OBJECTIVE: Extracellular matrix (ECM) deposition is a major reason of pulmonary fibrosis in hyperoxia-induced lung injury. However, the relevant mechanism has not been identified. This study examined the gene expressions of matrix metalloproteinases-8 (MMP-8, a catabolic enzyme of type I collagen) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in neonatal rats with hyperoxi-induced pulmonary injury in order to explore the role of MMP-8 and TIMP-1 in pulmonary fibrosis. METHODS: Eighty term newborn rats were randomly exposed to hyperxia (FiO2=0.90, hyperxia group) and to room air (FiO2=0.21, control group) (n =40 each). Lung injury was induced by hyperxia exposure. The content of type I collagen and the expressions of type I collagen protein and MMP-1 mRNA and TIMP-1 mRNA were assayed with enzyme linked immunoadsorbent (ELISA), immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) respectively on days 1, 3, 7, 14 and 21 after exposure. RESULTS: The content of type I collagen and the expression of type I collagen protein in the hyperxia group were statistically higher than those in the control group at 14 and 21 days post-exposure. The MMP-8 mRNA expression decreased while the TIMP-1 mRNA expression increased significantly in the hyperxia group as compared to the control group at 14 and 21 days post-exposure. CONCLUSIONS: Hyperxia exposure down-regulates MMP-8 mRNA expression and up-regulates TIMP-1 mRNA expression. This results in a reduction of ECM degradation, thereby ECM deposition occurs in lung tissue, which may be an important mechanism of pulmonary fibrosis following hyperoxia-induced lung injury.［Chin J Contemp Pediatr, 2007, 9 (1):1- 5］

OBJECTIVE: To evaluate the effect of epilepsy on sleep in children. METHODS: Whole night polysomnography was performed in 48 epileptic children and 12 healthy controls. The 48 epileptic children were divided into focal seizure and generalized seizure groups and into waking seizure and sleeping seizure groups according to the time of occurrence of the seizures. Various parameters of sleep structure were analyzed. RESULTS: The sleep efficiency of epileptic children was significantly lower than that of the healthy controls (85.4 ± 8.6% vs 90.9 ± 5.8%; P<0.05). The total recording time (TRT) of sleep was significantly longer and the sleep efficiency was significantly lower in the focal seizure group compared to the control group (P<0.05). The percentage of stage 1 non-rapid-eye-movement sleep (S1 sleep) increased and the percentage of rapid-eye-movement (REM) sleep decreased in the generalized seizure group compared to the control group (P<0.05). The percentage of S1 sleep increased and both the percentage of REM sleep and the sleep efficiency decreased in the sleeping seizure group as compared with the control group (P<0.05). There were no significant differences in the parameters of sleep structure between the waking seizure and the control group. Among the sleeping seizure group, the children with generalized seizure showed significantly lower REM sleep percentage and sleep efficiency, and those with focal seizure had significantly longer TRT and higher S1 sleep percentage as compared with the controls. CONCLUSIONS: Epilepsy affects sleep structure of patients, and different types of seizure have different influences on sleep structure. Children with generalized seizure have prolonged light sleep and shortened REM sleep. When generalized seizures occur during waking, the increase of light sleep is more pronounced. While generalized seizures occur during sleeping, REM sleep reduction is more prominent. Children with focal seizures have decreased sleep efficiency. When focal seizures occur during waking, the sleep structure of patients is normal. However, when seizures occur during sleeping light sleep increases and sleep efficiency decreases.［Chin J Contemp Pediatr, 2007, 9 (1):6-10］

OBJECTIVE: P-glycoprotein 170 (P-gp) is a plausible biologic candidate for pharmacoresistance in epilepsy. The expression and efflux efficiency of P-gp is influenced by a polymorphism (C3435T) in the encoding gene (MDR1). The CC genotype at the MDR1 C3435T polymorphism was reported to be associated with the response to antiepileptic drug treatment. This study attempted to replicate this finding by examining the association of this genetic polymorphism with response to antiepileptic drug treatment in ethnic Han Chinese children with epilepsy. METHODS: Two hundred and fourteen ethnic Han Chinese children with epilepsy were classified based on the response to antiepileptic drug treatment: drug-nonresponsive and drug-responsive. DNA samples were obtained from the patients. Genotypes of the C3435T polymorphism were determined by traditional polymerase chain reaction followed by restriction digestion (PCR-RFLP). The frequency of genotypes and alleles between the two groups was compared by Chi-square test. RESULTS: Of the 214 patients, 164 were dru-responsive and 50 were drug-nonresponsive. There were no significant differences in the allele frequency and genotype frequency between the two groups. CONCLUSIONS: There is no an association between the CC genotype or C allele at the locus of C3435T in MDR1 gene and response to antiepileptic drug treatment in ethnic Han Chinese children with epilepsy.［Chin J Contemp Pediatr, 2007, 9 (1):11-14］

OBJECTIVE: To identify the risk factors for bronchopulmonary dysplasia (BPD) in neonates with respiratory distress syndrome (RDS). METHODS: Data from 72 patients with RDS (birth weight 1 607±277 g; gestational age 29.47±2.54 weeks)who were hospitalized for >28 days and who received mechanical ventilation treatment between January 2001 and August 2005 were studied retrospectively. A logistic regression analysis was used to identify the risk factors associated with the development of BPD. RESULTS: Of the 72 patients, 17 developed BPD (23.6%). Uniovariate analysis revealed that in addition to a gestational age of ≤ 30 weeks and a birth weight below 1 250 g, the times of mechanical ventilation treatment (≥2 times), concurrent pulmonary infection and pneumorrhagia, prolonged mechanical ventilation (≥5 days), and positive sputum bacterial cultures on 2 occasions were all associated with an increase in the incidence of BPD. Multivariate logistic analysis revealed that birth weight below 1 250 g, prolonged mechanical ventilation (≥10 days),and positive sputum cultures on 3 or more occasions were independent risk factors for BPD (OR=6.614,14.997and 39.752 respectively). CONCLUSIONS: The risk for BPD is multifactorial. Preventing small gestational age and low birth weight prematurity, decreasing the duration of mechanical ventilation and treatment of pulmonary infection are necessary to prevent BPD.［Chin J Contemp Pediatr, 2007, 9(1):15-18］

OBJECTIVE: To study the correlation of erythrocyte immune function between normal neonates and their mothers and the influence of various obstetric factors on neonatal erythrocyte immune function. METHODS The adherent rate of complement 3b-receptor on the surface of red blood cells (RBC-C3bRR) and the immune complex adherent rate of red blood cells (RBC-ICR) were detected using the erythrocyte saccharomyces rosette test in 104 normal neonates and their mothers. The correlation of erythrocyte immune function between neonates and their mothers was evaluated by the maternal-infant paired test. RESULTS: The levels of RBC-C3bRR (16.80±1.56% vs 16.23±1.63%; P<0.05) and RBC-ICR (5.72±1.63% vs 5.02±1.38%; P<0.01)) in neonates were significantly higher than those in their mothers. There was a significantly positive correlation in RBC-ICR levels between neonates and their mothers (r = 0.28, P<0.05). No correlation was found in RBC-C3bRR levels between the two groups. Neither RBC-C3bRR nor RBC-ICR levels of neonates were associated with various obstetric factors such as amniotic fluid, placenta, umbilical cord, parturient patterns, and puerpera anemia and pregnancy-induced hypertension syndrome. CONCLUSIONS: The erythrocyte immune function in neonates has a relatively mature level and correlates with their mothers' erythrocyte immune function. Various obstetric factors have no influences on neonatal erythrocyte immune function.［Chin J Contemp Pediatr, 2007, 9 (1):19-21］

OBJECTIVE: To study the serum levels of insulin-like growth factorⅠ(IGF-I) and growth hormone (GH) in neonates with hypoxic-ischemic encephalopathy (HIE) and to investigate the relationship of serum levels of IGF-I and GH with the severity of HIE. METHODS: Serum levels of IGF-I and GH were measured within 72 hrs (acute stage) and on the 26-28th days (convalescence stage) of life in 53 HIE neonates. There were 30 babies in the mild HIE group, 15 babies in the moderate HIE group, and 9 babies in the severe HIE group. Thirty normal newborns were used as the control group. Neonatal behavioral neurological assessment (NBNA) was performed on HIE neonates at the acute and convalescence stages. RESULTS: The IGF-I levels of the mild, moderate and severe HIE groups measured within 72 hrs of life were 59.65±29.61, 33.56±17.32, and 23.58±13.57 ng/mL respectively and those of the three HIE subgroups on the 26-28th days after birth were 89.26±48.65, 71.46±38.35, and 54.39±26.39 ng/mL respectively. The serum IGF-I levels of HIE neonates at both acute and convalescence stages were significantly lower than those of the control group(71.23±35.42 and 96.54±52.38 ng/mL respectively; both P< 0.01), and associated with the severity of HIE as well as NBNA scores. GH levels were not significantly correlated to the severity of HIE and NBNA scores. CONCLUSIONS: Serum IGF-I levels can be used as a marker for estimating the severity and the outcome of neonatal HIE. ［Chin J Contemp Pediatr, 2007, 9 (1) :22-24］

OBJECTIVE: The anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital coronary artery abnormality. This study aimed to investigate the clinical characteristics, diagnosis and treatment of the disorder. METHODS: The medical data, including common clinical presentations, the findings of the digital subtraction angiogram (DSA), echocardiograms and the electrocardiograph (ECG), surgical records and the outcome, of 10 children with ALCAPA between June 2001 and February 2005 were retrospectively reviewed. RESULTS: Diaphoresis, fantod, breathlessness and difficult feeding were commonly presented in the patients with ALCAPA. ECG, echocardiography and DSA examinations showed characteristic changes in these patients. The Takeuchi procedure was performed in 4 patients, direct aortic reimplantation in 4 cases and aortic reconstruction in 2 cases. After operation the symptoms of 8 patients were improved but 2 died. CONCLUSIONS: ALCAPA patients have characteristic clinical manifestations and lab findings. This is helpful in making an early diagnosis of ALCAPA. Early surgical treatment can improve the patients' outcome.［Chin J Contemp Pediatr, 2007, 9 (1):25-27］

OBJECTIVE: Acute promyelocytic leukemia (APL) is a specific type of hematopoietic malignancy, accounting for 10% of the de novo acute myeloid leukemia (AML). The data on long-term outcome of APL in children are limited. The aim of this study was to investigate the clinical biological features, diagnosis, prognosis and long-term survival of childhood APL. METHODS: A total of 46 children with newly diagnosed APL from April 1998 to October 2005 were enrolled into this study. Induction treatment containing all-trans retinoic acid (ATRA) plus daunorubicin (DNR) or pirarubicin (THP) was performed on these patients, followed by 6 courses of chemotherapy consolidation: DNR, homoharringtonine or etoposide plus Ara-C. A maintenance therapy was then administered once 3-6 months. The total period of treatment was 2.5 years. RESULTS: Of the 39 patients who had completed the regular treatment, 36 (92.3%) achieved a complete remission. The 5-year cumulative incidence of relapse (CIR) was 28.6%. The estimated overall survival (OS) rates at 1, 3 and 5 years were (86.1±5.8)%, (76.1±7.5)% and (70.2±8.9)％respectively, while the event free survival (EFS) rates were (78.4±6.8)%，(63.6±8.7)% and (53.1±10.0)% respectively. The 5-year OS rate of patients with WBC less than or equal to 10.0×109/L was (81.4±10.3)%, which was significantly higher than that with WBC greater than 10.0×109/L [(51.6±14.7)％, P<0.05]. Five patients with RT-PCR positive for PML/RARα S (short) subtype died eventually although all of them achieved CR, but none of the 13 patients with PML/RARα L (long) subtype died. CONCLUSIONS: Remission induction therapy with ATRA + DNR or THP is effective and safe for newly diagnosed childhood APL. The remission induction therapy combined with chemotherapy containing high/intermediate dose Ara-C can improve the long-term survival rates of APL patients. High WBC count and S subtype of PML-RARa are two poor prognostic factors for children with APL. ［Chin J Contemp Pediatr, 2007, 9 (1):28-33］

OBJECTIVE: To investigate Daxx expression and its clinical significance in children with acute leukemia. METHODS: The expression of Daxx protein was detected by immunohistochemical assay in 50 children with newly diagnosed acute leukemia (34 cases of acute lymphocytic leukemia and 16 cases of acute non-lymphocytic leukemia). Twenty children with normal bone marrow were used as the control group. RESULTS: Daxx protein was expressed in 38.0% of 50 children with acute leukemia, which was significantly higher than that of the control group (5.0%) (P<0.05). The children with acute non-lymphocytic leukemia had significantly higher Daxx expression levels (62.5%) than those with acute lymphocytic leukemia (26.5%; P<0.05) as well as the control group (P<0.05). There were no significant differences in the Daxx expression between acute lymphocytic leukemia children and the control group. Daxx protein was expressed in 55.6% of high risk group of acute lymphocytic leukemia but it was not expressed in standard risk group of acute lymphocytic leukemia (P<0.05). CONCLUSIONS: Daxx expression is abnormal in children with acute leukemia and associated with some clinical features of acute leukemia, suggesting that it may play an important role in the genesis and development of acute leukemia. ［Chin J Contemp Pediatr, 2007, 9 (1) :33-36］

OBJECTIVE: To investigate the effects of mild hypothermia on sequential events of neuronal apoptosis following hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHODS: A model of HIBD was prepared by ligating the left common carotid artery in 7-day-old rats, followed by 8% hypoxia exposure. HIBD rats were randomly assigned into a hypothermia group (rectal temperature = 33 ℃) and a normothermia group (rectal temperature = 36 ℃). TUNEL, Haematoxylin and Eosin, and Nissl staining were used to detect neuronal apoptosis. Western blotting, RT-PCR and enzyme activity measurement were used to evaluate the changes of plasma and mitochondrial cytochrome c (Cyt c), caspase-3 mRNA expression and caspase-3 enzyme activity, respectively. RESULTS: The number of apoptotic cells in the ipsilateral hemisphere of the hypothermia group was significantly reduced compared with that of the normothermia group at 72 hrs post-HI (6.4±1.7% vs 25.3 ± 1.5%) (P<0.01).Analysis of Western blotting showed that Cyt c levels increased in the cytosolic fraction, but decreased significantly in the mitochondrial fraction in the ipsilateral hemisphere of the hypothermia group at 24, 48 and 72 hrs of HI insult compared with the normothermia group (P<0.05). Caspase-3 mRNA increased significantly after 24 hrs post-HI in the normothermia group, and this change became more pronounced with time. Mild hypothermia treatment decreased significantly caspase-3 mRNA expression at 24, 48 and 72 hrs post-HI (P<0.05). Caspase-3 activity gradually increased 2 hrs after HI insult and peaked at 24 hrs in the normothermia group. Mild hypothermia treatment resulted in a significant reduction in caspase-3 activity in the ipsilateral hemisphere, with an optimal effect produced at 24 hrs post-HI (2.42 ± 0.5 RFU vs 34.7 ± 3.2 RFU; P＜0.01). CONCLUSIONS: Mild hypothermia treatment attenuates neuronal apoptosis following HIBD, possibly through a reduction in Cyt c release from mitochondria and an inhibition of caspase-3 mRNA expression and its enzyme activity. ［Chin J Contemp Pediatr, 2007, 9 (1) :37-41］

OBJECTIVE: To study the effect of endogeneous gangliosides (Gls) on integrin α2β1-mediated adhesion of neuroblastoma cells to collagen (Col). METHODS: Neuroblastoma SK-N-SH cell line was cultured in the modified eagle's medium with the presence of 10 μm D-threo-1-phenyl-2-decanolamino-3-morphinolin-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase. Flow cytometry was used to detect the expression of integrin α2β1 in the cell line. The effects of Mg2+ and monoclonal antibodies to integrin α2β1 on the adhesion of the cell line to immobilized Col were observed. The adhesion cell number was measured with the BCA method and presented with absorptance A570. RESULTS: There was a high expression of integrin α2β1 in the SK-N-SH cell line without D-PDMP treatment. Endogenous Gls in the cells were almost depleted after 6-day exposure to D-PDMP, but the integrin α2β1 expression was not significantly changed. 1 mmoL/L Mg2+ treatment increased significantly the number of adhesion cells in the SK-N-SH cell line. The adhesion to Col of the SK-N-SH cells exposed to D-PDMP which Gls was depleted was significantly reduced compared with the control SK-N-SH cells treated with 1 mmoL/L Mg2+ (A570：0.33±0.016 vs 0.57±0.033; P<0.01). After endogeneous Gls was added into the Gls-depleted SK-N-SH cells, the adhesion of the cells was restored (A570∶0.52±0.035). The adhesion of SK-N-SH cells was significantly blocked by anti-α2 and anti-β1 monoclonal antibodies, with A570 of 0.31± 0.018 and 0.36± 0.021 respectively. CONCLUSIONS: Endogenous tumor Gls increases neuroblastoma cell adhesion to Col by regulating the function of integrin α2β1, but has no effects on the integrin expression. It is suggested that tumor Gls may play a role in migration, invasion and metastasis of tumor cells.［Chin J Contemp Pediatr, 2007, 9 (1):42-46］

OBJECTIVE: To examine the feasibility and practicability of quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) with SYBR GREEN I fluorescence for detecting the MYCN mRNA expression in neuroblastoma cell line LA-N-5. METHODS: MYCN mRNA expression in LA-N-5 cells was measured using real time RT-PCR with SYBR GREEN I. Glyceraldehyde phosphate dehydrogenase (GAPDH) was used as internal control. The level of the MYCN mRNA was calculated as MYCN copies/GAPDH copies. RESULTS: Standard curves were linear and showed high correlations (R2>0.99). The ratio of MYCN mRNA copies to GAPDH mRNA copies was calculated based on specific PCR products. The MYCN mRNA level in LA-N-5 cells was obtained (17.4±1.2). CONCLUSIONS: Quantitative RT-PCR with SYBR GREEN I fluorescence may be a sensitive and reliable method for detecting the MYCN mRNA expression. It may also be potential applicable for detecting the MYCN mRNA expression in the small amount neuroblastoma tissues.［Chin J Contemp Pediatr, 2007, 9 (1):47-50］

OBJECTIVE: The activation of N-methyl-D-aspartate(NMDA) receptors plays critical roles in the pathogenesis of diseases of the brain. This study aimed to examine the expression of phosphor-NR1 S897 in the cerebral cortex after NMDA microinjection in vivo. METHODS: Forty seven-day-old Sprague-Dawley rats were randomly assigned into normal control and NMDA injection groups. The rats from the NMDA injection group were injected with 10 mmol of NMDA and were sacrificed 1 hr after injection. 2, 3, 5-triphenyltetrazolium chloride (TTC) and fluorescent immunohistochemical stainings were conducted and the fluorescence intensity OD value between the two groups was compared. RESULTS: TTC staining from the two groups was normal. Expression of phosphor-NR1 S897 in the cerebral cortex of the ipsilateral hemisphere to injection in the NMDA injection group decreased significantly compared with the normal control group, with OD values of 0.366±0.087 vs 1.364±0.268 (P<0.01). CONCLUSIONS: NMDA microinjection, as a hypoxia-ischemia (HI) insult, significantly decreased the expression of phosphor-NR1 S897. This indicates the importance of the HI-NMDA-phospho-NR1 S897 dephosphorylation-cell damage pathway in HI brain damage.［Chin J Contemp Pediatr, 2007, 9(1):51-53］

OBJECTIVE: Topiramate (TPM) has an evident efficacy in the treatment of childhood epilepsy for multiple pharmacologic properties. However it was reported that it may cause adverse effects such as liver failure and hepatitis, which arouses the attention of the medical field. This study aimed to investigate the hepatotoxicity of low-dosage, high-dosage TPM or TPM along with valproate sodium (VPA) in aspects of biochemistry indexes, oxidative stress indexes and liver pathomorphology in young rats. METHODS: Sixty 3-week-old male Wistar rats were randomly assigned into five groups of 12 rats (Groups A-E). The rats in the experimental groups (Groups A-C) were administered intragastrically with TPM 40 mg/(kg?d) , 80 mg/(kg?d) and TPM 40 mg/(kg?d) plus VPA 300 mg/(kg?d) respectively. The rats in the negative control group (Group D) were administered with the same volume of distilled water. The ones in the positive control group (Group E) were treated by injection of 10% carbon tetrachloride dissolved in olive oil subcutaneously at a dose of 5 mL/kg twice a week. After 3-month administration, the changes of body weight and liver pathomorphology were observed; biochemical markers in serum and indexes of oxidative stress in liver homogenate associated with hepatotoxicity were examined. RESULTS: The body weight of rats in the experimental groups were significantly lower than that of rats in the negative control group. The levels of serum alanine aminotransferase, alkaline phosphatase and the content of malondialdehyde, and the activity of superoxide dismutase in liver tissues did not change significantly in the experimental groups. The contents of glutathion in the high dosage of TPM group (29.85±1.62 mg/g prot ) or in the TPM plus VPA group (29.63±4.47 mg/g prot) were significantly reduced compared with those of the negative control group (33.09±1.69 mg/g prot) and that of the low dosage of TPM group (32.43±2.11 mg/g prot) (both P＜0.05). In the histopathological examination, extensive steatosis and diffuse punctate necrosis of hepatocytes distributed in the portal area were found by microscopy in the positive control group. There were granular degeneration of some hepatocytes near the central veins of hepatic lobules in the low dosage of TPM group and punctate necrosis of some hepatocytes in the high dosage of TPM group. In the TPM plus VPA group, histological examination showed granular degeneration and fatty degeneration of partial liver cells and punctate necrosis of some hepatocytes. CONCLUSIONS: Long-term use of TPM can decrease antioxidant capacity of organism, resulting in slight pathological changes of liver tissues. High dosage of TPM or TPM along with VPA administration enhances the risk of the side effects.［Chin J Contemp Pediatr, 2007, 9 (1):54-58］

OBJECTIVE: To investigate the gene expression of Kiss-1 in the hypothalamus of true precocious female rats at various stages of development. METHODS: Forty 5-day-old normal female Sprague-Dawley rats were randomly assigned into four groups of 10 rats: Control group 1, Control group 2, Model group 1 and Model group 2. The rats from the two model groups were injected with 300 μg of danazol at 5 days of age to induce true precocious puberty. The two control groups were injected with normal saline instead. For the determination of Kiss-1 mRNA expression in the hypothalamus, the rats of the Model group 1 were sacrificed during the first diestrus (early puberty) and meanwhile the rats of the Control group 1 were sacrificed when they were at prepuberty; the Control group 2 rats were sacrificed at the first diestrus (early puberty); the rats of the Model group 2 were sacrificed during the second diestrus (middle puberty). The expression of Kiss-1 mRNA in the hypothalamus in the four groups was detected using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Kiss-1 mRNA expression in the hypothalamus in Model group 1 and Model group 2 increased by 1.4-fold and 2.8-fold, respectively, compared with that of Control group 1 (P<0.05). Model group 2 showed significantly higher Kiss-1 mRNA levels than Model group 1 (P<0.05). There were no statistical differences in the Kiss-1 mRNA expression between Control group 2 and Model group 1. CONCLUSIONS: Gene expression of Kiss-1 is associated with the developmental period of true precicous puberty, suggesting that Kiss-1 might play a role in the pathogenesis of this disorder.［Chin J Contemp Pediatr, 2006, 9(1):59-62］

OBJECTIVE: Cigarette smoke extract (CSE) can induce injuries of pulmonary II epithelial cells, activate nuclear factor-κB and increase tumor necrosis factor-α(TNF-α) secretion. This study aimed to investigate whether azithromycin can protect pulmonary II epithelial cells from injuries induced by CSE and relevant mechanisms. METHODS: Pulmonary II epithelial cells (A549 cells) were cultured in vitro. After 48 hrs of culture the cells were randomly treated with serum-free DMEM only (blank control group), azithromycin + serum-free DMEM, CSE+ serum-free DMEM or CSE+azithromycin. Eight hours later the morphology of A549 cells, the activity of NF-κB and the levels of TNF-α were measured by inverted microscope, immunohistochemistry and ELISA. RESULTS: The morphology and structure of A549 cells were changed, NF-κB activity increased (dark brown staining ) and TNF-α levels (0.307±0.036 pg/mL vs 0.234±0.028 pg/mL)increased in the CSE+ serum-free DMEM group compared with the blank control group (P<0.01). CSE together with azithromycin treatment recovered partly the morphological injuries of A549 cells. It also attenuated NF-κB staining and decreased TNF-α levels from 0.307±0.036 pg/mL (CSE+serum-free DMEM group) to 0.269±0.009 pg/mL (P<0.05). CONCLUSIONS: Azithromycin may inhibit NF-κB activity, decrease TNF-α secretion and thus lessen cytotoxicity of CSE to A549 cells.［Chin J Contemp Pediatr, 2007, 9 (1) :63-66］