pressure increased significantly within 72 h after birth ( P<0.05). Blood pressure increased with age and GA. Conclusions:The blood pressure of EPIs will increase spontaneously during 7 days after birth. The ranges of blood pressure are measured for infants with different GA to provide clinical evidence for blood pressure management of EPIs during early postnatal period.
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Objective To evaluate the effect of dexmedetomidine pretreatment on the expression of mitochondrial transcription factor A ( TFAM) and succinate dehydrogenase ( SDHA) during lung ischemia-reperfusion ( I∕R) in mice. Methods Twenty-four clean-grade healthy male C57BL∕6J mice, aged 8-10 weeks, weighing 18-22 g, were divided into 3 groups ( n=8 each) using a random number table method:sham operation group ( group S ) , lung I∕R group ( group I∕R ) and dexmedetomidine pretreatment group ( group D) . In I∕R and D groups, lung I∕R was induced by clamping the left pulmonary hilum for 60 min followed by 120-min reperfusion in anesthetized mice. The chest was only opened, but the left pulmonary hilum was not occluded in group S. Dexmedetomidine 25μg∕kg was intraperitoneally injected at 30 min be-fore ischemia in group D, while the equal volume of normal saline was given instead of dexmedetomidine in I∕R and S groups. The mice were sacrificed at 120 min of reperfusion, and lungs were removed for determi-nation of wet∕dry weight ratio ( W∕D ratio) , cell apoptosis ( by TUNEL) and expression of TFAM and SDHA mRNA in lung tissues ( by real-time polymerase chain reaction ) and for examination of the pathological changes of lung tissues. The apoptosis index was calculated. Results Compared with group S, the W∕D ratio, apoptosis index and lung injury scores were significantly increased, and the expression of TFAM and SDHA mRNA was down-regulated in I∕R and D groups ( P<0. 05) . Compared with group I∕R, the W∕D ra-tio, apoptosis index and lung injury scores were significantly decreased, and the expression of TFAM and SDHA mRNA was up-regulated in group D ( P<0. 05) . Conclusion The mechanism by which dexmedeto-midine pretreatment attenuates lung I∕R injury is related to up-regulating the expression of TFAM and SDHA in mice.
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Objective:To explore the protective effect of sodium channels antagonists HOE642 on lung ischemia reperfusion and the role of the p38 mitogen activated protein kinase (p38MAPK) signaling pathway in this process.Methods:A total of 36 mice were randomly divided into a sham operation group (SHAM group),a lung ischemia reperfusion group (I/R group) and a lung ischemia reperfusion+HOE642 group (HOE group).The water content was detected by electronic scales,and the lung tissue pathological changes were observed under optical microscope.The inflammatory cytokines including IL-6 and TNF-α were examined by ELISA.The intracellular calcium fluorescence intensity was examined and observed under fluorescence microscope,and the protein expression of p38MAPK was detected by Western blot.Results:Lung water content in the HOE group was lower than that in the I/R group,but higher than that in the SHAM group (both P＜0.05).Lung interstitial edema,hemorrhage,lung tissue inflammatory cells infiltration were significantly alleviated in the HOE group than those in the I/R group,while the injury in the HOE group was aggravated than those in the SHAM group (both P＜0.05).T he IL-6 and TNF-α in lung tissues in the HOE group were lower than those in the I/R group,but higher than those in the SHAM group (both P＜0.05).Intracellular calcium fluorescence intensity in the HOE group was lower than that in the I/R group,but higher than that in the SHAM group (both P＜0.05).The protein expression of p38MAPK in lung tissues in the HOE group was lower than that in the I/R group,but higher than that in the SHAM group (both P＜0.05).Conclusion:HOE642 may exert protective effect on pulmonary I/R injury through regulation of the p38MAPK signaling pathway,resulting in reduction of intracellular calcium ion concentration and calcium overload,and decrease of inflammatory response.
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Objective To evaluate the role of mitochondrial ATP-sensitive potassium (mito-KATP) channels in attenuation of renal ischemia-reperfusion (I/R) injury by lidocaine pretreatment in rats.Methods Sixty healthy male Wistar rats,weighing 300-350 g,were randomly assigned into 5 groups (n =12 each) using a random number table:sham operation group (group S); renal I/R group (group I/R); lidocaine pretreatment group (group L) ; 5-HD (a specific blocker of the mito-KATP channel) group and 5-HD + lidocaine pretreatment group (group 5-HD + L).Renal ischemia was induced by occlusion of bilateral renal arteries for 60 min with atraumatic microclips followed by 4 h reperfusion.At 60 min before renal ischemia,lidocaine 5 mg/kg was intravenously injected followed by continuous infusion at 2 mg· kg-1 · h-1 in group L.5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia in group 5-HD.In 5-HD + L groups,5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia and the other procedures were similar to those previously described in group L.In S and I/R groups,the animals received equal volumes of normal saline instead of lidocaine.Blood samples were obtained at 6 h of reperfusion for determination of serum creatinine (Cr) and urea mitrogen (BUN) concentrations.Bilateral kidneys were removed for determination of mitochondrial membrane potential in the renal tubular epidural cells,malondialdehyde (MDA) content,and superoxide dismutase (SOD) activity and for microscopic examination.Results Compared with group S,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in I/R,L,5-HD and 5-HD + L groups (P ＜ 0.05).Compared with group I/R,the serum Cr and BUN concentrations and MDA content were significantly decreased,and SOD activity and mitochondrial membrane potential were increased in L and 5-HD + L groups (P ＜ 0.05),and no significant changes were found in the serum Cr and BUN concentrations,MDA content,SOD activity and mitochondrial membrane potential in group 5-HD (P ＞ 0.05).Compared with group L,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in 5-HD + L group (P ＜ 0.05).The pathological changes were significantly reduced in group L as compared with I/R and 5-HD + L groups.Conclusion Mito-KATp channels are involved in reduction of I/R-induced renal injury by lidocaine pretreatment in rats.
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Objective To investigate the effect of lidocaine pretreatment on renal HMGB1 expression during renal ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Wistar rats weighing 300-350 g were randomly divided into 3 groups ( n=12 each):sham operation group (group S),I/R group and lidocaine pretreatment group (group L).Renal I/R was induced by occlusion of bilateral renal arteries for 60 min followed by 4 or 24 h reperfusion.Lidocaine 5 mg/kg was injected iv at 60 min prior to ischemia followed by 2 mg· kg- 1· h- 1 infusion iv for 60 min in group L.Equal volume of normal saline was given in group I/R.Six rats in each group were sacrificed at 4 or 24 h of reperfusionand their kidneys were removed for microscopic examination and for determination of SOD activity,MDA content and the expression of HMGB1 mRNA and protein.Results Compared with group S,renal HMGB1 mRNA and protein expression,MDA content were significantly increased,while SOD activity were significantly decreased in groups I/R and L( P ＜ 0.05).Compared with group I/R,renal HMGB1 mRNA and protein expression,and MDA content were significantly decreased,while SOD activity were significantly increased in group L ( P ＜ 0.05 ).Conclusion Lidocaine pretreatment can attenuate renal I/R injury in rats by down-regulating HMGB1 expression