Effect of oral motor intervention in improving brain function development in preterm infants: a randomized controlled trial / 中国当代儿科杂志

OBJECTIVE@#To study the effect of oral motor intervention (OMI) on brain function development in preterm infants.@*METHODS@#A total of 112 preterm infants were stratified into small-gestational-age (30-31@*RESULTS@#On day 7 of OMI, the small-gestational-age intervention group had lower upper bounds of voltage and bandwidth and a higher aEEG score than the small-gestational-age control group (@*CONCLUSIONS@#OMI can promote the maturation of aEEG background activities, improve neurobehavioral manifestations, and accelerate brain function development in preterm infants.

Effect of red blood cell storage duration on the clinical effect of exchange transfusion and internal environment in neonates with hyperbilirubinemia / 中国当代儿科杂志

OBJECTIVE@#To study the effect of red blood cell (RBC) storage duration on the clinical effect of exchange transfusion (ET) and internal environment in neonates with hyperbilirubinemia.@*METHODS@#A retrospective analysis was performed for the clinical data of 135 neonates with hyperbilirubinemia who received ET between January 2015 and August 2018. According to RBC storage duration, the neonates were divided into short-term storage group (RBCs were stored for ≤7 days) with 56 neonates and long-term storage group (RBCs were stored for >7 days) with 79 neonates. The two groups were compared in terms of serum total bilirubin (TBIL) level and the rate of TBIL reduction at 0 and 12 hours after ET, as well as the duration of continued phototherapy and rate of repeated ET. Routine blood test parameters, electrolytes, blood glucose, and blood gas parameters were measured before ET and at 0 hour after ET.@*RESULTS@#At 0 hour after ET, there were no significant differences in the TBIL level and the rate of TBIL reduction between the two groups (P>0.05). At 12 hours after ET, the long-term storage group had a significantly higher TBIL level and a significantly lower rate of TBIL reduction than the short-term storage group (P7 days in ET for neonates with hyperbilirubinemia does not affect the immediate effect of ET, but these neonates tend to have a poor outcome after continued phototherapy and high risk of hyponatremia, hyperkalemia, and metabolic acidosis.

Dynamic observation of pulmonary function by plethysmography in preterm infants with bronchopulmonary dysplasia / 中国当代儿科杂志

OBJECTIVE@#To study the effect of bronchopulmonary dysplasia (BPD) on lung function in preterm infants.@*METHODS@#According to the presence/absence or the severity of BPD, 72 preterm infants were divided into non-BPD group (n=44), mild BPD group (n=15) and moderate BPD group (n=13). Lung function was assessed by plethysmography on days 7, 14 and 28 after birth.@*RESULTS@#The preterm infants in the three groups had gradual increases in tidal volume per kilogram (TV/kg), functional residual capacity (FRC), ratio of time to peak tidal expiratory flow to total expiratory time (%T-PF) and ratio of volume to peak tidal expiratory flow to total expiratory volume (%V-PF) on days 7, 14 and 28 after birth, while there were gradual reductions in effective airway resistance per kilogram (Reff/kg) and respiratory rate (RR) (P<0.05). Compared with the non-BPD group on days 7, 14 and 28 after birth, the mild and moderate BPD groups had significantly lower TV/kg, FRC, %T-PF, and %V-PF and significantly higher Reff/kg and RR (P<0.05). On day 7 after birth, the moderate BPD group had significantly higher airway resistance, Reff/kg and FRC/kg than the mild BPD group (P<0.05).@*CONCLUSIONS@#There is a certain degree of pulmonary function impairment in preterm infants with BPD. Dynamic monitoring of lung function by plethysmography is useful for assessing lung development in the neonatal period in these infants.

Preventive effect of caffeine on bronchopulmonary dysplasia in preterm infants / 中国当代儿科杂志

With the increase in the rescue success rate of critically ill preterm infants and extremely preterm infants, the incidence rate of bronchopulmonary dysplasia (BPD) is increasing year by year. BPD has a high mortality rate and high possibility of sequelae, which greatly affects the quality of life of preterm infants and brings a heavy burden to their families, and so the treatment of BPD is of vital importance. At present, no consensus has been reached on the treatment measures for BPD. However, recent studies have shown that early application of caffeine can prevent BPD. With reference to the latest studies on the effect of caffeine in the prevention of BPD, this article reviews the mechanism of action of caffeine in reducing pulmonary inflammation, improving morphological abnormalities of lung injury, reducing oxidative stress injury, and improving pulmonary function.

Monitoring of kidney injury in preterm infants / 中国当代儿科杂志

Acute kidney injury (AKI) is a common complication in the neonatal intensive care unit that causes a high mortality of preterm infants and various chronic kidney diseases in adulthood. Preterm infants have immature development of the kidneys at birth. The kidneys continue to develop within a specific time window after birth. However, due to various factors during pregnancy and after birth, preterm infants tend to develop AKI. At present, serum creatinine and urine volume are used for the assessment of kidney injury, and their early sensitivity and specificity have attracted increasing attention. In recent years, various new biomarkers have been identified for early recognition of AKI. This article reviews the features, risk factors, renal function assessment, and prevention/treatment of AKI of preterm infants, in order to provide a reference for improving early diagnosis and treatment of AKI in preterm infants and long-term quality of life.

Pathogen distribution, risk factors, and outcomes of nosocomial infection in very premature infants / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the pathogen distribution and risk factors of nosocomial infection in very preterm infants, as well as the risk of adverse outcomes.</p><p><b>METHODS</b>A retrospective analysis was performed for the clinical data of 111 very preterm infants who were born between January and December, 2016 and had a gestational age of <32 weeks and a birth weight of <1 500 g. According to the presence or absence of nosocomial infection after 72 hours of hospitalization, the infants were divided into infection group and non-infection group. The infection group was analyzed in terms of pathogenic bacteria which caused infection and their drug sensitivity. A multivariate logistic regression analysis was used to investigate the potential risk factors and risk of adverse outcomes of nosocomial infection in very preterm infants.</p><p><b>RESULTS</b>Gram-negative bacteria were the main pathogens for nosocomial infection in very preterm infants and accounted for 54%, among which Pseudomonas aeruginosa was the most common one; the following pathogens were fungi (41%), among which Candida albicans was the most common one. The drug sensitivity test showed that Gram-negative bacteria were highly resistant to β-lactam and carbapenems and highly sensitive to quinolones, while fungi had low sensitivity to itraconazole and high sensitivity to 5-fluorocytosine and amphotericin B. Early-onset sepsis, duration of peripherally inserted central catheter, steroid exposure, and duration of parenteral nutrition were risk factors for nosocomial infection in very preterm infants (P<0.05). Compared with the non-infection group, the infection group had significantly higher risks of pulmonary complications (P<0.05), as well as a significantly longer length of hospital stay and a significantly higher hospital cost (P<0.001).</p><p><b>CONCLUSIONS</b>Nosocomial infection in very preterm infants is affected by various factors and may increase the risk of adverse outcomes. In clinical practice, reasonable preventive and treatment measures should be taken with reference to drug sensitivity, in order to improve the prognosis of very premature infants.</p>

Resveratrol increases sirtuin 1 expression in peripheral blood mononuclear cells of premature infants and inhibits the oxidative stress induced by hyperoxia in vivo / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the effect of resveratrol on the levels of sirtuin 1 (SIRT1) and reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) of premature infants exposed to hyperoxia.</p><p><b>METHODS</b>Peripheral blood and isolated PBMCs from premature infants (gestational age<32 weeks) without oxygen supplement were collected and were randomly assigned into four groups: control, air+resveratrol, hyperoxia, and hyperoxia+resveratrol. The PBMCs were cultured in vitro for 48 hours, then the ROS content in PBMCs was measured by laser scanning confocal microscopy. Malondialdehyde (MDA) content in the medium was measured by the whole spectrum spectrophotometer. SIRT1 positioning was assessed by immunofluorescence. SIRT1 expression levels in PBMCs were measured by Western bolt.</p><p><b>RESULTS</b>Compared with the control group, the level of SIRT1 in the air+resveratrol group increased significantly (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate in the hyperoxia group increased significantly, while the expression level of SIRT1 decreased significantly compared with the control group (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate decreased significantly (P<0.05), and the expression level of SIRT1 increased significantly in the hyperoxia+resveratrol group (P<0.05).</p><p><b>CONCLUSIONS</b>Resveratrol can increase SIRT1 expression in PBMCs and inhibit SIRT1 shuttle from nucleus to cytoplasm in order to increase the ability of antioxidative stress in premature infants exposed to hyperoxia, thereby reducing the oxidative stress injury in premature infants.</p>

Roles of PKCβ/P66Shc oxidative stress signal pathway in mediating hyperoxia-induced ROS production in alveolar epithelial cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the roles of PKCβ/P66Shc oxidative stress signal pathway in mediating hyperoxia-induced reactive oxgen species (ROS) production in alveolar epithelial cells (A549) and the protective effects of PKCβ inhibitor on hyperoxia-induced injuries of alveolar epithelial cells.</p><p><b>METHODS</b>A549 cells were cultured in vitro and randomly divided into three groups: control, hyperoxia and PKCβ inhibitor LY333531 treatment. The hyperoxia group was exposed to a mixture of O2 (950 mL/L) and CO2 (50 mL/L) for 10 minutes and then cultured in a closed environment. The LY333531 group was treated with PKCβ inhibitor LY333531 of 10 µmol/L for 24 hours before hyperoxia induction. Cells were collected 24 hours after culture and the levels of PKCβ, Pin1, P66Shc and P66Shc-Ser36 were detected by Western blot. The intracellular translocation of P66Shc, the production of ROS and cellular mitochondria membrane potential were measured using the confocal microscopy.</p><p><b>RESULTS</b>Compared with the control group, the levels of PKCβ, Pin1, P66Shc and P-P66Shc-Ser36 in A549 cells 24 hours after culture increased significantly in the hyperoxia group. These changes in the hyperoxia group were accompanied with an increased translocation rate of P66Shc from cytoplasm into mitochondria, an increased production of mitochondrial ROS, and a reduced mitochondrial membrane potential. Compared with the hyperoxia group, the levels of Pin1, P66Shc and P66Shc-Ser36 in A549 cells, the translocation rate of P66Shc from cytoplasm into mitochondria and the production of mitochondrial ROS decreased significantly, while the mitochondrial membrane potential increased significantly in the LY333531 treatment group. However, there were significant differences in the above mentioned measurements between the LY333531 treatment and control groups.</p><p><b>CONCLUSIONS</b>Hyperoxia can increase the expression of PKCβ in alveolar epithelial cells and production of mitochondrial ROS and decrease mitochondrial membrane potential. PKCβ inhibitor LY333531 can partially disrupt these changes and thus alleviate the hyperoxia-induced alveolar epithelial cell injury.</p>

Silencing of Pin1 suppresses hyperoxia-induced apoptosis of A549 cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the effect of silence of Pin1 expression on hyperoxia-induced apoptosis in alveolar epithelial cells A549.</p><p><b>METHODS</b>A549 cells were divided into four groups: control, hyperoxia, negative lentivirus and Pin1-shRNA hyperoxia. The hyperoxia group was exposed to a mixture of 95%O2 and 5%CO2 for 10 minutes. Then cells were cultured in a closed environment. After 24 hours, the changes of morphology were observed under an inverted microscope. Cell apoptosis was detected by flow cytometry (FCM). The expression of X-linked inhibitor of apoptosis protein (XIAP) and Caspase-9 were detected by immunohistochemistry. The production of reactive oxygen species (ROS) and cellular mitochondria membrane potential (△Ψm) were determined by fluorescence microscopy.</p><p><b>RESULTS</b>Under the inverted microscope, the A549 cells grew slowly and the changes in morphology of the cells were most obvious in the hyperoxia and negative lentivirus groups. The changes in morphology of A549 cells were obviously improved in the Pin1-shRNA hyperoxia group. The FCM results showed that the apoptosis rate of A549 cells increased, Caspase-9 expression increased, XIAP expression decreased, mitochondrial ROS production increased and mitochondrial membrane potential decreased in the hyperoxia and negative lentivirus groups compared with the control group (P<0.05). Compared with the hyperoxia and negative lentivirus groups, the apoptosis rate of A549 cells decreased, Caspase-9 expression decreased, XIAP expression increased, mitochondrial ROS production decreased and mitochondrial membrane potential increased in the Pin1-shRNA hyperoxia group (P<0.05), although the levels of the indexes did not reach to those of the control group.</p><p><b>CONCLUSIONS</b>Silencing of Pin1 could suppress hyperoxia-induced apoptosis of A549 cells.</p>

Expressions of Caveolin-1 and Transforming growth factor betal 1 in A549 cells exposed to hyperoxia and their relationship / 中华实用儿科临床杂志

Objective To observe the expressions of Caveolin-1 (CAV-1) and transforming growth factor bata 1 (TGF-β1) in human adenocarcinoma of lung A549 cells exposed to hyperoxia,and to explore the changes in CAV-1 and TGF-β1 expressions and the role in hyperoxic lung injury.Methods After the A549 human lung cancer cell lines were resuscitated,the cells were packaged and cultured in 50 mL/L CO2 culture chamber,when approaching to the condition of confluence in CO2 culture chamber(37 ℃,50 mL/L CO2),the cells were randomly divided into control group and hyperoxia group.Eighteen bottles of A549 cells in each group.The hyperoxia group received attacking factor that was mixed with oxygen (950 mL/L)and CO2 (50 mL/L) at a velocity of 3 L/min for 10 min;then the flasks were enclosed and cultured in culture chamber,while those in control group were still exposed to 5 mL/L CO2.After cells were cultured for 12 h,24 h,48 h,the changes in morphology were observed under the inverted microscope,the expressions CAV-1 and TGF-β1 were detected by double immunofluorescence staining technique,followed by laser scanning under the focus microscope.Results In the control group,there was high expression of CAV-1 associated with low expression of TGF-β1 (44.25 ± 3.23,10.18 ± 2.74).Compared with control group,the content of CAV-1 reduced continuously (12 h:35.25 ± 1.88,24 h:20.75 ± 1.68,48 h:9.86 ± 2.80) under prolonged hyperoxia exposure,but TGF-β1 increased gradually(12 h:17.32 ± 1.50,24 h:26.51 ± 1.82,48 h:41.94 ±4.47),and the expression of CAV-1 had highly negative relation to TGF-β1 at the same time (r =-0.91,-0.62,-0.53,-0.88,all P ＜ O.05) in the control group and the hyperoxia group in 12 h,24 h,48 h.Conclusions The reduction of CAV-1 expression can attenuate the inhibitory effect of TGF-β1 and activate TGF-β1 signaling pathway,which may result in hyperoxic lung injury.

Protective effects of mitochondrial ATP-sensitive potassium channel on A549 cell apoptosis induced by hyperoxia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the protective effects of mitochondrial ATP-sensitive potassium channel opener diazoxide on hyperoxia-induced apoptosis of type II alveolar epithelial cells (A549 cells) and possible mechanisms.</p><p><b>METHODS</b>A549 cells were cultured in vitro and divided randomly into control, hyperoxia and diazoxide group. The hyperoxia group was exposed to a mixture of O2 (900 mL/L) and CO2 (50 mL/L) for 10 minutes, then cultured in a closed environment. The diazoxide group was pretreated with diazoxide of 100 μmol/L for 24 hrs before hyperxia induction. The cells were collected 12, 24 and 48 hrs after culture. The morphologic changes of A549 cells were observed under an inverted microscope. A549 cell apoptosis was detected by flow cytometry. The expression of Omi/HtrA2 in the endochylema of A549 cells was determined by immunohistochemistry.</p><p><b>RESULTS</b>A549 cells were damaged and the changes in morphology of the cells were serious in the hyperoxia group. The apoptosis rate of A549 cells and the expression of Omi/HtrA2 in the endochylema increased in the hyperoxia group compared with the control group (P<0.05). The growth and the morphology of A549 cells were greatly improved and the cell injuries were obviously alleviated in the diazoxide group. The expression of Omi/HtrA2 in the endochylema and the apoptosis rate of A549 cells were significantly reduced in the diazoxide group compared with the hyperoxia group (P<0.05).</p><p><b>CONCLUSIONS</b>Diazoxide as an opener of mitoKATP channel can reduce the expression of Omi/HtrA2 and the apoptosis rate of A549 cells, thus relieves the injury of A549 cells induced by hyperoxia.</p>

Effects of Ucf-101 on expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the expression of serine protease Omi/HtrA2 in kidneys of postasphyxial neonatal rats, and to study the effects of Ucf-101 on apoptosis and the expression of Omi/HtrA2 in these rats.</p><p><b>METHODS</b>Seventy-two neonatal Wistar rats of 7-10 days old were randomly divided into 3 groups: control, postasphyxial model, Ucf-101-treated postasphyxialThe postasphyxial model was established by normobaric asphyxiaExpression of Omi/HtrA2 was determined with streptavidin-peroxidase immunohistochemistry 2, 24 and 48 hrs after asphyxia. Terminal deoxynuleotidyl-mediated nick end labeling (TUNEL) was used to ascertain the apoptosis of renal cells.</p><p><b>RESULTS</b>Compared with the control group, OmiHtrA2 expression in renal cells began to increase 2 hrs after asphyxia and peaked at 24 hrs. The expression of Omi/HtrA2 in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group (P<0.01). TUNEL-positive cells began to increase 2 hrs after asphyxia and peaked at 24 hrs in the postasphyxial model group when compared with the control group. The number of TUNEL-positive cells in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group at all time points (P<0.01).</p><p><b>CONCLUSIONS</b>The expression of Omi/HtrA2 in kidneys is increased in postasphyxial neonatal rats. The increased Omi/HtrA2 expression may play an important role in the development of postasphyxial renal injury. Treatment with Ucf-101 can reduce the expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats and thus reduce renal tububar epithelial cell apoptosis.</p>

Effect of Astragalus injection on the signal conduction of neonatal postasphyxial-serum induced human renal tubular cell injury / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate, from cytoprotein and molecular levels, the action mechanism of astragalus injection (ASI) on the signal conduction of human renal tubular cells (HK-2) injury induced by neonatal postasphyxial-serum (NPS), whether it is through activating the nuclear factor kappaB (NF-kappaB) signaling pathway.</p><p><b>METHODS</b>Taking HK-2 as the target cell and the 20% NPS as the attacking factor, the experiment was conducted by dividing the target cells into two groups before attacking, the blank control group and the ASI pretreated group. The nuclear translocation of NF-kappaB was detected by confocal microscopy with indirect immunofluorescence stain, and the amount of NF-kappaB inhibitor subunit (I-kappaBalpha) was detected by Western blot before attacking. The detections were repeated at various time points in the experiment, i.e., 15 min, 1 h and 2 h after attacking, respectively.</p><p><b>RESULTS</b>Before attacking, the nuclear translocation of NF-kappaB and the amount of I-kappaBalpha were not different in the two groups. But the former increased and the latter decreased significantly in the ASI group at all the time points after attacking with the topmost changes presented at 1 h after attacking, and significantly different to those in the control group at corresponding time</p><p><b>CONCLUSION</b>ASI pretreatment could inhibit the activation of NF-kappaB induced by postasphyxial-serum.</p>

Pneumocephalus caused by neonatal Enterobacter cloacae infection in a case / 中华儿科杂志

<p><b>OBJECTIVE</b>Gas-containing encephalo-meningitis is very rare. There have only been a few cases reported in the literature. The majority of neonatal cases reported in literature died. We report a case of a 5-day-old neonate who developed diffuse pneumocephalus from Enterobacter cloacae septicemia and intracranial infection.</p><p><b>METHOD</b>This neonate was initially treated with penicillin and mezlocillin. He also received phototherapy, intravenous infusion, correction of acidosis and other supportive therapy. Complete blood count, C-Reactive protein, cranial CT scan, blood culture, cerebrospinal fluid culture and biochemistry were tested repeatedly.</p><p><b>RESULTS</b>This neonate's condition deteriorated after admission. He developed respiratory distress, increased muscle tone and decreased level of consciousness. His WBC and C-reactive protein were elevated, while blood gas, electrolytes, liver enzymes and renal function were within normal range initially. Cranial CT scan was done which demonstrated diffuse pneumocephalus. He was transferred to a higher level hospital for further management at the request of the family. Blood culture done in our hospital subsequently showed growth of Enterobacter cloacae. The infant developed seizures and further deterioration in level of consciousness after transfer. Antibiotics were switched to penicillin and ceftizoxime. Cranial CT scan repeated 2 days after transfer showed hydrocephalus and some resolution of pneumocephalus. Cerebrospinal fluid (CSF) was aspirated from the lateral ventricles two weeks after admission. CSF culture also showed growth of Enterobacter cloacae. Antibiotic was switched to imipenem according to antibiotic sensitivity. His general condition was improved. Blood and CSF cultures were negative 1 month after admission. His head circumference at discharge was 34.6 cm. Repeat cranial CT scan at 4 month of age demonstrated severe hydrocephalus, diffuse leukomalacia and calcification. This infant suffered significant neurodevelopmental deficit. Muscle tone was diffusely increased. Head circumference at 9 month of age was 48.4 cm.</p><p><b>CONCLUSION</b>This case suggests the importance of Enterobacter cloacae infection in the newborns. Our analysis of 34 cases of Enterobacter cloacae infection showed that 93.75% - 100% were sensitive to quinolones, 94.12% were sensitive to imipenem, 73.33% were sensitive to gentamicin, 50% were sensitive to piperacillin-tazobactam. Enterobacter cloacae is generally not sensitive to penicillin, first and second generation cephalosporins (0 - 21.4%). Enterobacter cloacae septicemia and intracranial infection in neonates have a high mortality rate and can result in severe neurodevelopmental deficit in survivors.</p>

Role of serum from asphyxiated neonates in the inducement of human renal tubular cell adhesion to neutrophils / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the role of serum from asphyxiated neonates in the inducement of human renal proximal tubular epithelial cells (HK-2) adhesion to neutrophils and possible mechanisms.</p><p><b>METHODS</b>HK-2 cells were cultured randomly with 20% serum from neonates (1, 3, and 7 days after asphyxia), pyrrolidine dithiocarbamate (PDTC) or placebo. The activity of myeloperoxidase (MPO), an indicator of adhesion ability of HK-2 cells to neutrophils in suspensions, was detected by the biochemistry assay. Intercellular adhesion molecule-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) of HK-2 cells were examined with the immunohistochemical staining.</p><p><b>RESULTS</b>The expression of MPO in the post-asphyxial 1-day serum treatment group were significantly higher than that in the PDTC treatment and the control groups as well as the post-asphyxial 3 and 7-day serum treatment groups (P<0.01). The expression of ICAM-1 and NF-kappaB in the post-asphyxial 1-day serum treatment group was also significantly higher than that in the other groups (P<0.01).</p><p><b>CONCLUSIONS</b>Serum from asphyxiated neonates can induce HK-2 cell adhesion to neutrophils, possibly through activating NF-kappaB and increasing the synthesis and expression of ICAM-1 on the surface of renal tubular epithelial cells.</p>

Role and mechanism of Salvia miltiorrhiza Bunge in alleviating injury induced by hypoxia/reoxygenation in HK-2 cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Salvia miltorrhiza Bunge (SMB) is a traditional Chinese herb, which is considered to promote blood flow and remove blood stasis. This study examined whether SMB can alleviate injury induced by hypoxia/reoxygenation (H/R) in human kidney proximal tubular cells-2 (HK-2 cells).</p><p><b>METHODS</b>There were 3 experimental groups: control, H/R injury and SMB-treated H/R injury. H/R injury of HK-2 cells was induced by first covering the cells with and then removing liquid paraffin wax. Different concentrations of compound SMB solution (0.05%, 0.10%, 0.15% or 0.20%) were administered to the SMB-treated H/R injury group before the hypoxic injury. After 4, 12 and 24 hrs of hypoxia and 4, 12, 24 and 48 hrs of reoxygenation, morphologic changes of HK-2 cells were observed under an inverted microscope. Cell viability was measured by the MTT method. Lactate dehydrogenase (LDH) activity in the culture supernatants was assayed using biochemical methods; TNF-alpha levels were determined by radioimmunoassay (RIA).</p><p><b>RESULTS</b>The number of HK-2 cells was significantly reduced in the H/R injury group after hypoxia, and reached a nadir 24 hrs after hypoxia treatment. Various concentrations of SMB-treated groups showed significantly greater number of HK-2 cells than the H/R injury group. SMB solution (0.10%) produced the best effect. The levels of LDH and TNF-alpha in the H/R injury group were significantly increased, and reached a peak between 24 hrs of hypoxia and 4 hrs of reoxygenation when compared to the control group. Pre-treating with 0.10% SMB resulted in significantly lower levels of LDH and TNF-alpha than in the untreated H/R injury group at various time points of H/R.</p><p><b>CONCLUSIONS</b>SMB has protective effects against H/R injury of HK-2 cells, possibly through inhibition of inflammatory cytokines.</p>

Monocyte chemotactic protein-1 expression in coronary atherosclerosis plaque of sudden coronary death patients / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the expression of monocyte chemotactic protein 1 (MCP-1) in coronary atherosclerosis plaque of sudden coronary death (SCD) patients and the relationship between MCP-1 expression and SCD.</p><p><b>METHODS</b>Autopsy heart samples (n = 90) collected during 2001 - 2003 were divided to SCD group (n = 36) and 2 control groups: control group I, non-SCD CHD (n = 28), control group II, non-cardiac death (n = 26). The immuno-histochemistry SABC techniques (R, positive MCP-1 cell area/totl area) and computerized images analysis (A) were performed to detect the expression of MCP-1 in different groups.</p><p><b>RESULTS</b>R and A in plaques are significant higher in SCD group than control group I and II (0.1264 +/- 0.013 vs 0.0269 +/- 0.0110 and 0.0267 +/- 0.0100, P = 0.04), (0.4534 +/- 0.083 vs 0.2303 +/- 0.040 and 0.2158 +/- 0.0400, P = 0.00), and similar between control group I and control group II.</p><p><b>CONCLUSIONS</b>MCP-1 expression is increased in coronary atherosclerosis plaque of SCD patients.</p>

Effect of Erythropoietin on Apoptosis of Human Renal Tubular Cells Induced by Postasphyxial-Serum of Neonates / 实用儿科临床杂志

Objective To explore the effect of erythropoietin(EPO) on apoptosis of human renal tubular(HK-2) cells induced by postasphyxial-serum of neonates.Methods HK-2 cells were used as target cells.The experiment was divided into 4 groups,control group(n=8):HK-2 cells were maintained in standard medium;asphyxia group(n=8):HK-2 cells were treated with serum obtained from neonates with asphyxia.Each culture medium replaced with 200 mL/L suffocation DMEM/F12 serum culture medium;EPO pretreatment group(n=8):HK-2 cells were pretreated 24 h with serum contains 5?104 IU/L EPO,and then deal as asphyxia group;EPO and 5-hydroxydecanoic acid sodium salt(5-HD) pretreatment group(n=8): HK-2 cells were pretreated 24 h with serum contains 5?104 IU/L EPO and 500 ?mol/L 5-HD,and then deal as asphyxia group.All cells were cultured at 37 ℃ in humidified atmosphere with 50 mL/L CO2 for 24 h.The apoptosis rate of HK-2 cells was detected by flow cytometer.The expressions of Caspase-3 and X-linked inlnibitor of apoptosis protein(XIAP) of HK-2 cells were detected by using immunohistochemical method.Results Compared with control group,after stimulated with postasphyxial-serum,the apoptosis rate and the expression of Caspase-3 of HK-2 cells were significantly increased(Pa

Protective Effects of Astragalus on Human Renal Tubular Cells Injury Induced by Postasphyxial-Serum from Neonate / 实用儿科临床杂志

Objective To explore the protective effects of astragalus on injury of renal tubular cells(HK-2) induced by postasphyxial-serum from neonate.Methods Human renal proximal tubular cell line HK-2 cells were taken as subjects.The experiment was designed as:control group,model group,astragalus pretreatment group.The astragalus pretreatment group had 5 subgroups,which were pretreated for 24 hours.The serum of neonates who suffured asphyxia for 1 day,which concentration were 200 mL/L(volume fraction),were applied as attacking factor.The injury of morphology were observed under inverted microscope.The cell viability was measured by methyl thiazolyl tetrazolium methods.The leakage rate of lactate dehydrogenase(LDH) was determined by biochemical methods.Results Compared with control group,cell morphous changed,leakage rate of LDH elvated and cell survival rate decreased in model group,the variances were obviously significant(Pa

Role of Na~+/H~+ Exchanger 1 on Injury of Human Renal Tubular Cell Induced by Postasphyxial-Serum of Neonates / 实用儿科临床杂志

Objective To explore the role of Na~+/H~+ exchanger 1(NHE1) in injury of human renal tubular cells(HK-2) induced by postasphyxial-serum of neonates.Methods HK-2 was used as the target cell.The attacking concentration of postasphyxial-serum of neonates was 200 mL/L.First,the experiment was designed as control group and asphyxia group,the expression of NHE1 in the HK-2 was detected by immunohisto chemical method in the cells.Second,the experiment group was designed as control group,asphyxia group,and pretreatment with 5-N-Ethyl-N-isopropylamiloride(EIPA) group,then the change of morphology was observed under inverted microscope,and the cell viability was measured by methyl thiazolyl tetrazolium(MTT) method,and the leakage rate of lactate dehydrogenase(LDH) was determined by biochemical methods.Results Compared with blank control group,the expression of NHE1 in the HK-2 was increased signi-ficantly in asphyxia group,the changes of morphology of HK-2 was most serious and obvious,the cell viability decreased,and the leakage rate of LDH increased significantly in asphyxia group.But compared with asphyxia group,the change of morphology of HK-2 was greatly improved,the cell injury was decreased obviously,the leakage rate of LDH was increased and viability was decreased in pretreatment group in a dose 2 ?mol/L.Conclusions The postasphyxial-serum may induce the expression of NHE1,which plays an important role in injury of renal tubular cell induced by postasphyxial-serum in neonates,and inhibiting activity of NHE1 may relieve the injury of renal tubular cells induced by postasphyxial-serum in neonates.