Association between airborne particulate matter（PM 2.5） concentration and the incidence of allergic rhinitis in Shanghai / 临床耳鼻咽喉头颈外科杂志

Objective:To explore the impact of PM 2.5 concentration in Shanghai on the incidence of allergic rhinitis（AR） in the population, and provide strategies for early warning and prevention of AR. Methods:Collect daily average concentrations of atmospheric pollutants monitored in Shanghai from January 1, 2017 to December 31, 2019, and clinical data of AR patients from five hospitals in Shanghai during the same period. We used a time-series analysis additive Poisson regression model to analyze the correlation between PM 2.5 levels and outpatient attendance for AR patients. Results:During the study period, a total of 56 500 AR patients were included, and the daily average concentration of PM 2.5 was（35.28±23.07）μg/m³. There is a correlation between the concentration of PM 2.5 and the number of outpatient attendance for AR cases. There is a positive correlation between the daily average number of outpatient for AR and levels of PM 2.5 air pollution（（P<0.05）） . We found that every 10 μg/m³ increase in PM 2.5, the impact of on the number of AR visits was statistically significant on the same day, the first day behind, and the second day behind, with the strongest impact being the exposure on the same day. Every 10 μg/m³ increases in PM 2.5, the number of outpatient visits increased by 0.526% on the same day（95%CI 1.000 50-1.010 04）. Conclusion:The atmospheric PM 2.5 concentration in Shanghai is positively correlated with the number of outpatient for AR, and PM 2.5 exposure is an independent factor in the onset of AR. This provides an important theoretical basis for AR.

Analysis of problems and countermeasures faced by the ethics committee in the context of the 2020 version Good Clinical Practice / 中华医学科研管理杂志

Objective:According to the requirements set forth by the " regulations on the management of drug clinical trial institutions" and the 2020 version of Good Clinical Practice, problems faced by the construction of Institutional Review Board (hereinafter referred to as the IRB) in the implementation of the filing system is solved.Methods:According to the study of laws and regulations, combined with problem analysis during the early construction of IRB, problems during the IRB filing are identified and analyzed.Results:The IRB faced many problems that including the organizational structure, continuing review, informed consent and multicenter ethical review. We can gradually improve the ability of ethical review through continuous in-depth study of relevant laws and regulations, so as to ensure the scientific validity and ethical acceptability of drug clinical trials.Conclusions:It is of great significance for the high-quality development of IRB to improve its organizational structure, optimize its review mechanism and improve its review efficiency.

Effect of PM2.5 on inflammatory factors and pathology of nasal mucosa in a rat model of allergic rhinitis / 中华耳鼻咽喉头颈外科杂志

Objective@#To investigate the effect of PM2.5 exposure on nasal inflammatory cytokines and nasal mucosal pathology in a rat model of allergic rhinitis (AR).@*Methods@#Twenty-four healthy female SD rats were randomly divided into 3 groups by random number table method, with 8 rats in each group: normal control group (NC group), ovalbumin (OVA) induced AR model (AR group), and AR model group inhaled to PM2.5 at 200 μg/m3, 3 h/d, for 30 d (ARE group). Nasal symptoms including sneezing, nasal rubs and nasal secretion were recorded. Levels of OVA specific IgE in serum, interleukin 6 (IL-6) and tumor necrosis factor-ɑ (TNF-ɑ) in nasal irrigating solution were measured by enzyme-linked immunosorbent assay (ELISA). The histopathological changes of nasal mucosa were observed by HE staining. SPSS 17.0 software was used to analyze the data.@*Results@#The number of sneezing, nasal rubs and the amount of nasal secretion in the ARE group were significantly higher than that in the AR group and the NC group (number of sneezing (15.38±1.68) times/15 min vs (11.63±1.13) times/15 min vs (1.75±0.71) times/15 min, number of nasal rubs (27.75±2.12) times/15 min vs (21.25±2.96) times/15 min vs (5.25±1.04) times/15 min, amount of nasal secretion (18.90±2.07) mg vs (13.83±1.81) mg vs (3.78±0.41) mg, F values was 236.089, 224.139, 183.971, respectively, all P<0.001). Statistically significant differences in OVA specific IgE, IL-6 and TNF-ɑ levels were observed in ARE group exceeded AR group and NC group (OVA specific IgE (25.42±2.51) ng/ml vs (18.07±1.07) ng/ml vs (1.47±0.26) ng/ml, IL-6 (123.30±18.86) pg/ml vs (63.49±11.29) pg/ml vs (16.87±3.29) pg/ml, TNF-ɑ (162.50±38.15) pg/ml vs (72.96±11.28) pg/ml vs (27.52±4.15) pg/ml, F values was 481.604, 138.277, 63.938, respectively, all P<0.001). HE staining showed that the nasal epithelial cells of NC group were intact and neatly arranged. Nasal mucosa epithelial cells were arranged in disorder in AR group, with tissue structure swelling. Partial shedding of nasal epithelial cells, mucosal basement membrane thickening, submucosal tissue interstitial edema, vasodilation and gland hyperplasia were found in ARE group.@*Conclusion@#An increase inflammatory factors level such as IL-6 and TNF-ɑ aggravates pathological damage of nasal mucosa in a rat model of AR by exposure to PM2.5.

The effect of NK-1R-siRNA on expression of inflammatory factors in allergic rhinitis / 中华耳鼻咽喉头颈外科杂志

Objective@#To explore the effect of neurokinin-1 receptor small interfering RNA (NK-1R-siRNA) on the expression of inflammation factors in allergic rhinitis (AR).@*Methods@#Twenty-four male SD rats were divided into three groups randomly (by random number table methord): NK-1R-siRNA group, negative control siRNA (NC-siRNA) group and saline group, with 8 rats in each group. SD rats were sensitized and challenged with ovalbumin (OVA) to induce AR. The rats were treated intranasally with NK-1R-siRNA, NC-siRNA or saline before and during the challenge period. The AR symptoms were observed. The levels of OVA-specific IgE were measured by enzyme-linked immunosorbent assay (ELISA). The levels of NK-1R expression in the nasal mucosal tissues were determined by real time PCR (RT-PCR) and immunohistochemistry. Antibody array was used in studying the expression of inflammation cell factors in nasal mucosa. SPSS 11.0 software was used for one-factor analysis of variance.@*Results@#Compared with saline group, AR symptoms relived significantly in NK-1R-siRNA group (nose rubbing (31.4±8.9)/15 min vs (69.5±17.9)/15 min, sneezing (7.2±1.9)/15 min vs (23.7±9.2)/15 min, nasal secretions (7.1±2.3) mg vs (24.1±4.4) mg, t value was 38.100, 17.125, 16.837, respectively, all P<0.01), and the level of serum OVA-specific IgE was also reduced ((8.56±0.73) ng/ml vs (18.05±1.22) ng/ml, t=9.787, P<0.01). The RT-PCR and immunohistochemistry results showed that the expression of NK-1R in nasal mucosa of NK-1R-siRNA group was remarkably reduced than that of the NC-siRNA group and saline group. After the treatment of NK-1R-siRNA, the expression of interleukin (IL) 1α, IL-1β, IL-4, IL-6 and IL-13 decreased, while the interferon-γ (IFN-γ) and IL-10 increased.@*Conclusion@#NK-1R-siRNA could regulate the release of inflammation factors in AR nasal mucosa, thus relive the allergic inflammation.

The role of autophagy in PM2.5-induced inflammation in human nasal epithelial cells / 中华耳鼻咽喉头颈外科杂志

Objective@#To explore the role of autophagy in PM2.5-induced inflammation in human nasal epithelial cells and related mechanism.@*Methods@#Human nasal epithelial cells were exposed to different concentration of PM2.5 for different times, and the expression levels of microtubule-associated protein-1 light chain-3 Ⅱ (LC3 Ⅱ) and Beclin1 proteins were measured by Western blot. The typical autophagosome and autolysosome were observed by using transmission electron microscopy (TEM). To observe autophagic flux, mRFP-GFP-LC3 plasmid was transfected to nasal epithelial cells and the punctate staining of mRFP-GFP-LC3 were determined by confocal laser scanning microscope. The expression of inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell culture supernatant were assessed by enzyme-linked immunosorbent assay (ELISA). To assess the role of autophagy in PM2.5-mediated inflammation, autophagy related gene Atg5 and Beclin-1 were silenced by siRNA knockdown, and inflammatory cytokines were analyzed.GraphPad Prism 6.0 was used for statistical analysis.@*Results@#PM2.5 exposure increased the expression of LC3 Ⅱ and Beclin-1 proteins in a dose- (in PM2.5 group with concentration of 0, 15, 30, 60, 120 μg/ml, the expression of LC3 Ⅱ was 0.021±0.001(±s), 0.037±0.002, 0.058±0.005, 0.075±0.006, 0.085±0.004, respectively, F=126.8, P<0.05; the expression of Beclin-1 was 0.002±0.000, 0.003±0.000, 0.005±0.000, 0.007±0.001, 0.008±0.001, respectively, F=137.3, P<0.05) and time-dependent manner (in PM2.5 group with exposure time of 0, 3, 6, 12, 24 h, the expression of LC3Ⅱ was 0.160±0.007, 0.222±0.003, 0.251±0.015, 0.483±0.029, 0.585±0.035, respectively, F=215.3, P<0.05; the expression of Beclin-1 was 0.059±0.002, 0.080±0.002, 0.087±0.002, 0.183±0.007, 0.228±0.005, respectively, F=137.3, P<0.05) in human nasal epithelial cells. TEM analysis showed typical autophagosome and autolysosome in cells after PM2.5 exposure for 24 h. PM2.5 significantly increased the number of yellow and red dots representing autophagosomes and autolysosomes respectively, indicating autophagic flux was elevated. Moreover, PM2.5 enhanced the secretion of inflammatory cytokines such as IL-6 and TNF-α, which was dramatically prevented by Atg5-siRNA and Beclin-1-siRNA.@*Conclusion@#Autophagy plays an important role in PM2.5-caused inflammation response in nasal epithelial cells, which can induce release of inflammatory factors such as IL-6 and TNF-α and advance the inflammatory reaction.

Chinese Society of Allergy Guidelines for Diagnosis and Treatment of Allergic Rhinitis

Allergic rhinitis (AR) is a global health problem that causes major illnesses and disabilities worldwide. Epidemiologic studies have demonstrated that the prevalence of AR has increased progressively over the last few decades in more developed countries and currently affects up to 40% of the population worldwide. Likewise, a rising trend of AR has also been observed over the last 2–3 decades in developing countries including China, with the prevalence of AR varying widely in these countries. A survey of self-reported AR over a 6-year period in the general Chinese adult population reported that the standardized prevalence of adult AR increased from 11.1% in 2005 to 17.6% in 2011. An increasing number of original articles and imporclinical trials on the epidemiology, pathophysiologic mechanisms, diagnosis, management and comorbidities of AR in Chinese subjects have been published in international peer-reviewed journals over the past 2 decades, and substantially added to our understanding of this disease as a global problem. Although guidelines for the diagnosis and treatment of AR in Chinese subjects have also been published, they have not been translated into English and therefore not generally accessible for reference to non-Chinese speaking international medical communities. Moreover, methods for the diagnosis and treatment of AR in China have not been standardized entirely and some patients are still treated according to regional preferences. Thus, the present guidelines have been developed by the Chinese Society of Allergy to be accessible to both national and international medical communities involved in the management of AR patients. These guidelines have been prepared in line with existing international guidelines to provide evidence-based recommendations for the diagnosis and management of AR in China.

Diagnostic value of portable monitor device in patients with potential obstructive sleep apnea hypopnea syndrome / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To evaluate the diagnostic value of portable monitor device (PMD) in potential obstructive sleep apnea hypopnea syndrome (OSAHS) patients.</p><p><b>METHODS</b>All patients met the inclusion criteria were asked to finish the questionniar and underwent anthropometric measurements, and then completed polysomnography (PSG) test and PMD test simultaneously. The correlation between AHI-PMD and AHI-PSG, between MinSaO2-PMD and MinSaO2-PSG were analyzed by Spearman analysis. T test was used to compare the correlation coefficient between the two groups; ROC analysis was used to evaluate the sensitivity and specificity of PMD in diagnosis of OSAHS, and got the Cut-off value between moderate and severe OSAHS and mild OSAHS.</p><p><b>RESULTS</b>Through PSG test, of all the 111 cases, including 4 simple snoring cases, accounting for 3.6%, OSAHS patients with 107 cases, accounting for 96.4% which including 11 patients (9.9%) with mild, 17 patients (15.3%) with moderate, 79 patients (71.2%) with severe. The correlation of AHI-PMD and AHI-PSG between moderate and severe OSAHS patients was stronger than simple snoring and mild OSAHS patients. The coefficient test between the two groups was statistically significant (P=0.026). The correlation of MinSaO2-PMD and MinSaO2-PSG was statistically significant (P<0.001), the correlation of MinSaO2-PMD and MinSaO2-PSG between moderate and severe OSAHS group and snoring and mild OSAHS group was not statistically significant (P=0.270). A statistically significant correlation between AHI-PMD and AHI-PSG was found (P<0.001). PMD had a sensitivity and specificity of 96.9% and 86.7%, respectively (AUC=0.990, 95%CI 0.970-1.000). The cut-off value between moderate and severe OSAHS and mild OSAHS was AHI-PMD≥12 times/h.</p><p><b>CONCLUSION</b>PMD had a satisfactory sensitivity and specificity for diagnosing and judging the severity of moderate and severe OSAHS.</p>

Altered microRNA Expression Profiles of Extracellular Vesicles in Nasal Mucus From Patients With Allergic Rhinitis

PURPOSE: Allergic rhinitis (AR) is an inflammatory disorder of the upper airway. Exosomes or extracellular vesicles are nanosized vesicles of endosomal origin released from inflammatory and epithelial cells that have been implicated in allergic diseases. In this study, we characterized the microRNA (miRNA) content of exosomes in AR. METHODS: Extracellular vesicles were isolated from nasal mucus from healthy control subjects (n=10) and patients with severe AR (n=10). Vesicle RNA was analyzed by using a TaqMan microRNA assays Human Panel-Early Access kit (Applied Biosystems, Foster City, CA, USA) containing probes for 366 human miRNAs, and selected findings were validated with quantitative RT-PCR. Target prediction and pathway analysis for the differentially expressed miRNAs were performed using DIANA-mirPath. RESULTS: Twenty-one vesicle miRNAs were up-regulated and 14 miRNAs were under-regulated significantly (P<0.05) in nasal mucus from AR patients when compared to healthy controls. Bioinformatic analysis by DIANA-mirPath demonstrated that 32 KEGG biological processes were significantly enriched (P<0.05, FDR corrected) among differentially expressed vesicle miRNA signatures. Among them, the B-cell receptor signaling pathway (P=3.709E-09), the natural killer cell-mediated cytotoxicity (P=8.466E-05), the T-cell receptor signaling pathway (P=0.00075), the RIG-I-like receptor signaling pathway (P=0.00127), the Wnt signaling pathway (P=0.00130), endocytosis (P=0.00440), and salivary secretion (P=0.04660) were the most prominent pathways enriched in quantiles with differential vesicle miRNA patterns. Furthermore, miR-30-5p, miR-199b-3p, miR-874, miR-28-3p, miR-203, and miR-875-5p, involved in B-cell receptor and salivary secretion signaling pathways, were selected for validation using independent samples from 44 AR patients and 20 healthy controls. MiR-30-5p and miR-199b-3p were significantly increased in extracellular vesicles from nasal mucus when compared to healthy controls, while miR-874 and miR-28-3p were significantly down-regulated. In addition, miRNA-203 was significantly increased in AR patients, while miRNA-875-5p was found to be significantly decreased in AR patients. CONCLUSIONS: This study demonstrated that vesicle miRNA may be a regulator for the development of AR.

Clinical efficacy of ulinastatin combined with naloxone in patients with cardiogenic shock after acute myocardial infarction / 中国综合临床

Objective To study clinical efficacy of ulinastatin combined with naloxone in patients with cardiogenic shock(CS) after acute myocardial infarction (AMI).Methods Eighty patients with CS after AMI were randomly divided into routine treatment group (n =19),ulinastatin group (n =20),naloxone group (n =21) and ulinastatin combined with naloxone group (n =20).The levels of serum cardiac troponin I (cTnI),brain natriuretic peptide(BNP),tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6)were measured before and a week after treatment.In the meantime,recovery time of shock,the average hospitalization days and 28-day mortality rate were recorded.Results After the treatment,the levels of serum cTnI,BNP,TNF-α and IL-6decreased in all groups(P ＜ 0.01),and there was significant difference on the decreasing degree of cTnI,BNP,TNF-α and IL-6 in ulinastatin combined with naloxone group when compared with those in routine treatment group,ulinastatin group and naloxone group(cTnI:(1.04 ± 0.17) ng/L vs.(2.06 ± 0.15) ng/L,(1.59 ± 0.16)ng/L,(1.97 ± 0.14) ng/L; BNP:(143.21-56.94) ng/L vs.(261.07 ± 71.43) ng/L,(203.46 ± 65.73) ng/L,(252.96 ± 68.85) ng/L; TNF-α:(13.42 ± 8.93) ng/L vs.(31.21 ± 12.32) ng/L,(20.39 ± 11.08) ng/L,(28.98 ± 11.76) ng/L ; IL-6:(37.58 ± 11.14) ng/L vs.(80.46 ± 27.15) ng/L,(59.84 ± 20.72) ng/L,(76.15 ±26.45) ng/L; P ＜ 0.01).The recovery time of shock,the average hospitalization days and 28-day mortality rate in ulinastatin combined with naloxone group were significantly lower than those in routine treatment group,ulinastatin group and naloxone group(recovery time of shock:(7.16 ± 1.52) d vs.(11.43 ± 2.40) d,(8.05 ±1.81)d,(8.74 ± 1.98)d;the average hospitalization days:(15.03 ±3.23)d vs.(22.64 ±4.18)d,(18.93 ±3.97)d,(19.21 ±3.94)d ;28-day mortality rate:(41.62％ vs.61.20％,50.74％,52.31％ ; P ＜0.01)).Conclusion The application of ulinastatin combined with naloxone can effectively inhibit the cardiac injury and inflammatory response,promote the recovery of circulation function and improve prognosis in patients with CS after AMI.

Microarray analysis of differentially expressed microRNAs in allergic rhinitis.

BACKGROUND: Allergic rhinitis (AR) is a common disease characterized by chronic inflammation of the nasal mucosa, but we have not fully understood the mechanism responsible for the development of AR. MicroRNAs (miRNAs) are short endogenous noncoding RNAs regulating protein translation through a mechanism known as RNA interference. To understand the molecular mechanisms of miRNA involved in the pathogenesis of AR, expressed miRNAs in AR were investigated through genomewide microarray analysis. METHODS: Mammalian miRNA microarrays containing whole human mature and precursor miRNA sequences were used for analyzing eight samples of nasal mucosa of AR and eight samples of nonallergic patients. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) of some different expressed miRNAs was used to confirm the array results. RESULTS: The miRNA microarray chip analysis identified 421 miRNAs differentially expressed in the nasal mucosa of AR, and a total of 9 miRNAs were identified in the AR group with twofold change compared with control samples (p < 0.05). These included up-regulated miRNAs, hsa-hsa-miR-7, and hsa-miRPlus-E1194, and down-regulated miRNAs, hsa-miR-498, hsa-miR-187, hsa-miR-874, hsa-miR-143, hsa-miR-886-3p, hsa-miR-224, and hsa-miR-767-5p. RT-PCR results also confirmed that part of differentially expressed miRNAs as hsa-miR-224, hsa-miR-187, and hsa-miR-143 were down-regulated in AR. CONCLUSION: The report indicated that many miRNA expressions were altered in AR and differentially expressed miRNAs appear to be involved in the development of AR. The study of miRNAs may lead to a better understanding about the roles of identified miRNAs in the pathogenesis of AR; this would be considered in future therapeutic strategies.

A meta-analysis of the association of exhaled carbon monoxide on asthma and allergic rhinitis.

The objective of this study is to evaluate the effect of exhaled CO (eCO) on the development of asthma and allergic rhinitis (AR) by means of reviewing published literature. The literatures published between January 1997 and December 2008 from the US National Library of Medicine (NLM) Database were obtained according to inclusion criteria. Meta-analysis of randomized controlled trials (RCTs) was performed. CO levels of asthma and AR patients were compared with that of normal controls. HO-1(heme oxygenase-1) expression and effect of corticosteroids on eCO levels were also analyzed. Fifteen studies concerning asthma and four studies concerning AR were included in this analysis. Heterogeneity from different studies was evident (P < 0.0001), so a random-effects model was preferred. The meta-analysis revealed that asthmatic patients had significantly higher levels of eCO compared to normal controls. There was significant difference between asthma and control groups in terms of eCO (combined weighted mean difference (WMD) 1.33 (95% confidence interval 0.72 to 1.95), P < 0.0001), and no significant difference between AR and control (combined WMD 0.93 (95% confidence interval -0.54 to 2.40), P = 0.22). HO-1 expression were also reviewed, asthma group produced greater expression of HO-1 than control group with significant difference (combined standardized mean difference (SMD) 2.98 (95% confidence interval 1.13 to 4.84), P = 0.002). After corticosteroid therapy, significantly different levels of eCO were produced after corticosteroid therapy than did asthma group (combined WMD -1.23 (95% confidence interval -2.43 to -0.03), P = 0.04). The analysis reveals that eCO levels were significantly raised in asthma and it may attribute to high expression of HO-1, but there were no significantly high eCO levels between AR and control groups. Due to sensitivity to corticosteroid inhibition, eCO may be used as a practical marker to detect and monitor exacerbation of asthma.

Content of CD4+ CD25+ regulatory T cells in peripheral blood lymphocytes in patients with allergic rhinitis / 临床耳鼻咽喉头颈外科杂志

OBJECTIVE@#To investigate the change of CD4- CD25 regulatory T cells (Tregs) of peripheral blood in allergic rhinitis (AR) patients.@*METHOD@#T lymphocytes of twenty AR patients and eight healthy subjects were separated and the flow cytometry was used to measure the percentage of CD4+ CD25+ Treg.@*RESULT@#Compared with control group, the percentage of Treg and CD4- CD25high Tregs of AR patients was decreased significantly (P < 0.05).@*CONCLUSION@#The proportion of CD4+ CD25+ Tregs decreased in AR patients conspicuously, which might be one of the pathogenesis of AR.

Study on the expression of Eotaxin and the role of histamine in allergic rhinitis / 临床耳鼻咽喉头颈外科杂志

OBJECTIVE@#To explore the expression of Eotaxin and the effect of histamine in allergic rhinitis model (AR), and aim to explore the pathogenesis of AR.@*METHOD@#The AR models were established by application of ovum albumin in rats. The expression of Eotaxin in nasal mucosa, serum and nasal cavity lavage fluid, were observed before and after treatment of histamine or its antagonist by immunochemistry, RT-PCR and ELISA technique.@*RESULT@#The expression of Eotaxin in nasal lavage fluid and nasal mucosa increased after treatment of histamine (P < 0.05). Contrarily, the expression of Eotaxin in nasal lavage fluid, nasal mucosa and serum decreased after treatment of the antagonist of histamine.@*CONCLUSION@#Both histamine and its receptor can involve in the pathogenesis of AR by affecting the expression of Eotaxin.

Study on the expression of Eotaxin and the role of histamine in allergic rhinitis / 临床耳鼻咽喉头颈外科杂志

Objective: To explore the expression of Eotaxin and the effect of histamine in allergic rhinitis model (AR),and aim to explore the pathogenesis of AR. Method:The AR models were established by applicating of ovain albumin in rats. The expression of Eotaxin in nosal mucosa,serum and nasal cavity lavage fluid,were observed before and after treatment of histamine or its antagonist by immunochemistry,RT-PCR and ELISA technique. Result:The expression of Eotaxin in nasal lavage fluid and nasal mueosa increased after treatment of histamine(P＜0.05). Contrarily,the expression of Eotaxin in nasal lavage fluid,nasal mucosa and serum decreased after treatment of the antagonist of histamine. Conclusion:Both histamine and its receptor can involve in the pathogenesis of AR by affecting the expression of Eotaxin.

Possible contribution of endogenous carbon monoxide to the development of allergic rhinitis in guinea pigs.

BACKGROUND: The mechanisms responsible for the development of allergic rhinitis(AR) are not fully understood. The present study was designed to explore the possible roles of carbon monoxide(CO) on the pathogenesis of AR. METHODS: AR guinea pig model was established by nasal ovalbumin sensitization. Twenty-four AR guinea pigs were divided into four groups, 6 in each: Saline control group, AR sensitized group, Hemin treated group, and Zinc protoporphyrin (ZnPP) treated group. The frequency of sneezing and nose rubbing was recorded. Leukocyte infiltration in nasal lavage fluid, serum IgE level and plasma CO were measured. Expression of heme oxygenase-1 (HO-1) mRNA in nasal mucosa was determined by real time RT-PCR, and expression of HO-1 protein was detected by immunohistochemistry. RESULTS: The frequency of sneezing and nose rubbing, leukocyte infiltration, serum IgE, plasma CO, and HO-1 mRNA levels in sensitized guinea pigs were higher than those of control (P < 0.05). Except for serum IgE level, all above parameters were even higher (P < 0.05) when treated with Hemin, a heme oxygenase-1 inducer; but significantly decreased (P < 0.05) when treated with ZnPP, a heme oxygenase inhibitor. Immunohistochemical results showed that positive staining of HO-1 was present in the lamina of mucosa of sensitized guinea pigs, and there was an increase of HO-1 immunoreactivity with Hemin administration (P < 0.05) and a decrease with ZnPP treatment. CONCLUSION: The endogenous CO may take part in the inflammation process of AR and is positively correlated with expression of HO-1 in nasal mucosa. Endogenous CO plays a significant role in the pathogenesis of AR.

The role of hydrogen sulfide and cystathionine-gamma-lyase in allergic rhinitis guinea pigs / 临床耳鼻咽喉头颈外科杂志

OBJECTIVE@#To study the change of endogenous hydrogen sulfide (hydrogen sulfide, H2S) and its rate-limiting enzyme Cystathionine-gamma-lyase (CSE) in allergic rhinitis through guinea pigs with intervention treatment.@*METHOD@#Twenty-four guinea pigs were divide into 4 groups at random, one group were models of allergic rhinitis (AR) which were established by using ovalbumin, the second group were treated with NaHS after sensitized, the third group were treated with Propargylglycine (PPG) which was suppression of CSE after sensitized, and the last group were treated with saline for control. The concentration of eotaxin of nasal lavage and H2S in plasma were recorded, and then the expression of CSE in nasal mucosa was determined by real-time fluorescence RT-PCR.@*RESULT@#The concentration of eotaxin in nasal lavage of sensitized group were higher than those of control (P < 0.01), and concentration of H2S in plasma and expression of CSE in nasal mucosa were lower than control (P < 0.05). The concentration of eotaxin decreased when treated with NaHS and increased when treated with PGG (P < 0.05). Level of H2S in plasma and expression of CSE increased when treated with NaHS and decreased when treated with PGG (P < 0.05), and the level of H2S was positive linear correlate with the expression of CSE.@*CONCLUSION@#Endogenous H2S perhaps plays a significant role in the pathogenesis of allergic rhinitis, and it was mainly regulated by CSE.

Experimental study of basophil histamine releasability in guinea-pigs with allergic rhinitis / 第二军医大学学报

Objective: To investigate the pathogenesis of allergic rhinitis at cell level by determing basophil histamine releasability in guinea pigs and attempt to find an objective way for the diagnosis of allergic rhinitis. Methods: A model of allergic rhinitis was established after healthy guinea pigs were randomly divided into 2 groups. The basophil histamine releasability to the stimulant of concanavalin A between normal and experimental guinea pigs was compared by means of fluorometric assay of histamine. Results: Basophil histamine release to various concentrations of concanavalin A in allergic rhinitis group was significantly enhanced as compared with that in normal control ( P

Influence of histamine content in nasal mucosa of allergic rhinitis guinea-pigs on blood flow / 第二军医大学学报

Objective: To investigate the influence of histamine content in nasal mucosa on blood flow. Methods: Sixty guinea pigs were randomly devided into control group and allergized group and guinea pigs were sacrificed before nasal challenge with allergen and immediately after nasal challenge, at 24, 48, 72 h. The content of histamine in nasal mucosa was examined. Nasal mucosa blood flow was examined in all guinea pigs before sacrifice. The data were analyzed using linear correlation and linear regression. Results: As compared with normal guinea pigs, the content of histamine and blood flow in nasal mucosa of allergic rhinitis guinea pigs were significantly increased before challengd with allergen( P

Histochemical changes of nitric oxide synthase in nasal mucosa of allergic rhinitis / 第二军医大学学报

Objective: The activity of nitric oxide synthase(NOS)in nasal mucosa of normal guinea pigs was compared with that of allergic rhinitis(AR)guinea pigs to investigate the relationship between NOS and AR. Methods: Localization of NOS in nasal mucosa of normal and AR guinea pigs was examined by means of NADPH diaphorase (NADPH d) histochemical stain. Results: Nasal mucosa of both normal and AR groups was positive for NADPH d, though the AR group reacted more strongly. Reaction was localized to the cytoplasm of glandular cell, epithelium and vascular endothelium. Conclusion: There is distribution of NOS in nasal mucosa of normal guinea pigs. The activity of NOS in guinea pig AR model was significantly stronger than that in normal group. NOS is related to AR. [