Therapeutic effects and modulatory mechanism of Alpiniae oxyphyllae Fructus in chronic intermittent hypoxia induced enuresis in rats.

OBJECTIVE: The objective of this study was to explore the effect of Alpiniae oxyphyllae Fructus (AOF) on a rat model of chronic intermittent hypoxia (CIH)-induced enuresis. Findings of this study may help identify therapeutic targets in children with nocturnal enuresis (NE). METHODS: Female rats were randomly divided into a control group (saline gavage, 4 weeks of normal air), CIH group (saline gavage, 4 weeks of CIH), and AOF group (AOF gavage, 4 weeks of CIH). The variables measured in this study included water intake, urine output, bladder leak point pressure (BLPP), malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity. The expression levels of the purinergic P2X3 receptor, muscarinic M3 receptor, and ß3-adrenergic receptor (ß3-AR) in the bladder were also measured. The bladder was subjected to haematoxylin and eosin (HE) and Weigert staining, and histological changes were observed under a light microscope to evaluate the morphological changes in the bladder in each group. RESULTS: Compared with the control group, urine output was increased, and the BLPP was decreased in the CIH group, but AOF administration decreased urine output and increased BLPP. In addition, the serum MDA level increased and the SOD activity decreased in the CIH group compared with the control group. Administration of AOF decreased the MDA level and increased the SOD activity. Additionally, compared with the control group, HE and Weigert staining in the CIH group showed that the bladder detrusor muscle bundles were disordered and loose, some muscle bundles were broken, the content of collagen fibres in the gap was reduced, and the gap was significantly widened. However, following the administration of AOF, the bladder detrusor muscle bundles were neatly arranged, and the content of collagen fibres in the gap was increased. Furthermore, compared with the control group, the purinergic P2X3 receptor and muscarinic M3 receptor were expressed at higher levels, and ß3-AR was expressed at lower levels in the CIH group, but AOF administration decreased the expression of the purinergic P2X3 receptor and muscarinic M3 receptor and increased the expression of the ß3-AR. CONCLUSIONS: AOF improves enuresis by inhibiting oxidative stress and regulating the expression of the purinergic P2X3 receptor, muscarinic M3 receptor, and ß3 adrenergic receptor.

Current perspectives on the correlation of nocturnal enuresis with obstructive sleep apnea in children.

BACKGROUND: Obstructive sleep apnea (OSA) and nocturnal enuresis (NE) are common clinical problems in children. OSA and NE are thought to be interrelated, but the exact pathophysiological mechanisms are not yet clear. This review aims to explain the possible pathogenesis of NE in children with OSA. DATE SOURCES: We have retrieved all relevant original articles from Database that have been published so far, including the prevalence studies of NE and OSA in children, sleep characteristic studies that use polysomnography (PSG) to focus on children with NE, and studies on the relationship between OSA and NE. RESULTS: Clinical studies have revealed that the risk of NE in children with OSA was increased compared with that of their healthy peers. This increased risk may be associated with sleep disorders, bladder instability, detrusor overactivity, nocturnal polyuria, endocrine and metabolic disorders, and inflammation. CONCLUSIONS: Cardiopulmonary and renal reflex-induced neuroendocrine disorder may play an important role in the mechanism of NE in children with OSA, but this remains to be confirmed by animal studies. Other causes such as oxidative stress and inflammatory responses need to be further researched.

Association of T lymphocyte immune imbalance and IL-10 gene polymorphism with the risk of obstructive sleep apnea in children with obesity.

PURPOSE: The purpose of this study is to determine the role of T lymphocyte immune imbalance and interleukin (IL)-10 gene polymorphism in the development of obstructive sleep apnea (OSA) in obese children. METHODS: One hundred obese children at high-risk and low-risk for OSA based upon a sleep questionnaire were selected. Peripheral blood T lymphocyte subsets were measured by flow cytometry, and plasma IFN-γ, IL-4, and IL-10 cytokines were detected by ELISA. The relationships between OSA and the above variables were analyzed. IL-10 gene polymorphisms were analyzed by DNA sequencing. RESULTS: Ninety subjects completed all the tests. Forty-two patients were diagnosed as OSA by PSG. Compared with non-OSA children, the levels of CD4+ T cells, IFN-γ, and IL-4 were increased (P < 0.05) whereas the numbers of CD4+ CD25+ Treg and NKT cells and the levels of IL-10 were reduced (P < 0.05). Multiple linear regression analysis showed that IL-10 level was negatively associated with OAHI (OR 0.352, 95% CI 0.286-0.540; P < 0.05). In multivariate analysis, IL-10 also had a strong negative association with OSA after adjustment for confounding factors from models 1 to 3. Correlative analysis showed that IL-10 levels had a positive association with CD4+ CD25+ Treg (r = 0.628, P < 0.01). Furthermore, the IL-10/A-1082G gene polymorphism correlated with OSA. CONCLUSIONS: T lymphocyte immune imbalance was associated with OSA and IL-10 may play an important protective role in the pathogenesis of OSA in obese children.

Obesity in children with different risk factors for obstructive sleep apnea: a community-based study.

This study investigated the association between obesity and obstructive sleep apnea (OSA) in preschool and school-age children. Parents of obese and randomly chosen normal weight children completed a questionnaire on sleep-related symptoms, demography, family, and medical history. All subjects were invited to undergo polysomnography (PSG). OSA cases were defined as obstructive apnea hypopnea index (OAHI) ≥1. A total of 5930 children were studied with 9.5% obese (11.9% boys/6.1% girls), 205/2680 preschool and 360/3250 school children. There were 1030 children (535 obese/495 normal weight) who underwent PSG. OSA was higher in obese children and obese school children had higher OAHI, arousal index, and shorter total sleep time. However, there was no positive correlation between OSA and body mass index (BMI). The main risk factors for OSA in preschool children were adenotonsillar hypertrophy and recurrent respiratory tract infection. The main cause for OSA in school children was a history of parental snoring and obesity. Mallampati scores and sleep-related symptoms were found to be associated with OSA in both preschool and school children. CONCLUSION: We demonstrated differential risk factors for OSA in obese children, which suggest that a different mechanism may be involved in OSA development in preschool and school-age children. WHAT IS KNOWN: Various risk factors have been reported in obese children with OSA owing to the different age and different study design. Obese children have a higher prevalence and severity of obstructive sleep apnea (OSA). OSA risk factors in obese children are affected by different ages and study designs. WHAT IS NEW: A differential prevalence and risk factors for obese preschool and school-age children with OSA has been demonstrated.

[Control study on antimicrobial resistance of invasive and non-invasive Streptococcus pneumoniae in children].

OBJECTIVE: To investigate the antimicrobial resistance of invasive and non-invasive Streptococcus pneumoniae (SP) strains in children and to provide a basis for proper use of antimicrobial drugs in the treatment of SP infection. METHODS: Seventy children who were diagnosed with invasive pneumococcal diseases (IPD) between January 2009 and December 2013 were enrolled, and 164 children with lower respiratory tract infection caused by SP were randomly selected as the control group. The samples from sterile sites (blood, cerebrospinal fluid, etc) of children with IPD, as well as the sputum samples of children in the control group, were collected for bacterial culture, and the drug susceptibility tests for isolated SP strains were conducted. RESULTS: A total of 82 invasive strains of SP were isolated from sterile sites of 70 children with IPD; 49 strains (60%) were isolated from blood, and 19 strains (23%) from cerebrospinal fluid. The detection rate of invasive SP strains decreased from 2009 to 2013 (P<0.01). The total detection rates of penicillin-nonsusceptible SP from the invasive and non-invasive strains were 27% and 17% respectively (P>0.05). Among invasive strains, the penicillin-nonsusceptible SP strains had significantly higher rates of insusceptibility to cefotaxime, ceftriaxone, and cefepime than the penicillin-susceptible SP (P<0.01). There were significant differences in the rates of insusceptibility to cefotaxime, ceftriaxone, and meropenem between the sensitive and non-sensitive SP strains (P<0.05). The multidrug resistance rates of the invasive and non-invasive SP strains were 89% and 93% respectively (P>0.05). CONCLUSIONS: Invasive SP can easily invade the blood in children, but the total detection rate has decreased year by year. The results of drug sensitivity tests have guiding significance for proper use of antimicrobial drugs for different SP infections.

Multiple system morbidities associated with children with snore symptom.

OBJECTIVE: To exam the relationship between snoring and morbidities of multiple systems in children. STUDY DESIGN: Children with snoring were enrolled and divided into primary snorer (PS) group and obstructive sleep apnea hypopnea syndrome (OSAHS) group based on polysomnography. The healthy children served as the control group. The growth parameters, maxillofacial malformations, blood chemistry, electrocardiogram, and echocardiogram were recorded and intelligence testing was performed in the enrolled children who were ≥6 years old. RESULTS: The weight and height were similar in the control group (n = 60) and the PS group (n = 63), but lower in the OSAHS group (n = 89; P < 0.001). Occurrence of adenoidal face and dental malocclusion in the OSAHS and the PS group was significantly higher than that in the control group (P < 0.001). Compared with the control group, the OSAHS group had a lower serum high-density lipoprotein cholesterol level, higher low-density lipoprotein cholesterol level; and a possible higher pulmonary artery pressure based on the echocardiogram (P < 0.001). All the above parameters in the PS group were similar to those in the control group. Full-scale IQ and performance IQ of the OSAHS group was lower (P < 0.001), attention deficits were significantly higher in the OSAHS group (P < 0.001), but were similar in the PS group when compared to the control group. CONCLUSIONS: OSAHS in children is associated with delayed growth, maxillofacial malformations, impaired cognitive functions, abnormalities in lipid metabolism, and changes in pulmonary artery pressures. PS children also have higher incidence of maxillofacial malformations but have a normal growth and normal cognitive functions.

Nocturnal enuresis in children: prevalence, correlates, and relationship with obstructive sleep apnea.

OBJECTIVES: To examine the prevalence and correlates of nocturnal enuresis (NE) in primary school children, and to compare the prevalence of NE in children with and those without obstructive sleep apnea (OSA). STUDY DESIGN: Parents of children aged 6-11 years completed a questionnaire eliciting information on sleep-related symptoms, demography, and family and past medical history. Children screened due to high risk for OSA, along with a randomly chosen low-risk group, underwent overnight polysomnography (PSG). RESULTS: A total of 6147 children (3032 girls) were studied. The overall prevalence of NE (≥1 wet night/month) was 4.6% (6.7% of boys and 2.5% of girls). Boys had a significantly greater prevalence across all age groups. In 597 children (215 girls) who underwent PSG, the prevalence of NE was not greater in children with OSA, but was increased with increasing severity of OSA in girls only. Boys with NE had longer deep sleep duration. Sex and sleep-related symptoms were associated with NE. CONCLUSIONS: This community-based study demonstrated a sex-associated prevalence of NE in relation to increasing OSA severity.

[The role of phosphorylation of c-Jun NH2-terminal kinase in airway remodeling of asthmatic rats and the effect of glucocorticoids].

OBJECTIVE: To study the role of phosphorylation of c-Jun NH2-terminal kinase (JNK) in asthmatic airway remodeling and to explore the effect of glucocorticoids on IL-1beta, JNK and airway remodeling. METHODS: Forty-eight 4 - 6 week old male SD rats were randomly divided into 4 groups with 12 rats in each group: the control group, the asthma group, the budesonide (BUD) group, and the dexamethasone (DXM) group. The asthma airway remodeling models were made by intra-peritoneal injection of ovalbumin (OVA) on days 1 and 8 and inhalation of OVA every other day for 12 weeks since day 15. The BUD group underwent inhalation of BUD 30 min before every inhalation; the DXM group received intra-peritoneal injection of DXM 30 min before every inhalation; while the control group received normal saline instead of OVA. The histopathology and ultrastructural changes of pulmonary tissues were observed by light microscope and transmission electron microscope (TEM). The total bronchial wall thickness (Wat) and the airway smooth muscle thickness (Wam) were measured by image analysis system. The concentrations of IL-1beta in serum and BALF were tested by sandwich ELISA. The protein expressions of P-JNK and P-c-Jun were detected by immunohistochemistry technique. Lung tissue extracts were analyzed for phosphorylation of JNK by Western blot. Linear correlation analysis was used to evaluate correlations between Wat and P-JNK protein (mA), Wam and P-JNK protein (mA), P-JNK protein (mA) and levels of IL-1beta in serum, P-JNK protein (mA) and levels of IL-1beta in BALF. RESULTS: In the asthma group, HE-staining showed inflammatory cell infiltration around bronchi and mucous gland hyperplasia. TEM examination showed airway smooth muscle and collagen fiber proliferation, and widening of intercellular distance. The Wat and Wam of the asthma group were significantly higher than those of the control group, while the thickness of airway wall in the glucocorticoid intervention groups became significantly decreased. The concentrations of IL-1beta in serum and BALF of the asthma group [(81 +/- 4) ng/L, (331 +/- 15) ng/L] were significantly higher than those of the control group [(53 +/- 6) ng/L, (130 +/- 9) ng/L] (t = -8.62 and t = -24.10, both P < 0.01). Mean absorbance values (by immunohistochemistry) of P-JNK and P-c-Jun in the asthma group were significantly higher than those of the control group, and the mean absorbance values of P-JNK and P-c-Jun in the BUD and DXM groups were significantly lower than those of the asthma group, but higher than those of the control group (F = 223.59 and F = 76.53, both P < 0.01). Absorbance (by Western blot) of P-JNK in the control, asthma, BUD, and DXM groups were (1.00 +/- 0.00), (1.66 +/- 0.16), (1.18 +/- 0.12), and (1.29 +/- 0.14), respectively; that of the asthma group was significantly higher than that of the control group, while absorbance of P-JNK in the BUD and the DXM groups were significantly lower than that of the asthma group, but higher than that of the control group (F = 17.84, P < 0.05). Strong positive correlations were found between Wat or Wam and P-JNK (mA) (r = 0.700 and r = 0.769, P < 0.01, respectively, n = 48). Strong positive correlations were also found between P-JNK (mA) and concentration of IL-1beta in serum or BALF (r = 0.689 and r = 0.805, P < 0.01, respectively, n = 48). CONCLUSION: Phosphorylation of JNK is closely related to asthma airway remodeling. Glucocorticoids can inhibit phosphorylation of JNK, one mechanism of which may be down-regulation of IL-beta expression.

[Role of c-Jun N-terminal kinase signal transduction pathway in the course of airway remodeling of asthma rat].

OBJECTIVE: To study the role of c-Jun N-terminal kinase (JNK) signal transduction pathway in the course of asthma airway remodeling, to explore whether IL-1beta participates in asthma airway remodeling mediated by JNK signal transduction pathway. METHODS: Totally 72 male Sprague-Dawlay rats (6 - 8 weeks old, weighing about 120 g) were randomly divided into control groups (36 rats) and asthma groups (36 rats). The rats were sensitized for inducing asthma by intraperitoneal injection of ovalbumin and AL(OH)3 and were repeatedly exposed to aerosolized ovalbumin for 4, 8, 12 weeks (A4, A8, or A12 group), each had 12 rats, and correspondingly control rats were intraperitoneally injected with 0.9% NaCl, then were repeatedly exposed to 0.9% NaCl for 4, 8, 12 weeks (C4, C8, or C12 group), each had 12 rats. The ultrastructural changes of pulmonary tissues were observed by transmission electron microscope (TEM). The total bronchial wall thickness (Wat) and the airway smooth muscle thickness (Wam) were measured by an image analysis system. The concentrations of IL-1beta in serum and bronchoalveolar lavage fluid (BALF) were tested by a "sandwich" ELISA. The protein expressions of P-JNK and P-c-Jun were detected by immunohistochemical technique. Lung tissue extracts were analyzed for phosphorylation of JNK by Western blotting. Linear correlation analysis showed the correlation between Wat and P-JNK protein, Wam and P-JNK protein, levels of IL-1beta in serum and P-JNK protein, levels of IL-1beta in BALF and P-JNK protein. RESULTS: In asthma groups, TEM showed alveolar septal proliferation and alveolus type II epithelial cells swelling. Wat and Wam in all asthma groups were significantly higher than those in corresponding control groups (P < 0.01, respectively), and compared with group A4 and group A8, Wat and Wam of group A12 significantly increased (P < 0.01). The concentrations of IL-1beta in serum and BALF of asthma groups were all significantly higher than those of the corresponding control groups (P < 0.01, respectively), and compared with group A4 and group A8, the concentrations of IL-1beta in BALF of group A12 significantly increased (P < 0.01 or P < 0.05), but the levels of IL-1beta in serum were not significantly different among them (P > 0.05). Mean absorbance values (by immunohistochemistry) of P-JNK and P-c-Jun in asthma groups were significantly higher than those in corresponding control groups (P < 0.01, respectively), and compared with group A4 and group A8, those of group A12 significantly increased (P < 0.01 or P < 0.05). The absorbance (by Western Blot) of P-JNK in A4, A8, A12 group was significantly higher than that in C4, C8, C12 groups (P < 0.01, respectively), and compared with group A4, that of P-JNK of A12 significantly increased (P < 0.01), and compared with group A8, there was no significant difference (P > 0.05). Strong positive correlations were found between Wat or Wam and P-JNK (r = 0.823 and r = 0.818, P < 0.01, respectively, n = 68) and between P-JNK and concentration of IL-1beta in serum or BALF (r = 0.717 and r = 0.803, P < 0.01, respectively, n = 68). CONCLUSIONS: The expression of P-JNK and its downstream P-c-Jun in rats of asthma airway remodeling is increased, which implicates that JNK signal transduction pathway plays an important role in the course of asthma airway remodeling. IL-1beta participates in asthma airway remodeling possibly partly through activating JNK signal transduction pathway.

[Biological characteristics of human peripheric CD4+ CD25- T cells isolated and cultured in vitro].

AIM: To isolate peripheric CD4(+) CD25(-) T cells in vitro, and study their biological characteristics. METHODS: Human peripheric blood CD4(+) CD25(-) T cells were isolated by discontinuous density gradient centrfugal and dynal immunomagnetic beads, and then divided into three groups: control group(A), LPS group (B) and LPS+TGF-beta1 mAb group (D), After they were prepared 4 h, 3 d and 5 d, the percentage of CD4(+) CD25(+) T cells were tested by FCM, the levels of TGF-beta1 in cultured supernatants were detected by ELISA, and the expression of FOXP3 mRNA was examined by RT-PCR. RESULTS: (1)LM showed CD4(+) CD25(-) T cells were of spherical cell nucleus, After CD4(+) CD25(-) T cells were cultured by anti-CD3/CD28 in vitro, their cellular volume increased and cytoplasm contained more particles. TEM showed CD4(+) CD25(-) T cells were of oval or kidney-shaped caryon. (2)FCM showed the purity of CD4(+) CD25(-) T cells was 91.5%-96%. The trypan blue experiment showed the energometry before and after detachment had no obvious difference(P>0.05). (3)FCM showed the percentage of CD4(+) CD25(+) T cells in B5d group(55.99+/-1.42)% increased markedly compared with that in A5d group(1.29+/-0.04)%. (4)ELISA showed the levels of TGF-beta1 in B3d(1.60+/-0.09) microg/L, in B5d(1.83+/-0.14) microg/L were significantly increased compared with those in A3d (0.35+/-0.04) microg/L and A5d(0.33+/-0.08) microg/L(P<0.01); but the levels in group D and group A had no significant difference; (5)RT-PCR showed FOXP3 mRNA in B3d group(0.84+/-0.07) and B5d group(1.85+/-0.24) increased strikingly compared with those in A3d(0.05+/-0.02) and A5d(0.04+/-0.02)(P<0.01), but those in group A and group D had no significant difference. (6)There was significantly positive correlation between the expression of TGF-beta1 and FOXP3 mRNA in the induced CD4(+) CD25(-) T cells (r=0.812, P<0.01). CONCLUSION: Human peripheric blood CD4(+) CD25(-) T cells can be isolated in vitro by discontinuous density gradient centrfugal and dynal immunomagnetic beads. The expression of FOXP3 mRNA in E.coli LPS-induced human CD4(+) CD25(-) T cells may correlate with the expression of TGF-beta1.

[Effect of Radix Astragali on signal transducer and activator of transcription activator-4 and its mRNA expression in a rat model of asthma].

OBJECTIVE: To study the effect of Radix Astragali (RA) on the expression of signal transducer and activator of transcription-4 (STAT4) and its mRNA in the bronchus of a rat model of asthma. METHODS: Forty male SD rats were randomly divided into four groups: the control group, asthma group, high dosage of RA group and low dosage of RA group. In the experiment, the rat model of asthma was established by the ovalbumin (OVA) challenge methods. The lung tissue was gainedfrom the left lung, bronchoalveolar lavage fluid (BALF) was gained from the right lung. The eosinophils (EOS) numbers and differentiated cell numbers in BALF were counted by different counting fluids; the protein expressions of STAT4 were detected by immunohistochemistry; the mRNA expressions of STAT4 were detected by in situ hybridization. RESULTS: (1) In the BALF of the asthma group, the absolute numbers of EOS, the ratios of EOS to the total cell numbers (EOS%) of asthma group [(35.81 +/- 7.30) x 10(7)/L, (8. 20 +/- 1.75)%] were all significantly higher than those of the control group [(1.51 +/- 1.04) x 10(7)/L, (0.70 +/- 0.48)%] (P < 0.01); the total cell numbers in BALF, the absolute numbers of EOS and EOS% of RA groups [(14.89 +/- 2.35) x 10(7)/L, (4.70 +/- 0.82)%; (10.98 +/- 1.81) x 10(7)/L, (3.56 +/- 0.53)%] were all significantly lower than those of asthma group (P < 0.01); (2) The concentration of IL-4 in BALF of asthma group (25.70 +/- 7.36) was significantly higher than that of the control group (8.55 +/- 2.97) (P < 0.01); the concentration of IL-4 of BALF of RA groups [(31.89 +/- 5.46), (35.26 +/- 6.03)] was significantly lower than that of asthma group (P < 0.01); the concentration of IL-12 of BALF of asthma group (16.10 +/- 3.38) was significantly lower than that of the control group (42.33 +/- 9.66) (P < 0.01); the concentration of IL-12 of BALF of the RA groups [(31.89 +/- 5.46), (35.26 +/- 6.03)] was significantly higher than that of the asthma group (P < 0.01); (3) Immunohistochemistry and in situ hybridization showed that the protein content of STAT4 and the STAT4 mRNA expression around the bronchus of asthma group [(0.096 +/- 0.012), (0.098 +/- 0.011)] were lower than those of the control group [(0.216 +/- 0.034), (0.228 +/- 0.032)], while those of RA groups [(0.176 +/- 0.012), (0.185 +/- 0.023); (0.183 +/- 0.011), (0.201 +/- 0.019)] were all significantly higher than that of the asthma group (P < 0.01), the airway smooth muscle cells, the pulmonary arterial smooth muscle cells and endothelial cells were the chief expression cells; (4) the STAT4 and the STAT4mRNA expression around the bronchus had positive correlation with the concentration of IL-12 in BALF while had negative correlation with the concentration of IL-4, absolute numbers of EOS in BALF. CONCLUSIONS: RA has an inhibitory effect on airway inflammation cells infiltration such as EOS, it raises the STAT4 protein and its mRNA expression in the airway smooth muscle cells, the pulmonary arterial smooth muscle cells and endothelial cells, and the key mechanism may be that the IL-12 composition is increased.

[Regulative mechanism of dexamethasone on Toll-like receptor 4 signal transduction of infant asthma rat].

OBJECTIVE: Eosinophilic airway inflammation is one of the basic characteristics of allergic asthma. Toll-like receptor is one of the most important innate immunity pattern recognition receptors. Glucocorticoids (GCS) are still the most effective treatment for asthma. However, few reports of studies on regulatory mechanism of GCS on the innate immunity system are available. The mechanism of effects of GCS on TLR4 is unclear. The present study aimed at understanding the effect of dexamethasone (DXM) on change of TLR4 and mechanism of regulatory effect of TLR4 on eosinophil (EOS) apoptosis. METHODS: Twenty-seven Sprague-Dawley (SD) rats (age 28 to 42 days, body weight 120 to 180 gram) were randomly divided into the control group, asthma group and DXM group with 9 in each. Asthma model rats were sensitized with the mixture of ovalbumin (OVA, 1 mg) and Al (OH)(3), 100 mg on day 1 and day 8, repeatedly exposed to aerosolized OVA after day 15, once a day for three days and continued for 30 minutes at every time. During the sensitization stage, 100 microg/ml DXM were prepared with DXM group for every other day, and the same doses DXM were prepared for every day on the stage of challenge. The histopathological changes of lung tissues were observed with light microscope (LM). EOS and other inflammatory cells in bronchoalveolar lavage fluid (BALF) were counted; the concentrations of OVA-sIgE in serum were measured by using "sandwich" ELISA; The expressions of TLR4 mRNA were determined by in situ hybridization, the apoptosis of EOS was detected by TUNEL. RESULTS: (1) LM showed many inflammatory cells infiltration around the bronchi and blood vessels, bronchus mucus increased, airway epithelium damage and desquamation, and airway mucous plugs in asthma group, whereas DXM group showed significantly milder changes. (2) Inflammationary cells count in BALF of asthma group was significantly higher as compared to control group (P < 0.01); compared with asthma group, the total cell count, EOS absolute count and EOS% were all significantly decreased in DXM group [(2.14 +/- 0.10) x 10(9)/L, (4.78 +/- 1.23) x 10(7)/L, (2.17 +/- 0.25)%]. (3) Levels of OVA-sIgE in serum of asthma group [(83.40 +/- 6.80) microg/ml] were significantly higher than those of the control group [(14.38 +/- 4.25) microg/ml] (P < 0.01), while those of DXM group [(45.02 +/- 7.47) microg/ml] were significantly lower than asthma group (P < 0.0 1). (4) There were no significant differences in TLR4 mRNA detected by in situ hybridization between control group (24.71 +/- 0.85) and asthma group (25.81 +/- 3.56) (P > 0.05); but it significantly increased in DXM group (29.86 +/- 3.92) as compared to asthma group. (5) The percentages of apoptotic EOS in asthma group [(7.39 +/- 1.93)%] were significantly lower than those in control group [(9.06 +/- 1.52)%] (P < 0.01); and significantly higher in DXM group [(13.33 +/- 1.09)%] than in asthma group (P < 0.01). There were significantly positive correlations between TLR4 mRNA and the percentage of apoptotic EOS (r = 0.612, P < 0.01). CONCLUSION: DXM can decrease OVA-sIgE level, induce EOS apoptosis, which may correlate with the activation of TLR4 signal transduction.

[Effect of achyranthes bidentata polysaccharides on signal transducer and activator of transcription 6 and its mRNA expression in a rat model of asthma].

AIM: To study the effect of achyranthes bidentata polysaccharides(ABPS) on the expression of signal transducer and activator of transcription 6 and its mRNA in bronchus of a rat model of asthma. METHODS: Thirty male SD rats were randomly divided into three groups: the control group, asthma group and ABPS group. The total cell numbers, eosinophils (EOS) numbers and differentiated cell numbers in bronchoalveolar lavage fluid (BALF) were counted by different count fluids. The concentrations of IL-4 in serum and BALF were measured by sandwich ELISA. The protein expressions of STAT6 were detected by immunohistochemistry techniques. The mRNA expressions of STAT6 were detected by hybridization in situ. RESULTS: (1) The total cell numbers in BALF, the absolute numbers of EOS, the ratios of eosinophils to the total cell numbers (EOS%) of asthma group were all significantly higher than those of the control group (P < 0.01). The total cell numbers in BALF, the absolute numbers of EOS and EOS% of ABPS group were all significantly lower than those of asthma group (P < 0.01). (2) The concentrations of IL-4 in BALF and serum of asthma group were significantly higher than those of control group (P < 0.01), while the concentrations of IL-4 in BALF and serum of ABPS group were significantly lower than those of asthma group. (3) Immunohistochemistry showed that the protein content of STAT6 around the bronchus of asthma group was significantly higher than that of the control group (P < 0.01), while that of ABPS group was significantly lower than that of asthma group , the epithelial cells were the chief expression cells; hybridization in situ showed that the mRNA expression of STAT6 around the bronchus of asthma group was significantly higher than that of the control group (P < 0.01), while that of ABPS group was significantly lower than that of asthma group , the epithelial cells were the chief expression cells. CONCLUSION: STAT6 protein and STAT6 mRNA were found strongly expressed in rat asthma model, the epithelial cells were the chief expression cells. ABPS had an inhibitory effect on airway inflammation cells infiltration such as EOS, it significantly depressed STAT6 and its mRNA expression, thus reduced the synthesis of IL-4 might be key in modulating mechanism of asthma.