Ovalbumin-induced Mouse Asthma Research Articles

Retracted: Dioscorea nipponica Makino Relieves Ovalbumin-Induced Asthma in Mice through Regulating RKIP-Mediated Raf-1/MEK/MAPK/ERK Signaling Pathway.

[This retracts the article DOI: 10.1155/2022/8077058.].

Short-term administration of Qipian®, a mixed bacterial lysate, inhibits airway inflammation in ovalbumin-induced mouse asthma by modulating cellular, humoral and neurogenic immune responses

AimsQipian® is a commercialized agent composed of extracts of three genera of commensal bacteria, and its mechanism of action on asthma is unclear. This study aimed to examine the impact of Qipian® on airway inflammation and investigate the underlying mechanisms. Materials and methodsQipian® or dexamethasone (DEX) was administered before OVA challenge in an ovalbumin-induced asthma mouse model, and then asthmatic symptoms were observed and scored. Samples of lung tissues, blood, and bronchoalveolar lavage fluid (BALF) were collected, and eosinophils (Eos), immunoglobins (Igs), and type 1 T helper (Th1)/Th2 cell cytokines were measured. Mucus production in the lung was assessed by periodic acid-Schiff (PAS) staining. The effects of Qipian® on dendritic and T regulatory (Treg) cells were investigated using flow cytometry. Key findingsThe short-term administration of Qipian® significantly inhibited the cardinal features of allergic asthma, including an elevated asthmatic behaviour score, airway inflammation and immune response. Histological analysis of the lungs showed that Qipian® attenuated airway inflammatory cell infiltration and mucus hyperproduction. Qipian® restored Th1/Th2 imbalance by decreasing interleukin (IL)-4, IL-5, and IL-13 while increasing interferon (IFN)-γ and IL-10. Further investigation revealed that Qipian® treatment induced the upregulation of CD4+CD25+Foxp3+ Treg cells and CD103+ DCs and downregulation of tachykinins neurokinin A (NKA) and NKB in the lung. SignificanceOur findings suggested that short-term treatment with Qipian® could alleviate inflammation in allergic asthma through restoring the Th1/Th2 balance by recruiting Treg cells to airways and inducing the proliferation of CD103+ DCs, which actually provides a new treatment option for asthma.

Effects of human umbilical cord blood mononuclear cells on ovalbumin-induced asthma in mice.

Umbilical cord blood mononuclear cells (UCMNCs) show broad immune-modulation effects, which may be helpful for treating asthma. Effects of UCMNCs on asthma were investigated with mouse model in present study. Asthma was induced in BALB/c mice by ovalbumin (OVA) immunization and challenge. Asthmatic mice were then treated on days 7 and 20 with intravenous injections of UCMNCs in doses of 4×105, 2×106, and 107 cells per mouse for the low-dose UCMNC (UCMNCL), medium-dose UCMNC (UCMNCM), and high-dose UCMNC (UCMNCH) groups, respectively. Fetal mouse blood mononuclear cells (FMMNCs) were administered to FMMNC group at a dose of 2×106 cells per mouse as approximate allograft control. Airway hyperresponsiveness (AHR), airway inflammation indexes, and CD4/CD8 T cell subsets were measured at day 25. Compared with the model group, AHR in the UCMNCL group, inflammation score of lung tissue in the UCMNCM group, interleukin (IL)-5 in bronchoalveolar lavage fluid (BALF) in UCMNCL group, IL-5 and IL-13 in BALF in UCMNCM group, and IL-17 in serum in UCMNCH group were significantly inhibited. Compared with the model group, CD4+CD8+ T cells were reduced in the UCMNCL group, while decrease of CD4-CD8- T cells and increase of CD4+CD8- T cells were further strengthened in UCMNCM group. FMMNC treatment significantly reduced the IL-13 and IL-17 in serum, decreased CD4-CD8- and CD4+CD8- T cells, and increased the CD4+CD8+ and CD4-CD8+ T cells in BALF. UCMNCs can modulate AHR, T-helper (Th)2 inflammation, and airway injury in experimental asthma at appropriate dose.

Antiinflammatory effect of Cissus quadragularis in asthma induced by ovalbumin in mice

Asthma is a disease characterized by difficulty breathing. According to the WHO, asthma affects approximately 300 million people worldwide. In Africa, its prevalence is between 1 and 12 % depending on the country. In Cameroon, about 5.7 % of the population suffers from asthma. The objective of our work was to evaluate the antiinflammatory effect of Cissus quadrangularis in asthma induced by ovalbumin in mice. For this purpose, thirty (30) female mice subdivided into 6 groups of 5 mice each were distributed. All animals (except normal control) were subjected to disease induction for 16 days. The animals were injected intraperitoneally on days 0 and 7 with 20 μg of ovalbumin mixed with 1 mg of aluminum hydroxide (as adjuvant) in a total volume of 200 μl of phosphate buffered saline (PH=7.4). Days 14, 15, and 16 after the initial injection with ovalbumin, mice were re-exposed by intranasal instillation with 20 μg ovalbumin in 20 μl phosphate saline once daily. The extract as well as dexametasone were administered daily to the mice for 17 days orally at doses of 75, 150, 300 and 1 mg/kg respectively to the test batches and to the positive control 1 h before the initial sensitization. The animals were sacrificed 24 h after the last instillation. Blood, liver, lungs, and pulmonary fluid were collected. Dosages of IgE, cytokines (IL-4, IL-5 and IL-13), and counting of cells in the pulmonary fluid were carried out. Our results showed that the pretreatment with the extract significantly reduced (P < 0.001) the level of total IgE, there is also a significant inhibition (P < 0.001) of the recruitment of inflammatory cells in the lungs and a significant decrease (P < 0.001) the level of inflammatory cytokines. Similarly, the administration of the extract at a dose of 150 mg/kg significantly reduced (P < 0.001) the level of MDA correlated with a significant increase (P < 0.001) in the level of SOD, CAT and GHS compared to the control negative. Furthermore, the histological analyzes of the lungs showed that the pretreatment with the extract leads to an improvement in the histopathological changes; these results suggest that the aqueous extract of Cissus quadrangularis improves inflammation in ovalbumin-induced asthma in mice.

Effect of Ximenia americana (Olacaceae) leaves on ovalbumin induced asthma in mice

Ximenia americana commonly known as Sea Lemon is a plant of the Olacaceae family with anti-inflammatory, antioxidant and antiviral properties. Ximenia americana is used in traditional medicine for the treatment of diseases such as cancer, diabetes, asthma, etc. In this work, six groups of five mice were formed. The prevalence of clinical asthma is estimated at around 4.3% of the world's population, which is a real public health problem. Hence the aim of this work, which was to evaluate the effects of the aqueous extract of the leaves of X. americana on ovalbumin-induced asthma (OVA) in mice. The test animals received aqueous extract from Ximenia americana at doses 75 mg / kg, 150 mg / kg and 300 mg / kg. In order to measure the intensity of bronchial inflammation, the inflammatory cell rate has been evaluated. The results obtained after analysis of the different biochemical parameters show a significant decrease (p < 0.05) of the white blood cells in the positive lots, tests at 75 mg / kg, 150mg / kg, 300mg / kg compared to the negative light. In addition, a significant decrease in the average globular volume (MCV), blood platelets were recorded in these same animals (p < 0.01); (p < 0.001) respectively with respect to the negative group. The results also show that this allergen causes intense lipid peroxidation, as well as a significant reduction in the activity of different antioxidant systems (GSH, SOD and CAT). However, the pretreatment of Ximenia americana aqueous extract is effective, as to the significant reduction in the MDA rate (p < 0.001) and significant increase (p < 0.05) of the activity of CAT. The rebalance of the balance between oxidant and antioxidant during the plant administration, would probably be attributed to the antioxidant and anti-inflammatory capacity of the compounds contained in our extract.

Anti-inflammatory effects of Rhizopus spp. fermentation products on ovalbumin-induced asthma in mice

Anti-inflammatory effects of Rhizopus spp. fermentation products on ovalbumin-induced asthma in mice

Overexpression of Homeobox A1 Relieves Ovalbumin-Induced Asthma in Mice and Is Associated with Blocking of the NF-κB Signaling Pathway.

Homeobox A1 (HOXA1) is a protein coding gene involved in regulating immunity signaling. This study aims to explore the function and mechanism of HOXA1 in asthma. An asthma mouse model was established via ovalbumin (OVA) induction. Airway hyperresponsiveness was evaluated by the value of pause enhancement (Penh). Inflammatory cells in bronchoalveolar lavage fluid (BALF) were detected by Trypan blue and Wright staining. The pathological morphology of lung tissues was assessed by H&E staining. The IgE and inflammatory biomarkers (IL-1β, IL-6, IL-17, and TNF-α) in BALF and lung tissues were measured by ELISA. Western blot was performed to detect the expression of NF-κB pathway-related proteins. HOXA1 was down-regulated in OVA-induced asthmatic mice. Overexpression of HOXA1 decreased Penh and relieved pathological injury of lung tissues in OVA-induced mice. Overexpression of HOXA1 also reduced the numbers of total cells, leukocytes, eosinophils, neutrophils, macrophages, and lymphocytes, as well as the levels of IgE, IL-1β, IL-6, IL-17, and TNF-α in BALF of OVA-induced mice. The inflammatory biomarkers were also decreased in lung tissues by HOXA1 overexpression. In addition, HOXA1 overexpression blocked the NF-κB signaling pathway in OVA-induced mice. Overexpression of HOXA1 relieved OVA-induced asthma in female mice, which is associated with the blocking of the NF-κB signaling pathway.

Possible Anti-asthmatic Effect of Iraqi Ammi majus Seeds Extract Induced by Ovalbumin in Mice


 
 
 
 Asthma is a chronic and complex condition of the respiratory tract, that occurs in both children and adults. Currently available medications have side effects; therefore, new therapies with fewer side effects are needed. Thus, present study was designed to evaluate the potential anti-asthmatic effects of alcoholic extract of Ammi majus on ovalbumin-induced asthma in mice. Forty-eight female Albino mice were randomly assigned to one of six groups with 8 animals each. Group I received distilled water as a negative control, Group II received ovalbumin as a positive control, Groups III and IV received Ammi majus orally at 64 and 128 mg/kg/day, respectively, with sensitization, and Groups V and VI received Ammi majus orally at 64 and 128 mg/kg/day, respectively, without sensitization. Bronchoalveolar lavage fluid (BALF) was obtained 24 h after the 1st challenge to measure the number of inflammatory cell counts. In addition, lung tissue was removed for histopathological examination. Oral administration of alcoholic extract of Ammi majus at both doses (64 and 128 mg/kg) significantly inhibited ovalbumin-induced increases in total and differential cell counts of eosinophile, neutrophile, monocyte, and lymphocyte) in BALF, in addition, improve histopathologic events of asthma in lung tissue of ovalbumin-induced asthma in mice. These results demonstrated that Ammi majus alcoholic extract has a potent anti-asthmatic activity that improved ovalbumin-induced asthma.
 
 
 

Lactoferrin Ameliorates Ovalbumin-Induced Asthma in Mice through Reducing Dendritic-Cell-Derived Th2 Cell Responses.

Asthma is a chronic respiratory disease with symptoms such as expiratory airflow narrowing and airway hyperresponsiveness (AHR). Millions of people suffer from asthma and are at risk of life-threatening conditions. Lactoferrin (LF) is a glycoprotein with multiple physiological functions, including antioxidant, anti-inflammatory, antimicrobial, and antitumoral activities. LF has been shown to function in immunoregulatory activities in ovalbumin (OVA)-induced delayed type hypersensitivity (DTH) in mice. Hence, the purpose of this study was to investigate the roles of LF in AHR and the functions of dendritic cells (DCs) and Th2-related responses in asthma. Twenty 8-week-old male BALB/c mice were divided into normal control (NC), ovalbumin (OVA)-sensitized, and OVA-sensitized with low dose of LF (100 mg/kg) or high dose of LF (300 mg/kg) treatment groups. The mice were challenged by intranasal instillation with 5% OVA on the 21st to 27th day after the start of the sensitization period. The AHR, cytokines in bronchoalveolar lavage fluid, and pulmonary histology of each mouse were measured. Serum OVA-specific IgE and IgG1 and OVA-specific splenocyte responses were further detected. The results showed that LF exhibited protective effects in ameliorating AHR, as well as lung inflammation and damage, in reducing the expression of Th2 cytokines and the secretion of allergen-specific antibodies, in influencing the functions of DCs, and in decreasing the level of Th2 immune responses in a BALB/c mouse model of OVA-induced allergic asthma. Importantly, we demonstrated that LF has practical application in reducing DC-induced Th2 cell responses in asthma. In conclusion, LF exhibits anti-inflammation and immunoregulation activities in OVA-induced allergic asthma. These results suggest that LF may act as a supplement to prevent asthma-induced lung injury and provide an additional agent for reducing asthma severity.

Dioscorea nipponica Makino Relieves Ovalbumin-Induced Asthma in Mice through Regulating RKIP-Mediated Raf-1/MEK/MAPK/ERK Signaling Pathway.

Purpose Dioscorea nipponica Makino (DNM) is a traditional herb with multiple medicinal functions. This study is aimed at exploring the therapeutic effects of DNM on asthma and the underlying mechanisms involving RKIP-mediated MAPK signaling pathway. Methods An ovalbumin-induced asthma model was established in mice, which was further administrated with DNM and/or locostatin (RKIP inhibitor). ELISA was performed to detect the serum titers of OVA-IgE and OVA-IgG1, bronchoalveolar lavage fluid (BALF) levels of inflammation-related biomarkers, and tissue levels of oxidative stress-related biomarkers. The expression of RKIP was measured by quantitative real-time PCR, Western blot, immunohistochemistry, and immunofluorescence. HE staining was used to observe the pathological morphology of lung tissues. The protein expression of MAPK pathway-related proteins was detected by Western blot. Results Compared with the controls, the model mice exhibited significantly higher serum titers of OVA-IgE and OVA-IgG1, BALF levels of IL-6, IL-8, IL-13, TGF-β1, and MCP-1, tissue levels of MDA and ROS, lower BALF levels of IL-10 and IFN-γ, and tissue level of GSH. DNM relieved the allergic inflammatory response and oxidative stress in the model mice. DNM also recovered the downregulation of RKIP and the pathological injury of lung tissues in asthma mice. In addition, the Raf-1/MEK/MAPK/ERK pathway in the model mice was blocked by DNM. Silencing of RKIP by locostatin weakened the relieving effects of DNM on asthma through activating the Raf-1/MEK/MAPK/ERK pathway. Conclusion DNM relieves asthma via blocking the Raf-1/MEK/MAPK/ERK pathway that mediated by RKIP upregulation.

Immunomodulatory Effect of SINA 1.2 Therapy Protocol in Asthmatic Mice Model: A Combination of Oxymel and Sauna.

Alternative medicine, has become popular in asthmatic patients. We evaluated the immunomodulatory effects of SINA 1.2 therapy protocol derived from Persian medicine in an asthmatic mice model. Forty-two male BALB/c mice divided into six groups: one control (sham) and five sensitized groups (by parenteral injection of 20 μg ovalbumin in 100 μL normal saline plus 50 μL alum on days 1 and 14). Sensitized groups were as: untreated, budesonide (1 mg nebulized budesonide: 200 μg/puff every 5 min for 25 min), dry sauna (30 min, 37°C), oral oxymel (gavaged: 0.2 mL of the syrup plus 0.8 mL of water), and SINA protocol No.1.2 (oxymel followed by sauna) groups. Treatments were given for 10 days from day 23 to 33 then sacrificed. Significant gene expression reduction of interleukin(IL)-4, IL-5, and MUC5AC and increase of interferon(IFN)-γ and IFN-γ/IL-4 ratio and decreased perivascular and peribronchial inflammation, goblet cell hyperplasia, and subsequent mucus hypersecretion in SINA group were seen compared to untreated group. SINA lowered IL-5 and MUC5AC gene expression levels similar to the budesonide and acted better than budesonide in increasing IFN-γ gene expression up to normal level. Compared with the asthma group, sauna alone only affected MUC5AC and IFN-γ gene expressions and oxymel alone, only reduced IL-4 gene expression, perivascular and peribronchial inflammation, and mucus hypersecretion. It seems that SINA therapy alleviates asthma via immune modulation of pro-inflammatory cytokines and improvement of pathological changes in ovalbumin-induced asthma in mice, supporting the notion of innate healing power mentioned in Persian medicine literature.

Human amniotic membrane mesenchymal stem cell-conditioned medium reduces inflammatory factors and fibrosis in ovalbumin-induced asthma in mice.

What is the central question of this study? Is mesenchymal stem cell-conditioned medium capable of improving the pathological alterations of ovalbumin-induced asthma in mice? What is the main finding and its importance? Our study indicated that human amniotic membrane mesenchymal stem cell-conditioned medium is capable of modulating inflammation, fibrosis, oxidative stress and the pathological consequences of ovalbumin-induced allergic asthma in mice. Paracrine factors secreted by mesenchymal stem cells (MSCs) have immunomodulatory, anti-inflammatory and antifibrotic properties, and the conditioned medium (CM) of these cells might have functional capabilities. We examined the effects of human amniotic membrane MSC-CM (hAM-MSC-CM) on ovalbumin (OVA)-induced asthma. Forty male Balb/c mice were randomly divided into the following four groups: control; OVA (sensitized and challenged with OVA); OVA+CM (sensitized and challenged with OVA and treated with hAM-MSC-CM); and OVA+Placebo (sensitized and challenged with OVA and treated with placebo). Forty-eight hours after the last challenge, serum and bronchoalveolar lavage fluid samples were collected and used for evaluation of inflammatory factors and cells, respectively. Lung tissue sections were stained with Haematoxylin and Eosin or Masson's Trichrome to evaluate pathological changes, and oxidative stress was assessed in fresh lung tissues. Treatment with hAM-MSC-CM significantly hindered histopathological changes and fibrosis and reduced the total cell count and the percentage of eosinophils and neutrophils in bronchoalveolar lavage fluid. Furthermore, it reduced serum levels of immunoglobulinE, interleukin-4, transforming growth factor-β and lung malondialdehyde. It also increased serum levels of interferon-γ and interleukin-10, in addition to the enzymatic activity of glutathione peroxidase, catalase and superoxide dismutase in lung tissue in comparison to the OVA and OVA+Placebo groups. This study showed that administration of hAM-MSC-CM can improve pathological conditions, such as inflammation, fibrosis and oxidative stress, in OVA-induced allergic asthma.

Dihydroartemisinin Ameliorated Ovalbumin-Induced Asthma in Mice via Regulation of MiR-183C.

BackgroundThe purpose of the present study was to investigate the function and mechanism of dihydroartemisinin (DHA) in treating ovalbumin-induced asthma in BALB/c mice.Material/MethodsThirty female BALB/c mice were randomly separated into 3 groups: the control group, the asthma model group stimulated by ovalbumin (OVA group), and the DHA treatment group (DHA group). The therapeutic effects and potential pharmacological mechanisms of DHA were specifically clarified by examining its effects on asthma-related phenomena, such as body weight, lung function, cell counts in bronchoalveolar lavage fluid (BALF), and hemotoxin and eosin staining. In addition, the expression of inflammatory factors was checked by enzyme-linked immunosorbent assay kits, and fractions of Th17 cells were detected by FACS analysis. Moreover, the downstream molecular pathway of IL-6/Stat3 (interleukin-6/signal transducer and activator of transcription 3) and expression of miR-183C was investigated by western blot and/or quantitative real-time polymerase chain reaction. Luciferase assay was used to reveal the function of miR-183C on the transcriptional regulation of Foxo1 (forkhead box O).ResultsDHA administration significantly relieved the severity of the asthma through its effect on body weight, survival rate, and airway pressure. DHA was able to ameliorate lung damage in terms of pathological morphology and it reduced the percentage of helper T 17 (Th17) cells and the secretion of cytokines. As a result, the activity of the IL-6/Stat3 pathway was inhibited by DHA. In addition, the adoption of DHA decreased the expression of miR-183C but increased the expression of the transcription factor Foxo1.ConclusionsOur results suggest that the therapeutic effects of DHA on asthma are partially realized via the regulation of miR-183C and IL-6/Stat3 pathway.

Gallic acid attenuates allergic airway inflammation via suppressed interleukin-33 and group 2 innate lymphoid cells in ovalbumin-induced asthma in mice.

Asthma is an inflammatory disease characterized by airway hyperresponsiveness. Gallic acid is a powerful anti-inflammatory agent. In this study we aimed to investigate the efficacy of gallic acid in asthma treatment and its mechanisms. An ovalbumin-induced asthma mouse model was generated. Pro-inflammatory cell infiltration and T helper (Th2)-associated cytokine release in the bronchoalveolar lavage fluid (BALF) were analyzed to reflect the severity of asthma in mice. An interleukin-33 (IL-33)-induced asthma mouse model was also generated to study the mechanism by which gallic acid could improve asthma. Group 2 lymphoid cells (ILC2s) were identified using flow cytometry. Proteins were detected using Western blotting. Ovalbumin significantly increased the infiltration of pro-inflammatory cells, including eosinophils, macrophages, lymphocytes, and neutrophils, accompanied by enhanced airway hyperesponsiveness. Gallic acid reduced pro-inflammatory cell infiltration and improved airway hyperresponsiveness. Meanwhile, gallic acid reduced IL-5 and IL-13 levels in BALF and decreased expression of IL-33 in the lungs. Mechanistically, gallic acid inhibited MyD88 expression and downregulated nuclear factor (NF)-κB signaling to decrease IL-33 expression. Gallic acid can mollify ovalbumin-induced asthma in mice, possibly by inhibiting IL-33-mediated ILC2 activation and subsequent Th2 cytokine release via downregulation of the MyD88/NF-κB signaling pathway. ©2018 ARSAAOA, LLC.

Catalpol alleviates ovalbumin-induced asthma in mice: Reduced eosinophil infiltration in the lung

BackgroundRadix Rehmanniae Preparata is a traditional Chinese herbal medicine used to treat asthma, and catalpol is one of the main active ingredients in this herb. In the present study, the effects of catalpol on asthma and the underlying mechanism were explored. MethodsMice with ovalbumin (OVA)-induced asthma were given 5 or 10mg/kg catalpol from Day 15 to Day 28 (intraperitoneal injection). Histopathologic changes were detected by Hematoxylin and Eosin staining and Periodic Acid Schiff staining. The levels of IgE, interleukin (IL)-4, IL-5 and eotaxin were measured by ELISA. The numbers of lymphocytes, monocytes, basophils and eosinophils in the bronchoalveolar lavage fluid were determined by Wright-Giemsa staining. The expression and distribution of eotaxin and C-C chemokine receptor 3 (CCR3) were detected by immunohistochemistry and immunofluorescence. The expression of interleukin-5 receptor α (IL-5Rα) was detected by Western blot assay. ResultsCatalpol inhibited OVA-induced inflammation and IgE secretion in the lung. OVA-induced type 2 inflammation was suppressed by catalpol as evidenced by decreased levels of IL-4 and IL-5. Moreover, catalpol inhibited the aberrant eosinophil infiltration in the lungs, and also suppressed OVA-induced elevation of eosinophil chemokine eotaxin and its receptor CCR3. In addition, IL-5Rα expression in the bone marrow cells derived from catalpol-treated asthmatic mice was lower than that from the untreated asthmatic mice. ConclusionOur study demonstrated that catalpol attenuated OVA-induced asthma and inhibit the infiltration of inflammatory cells, especially eosinophils, into the lung. This study suggests that catalpol may become a promising drug for the treatment of asthma.

1′-Acetoxychavicol Acetate Isolated from Alpinia galanga Ameliorates Ovalbumin-Induced Asthma in Mice

The World Health Organization reports that 235 million people are currently affected by asthma. This disease is associated with an imbalance of Th1 and Th2 cells, which results in the upregulation of cytokines that promote chronic inflammation of the respiratory system. The inflammatory response causes airway obstruction and can ultimately result in death. In this study we evaluated the effect of 1′-acetoxychavicol acetate (ACA) isolated from Alpinia galanga rhizomes in a mouse model of ovalbumin (OVA)-induced asthma. To generate the mouse model, BALB/c mice were sensitized by intraperitoneal injection of OVA and then challenged with OVA inhalation for 5 days. Mice in the vehicle control group were sensitized with OVA but not challenged with OVA. Treatment groups received dexamethasone, 25 mg/kg/day ACA, or 50 mg/kg/day ACA for 5 days. Asthma-related inflammation was assessed by bronchoalveolar lavage fluid cell counts and histopathological and immunohistochemical analysis of lung tissues. Our results showed that ACA reduced the infiltration of white blood cells (especially eosinophils) and the level of IgE in the lungs of mice challenged with OVA and suppressed histopathological changes such as airway remodeling, goblet-cell hyperplasia, eosinophil infiltration, and glycoprotein secretion. In addition, ACA inhibited expression of the Th2 cytokines interleukin (IL)-4 and IL-13, and Th1 cytokines IL-12α and interferon-γ. Because asthmatic reactions are mediated by diverse immune and inflammatory pathways, ACA shows promise as an antiasthmatic drug candidate.

길경약침(桔梗藥鍼)의 천식억제(喘息抑制) 및 면역조절효과(免疫調節效果)에 대(對)한 실험적(實驗的) 연구(硏究)

Objectives : The aim of this study was to investigate the effect of Asthma-depression and Immunoregulation with PR-HAS(Herbal-acupuncture with Platycodi Radix infusion solution) infection at Joksamni(St36) on ovalbumin-induced asthma in mice. Methods : C57BL/6 mice were sensitized and challenged with OVA(ovalbumin) for 12 weeks(once a week). The experimental group(OVA-PR-HA) was treated with concentrations(1%) of PR-HAS at Joksamni(St36) for the later 8 weeks(3times/week). The second experimental group(OVA-Needle prick) was treated with Needle-Prick at Joksamni(St36) for the later 8 weeks(3times/week). Results : 1. The weight and total cells in the mice lung treated with PR-HA decreased significantly compared with that of control group. 2. Total leukocytes and eosinophils in BALF of the mice group treated with PR-HA decreased remarkably compared with those of control group. 3. The sticking of collagen on histological analysis of lung sections, the mice group treated with PR-HA decreased significantly compared with those of control group. 4. The concentrations of IL-4, IL-5, IgE in BALF, and IL-4, IL-5, IL-13 in serum of the mice group treated with PR-HA decreased significantly compared with those of control group. 5. The number of Gr-1+/CD11b+ and CD11b+ cells in the lungs of the mice group treated with PR-HA decreased significantly compared with that of control group. 6. The numbers of CCR3+ cells, CD4+ cells and CD8+ cells in the lungs, and CD3e+/CD69+ in the lungs of the mice group treated with PA-HA decreased significantly compared with those of control group. 7. The mRNA expression of -actin, TNF-, IL-4, IL-5, IL-13 in the mice group treated with PR-HA with RT-PCR decreased significantly compared with those of control group. Conclusions : These result suggests that Platycodi Radix Herbal-acupuncture at Joksamni(St36) in C57BL/6mice may be an effictive part to OVA-induced asthma in C57BL/6 mice.

소자약침(蘇子藥鍼)의 천식억제(喘息抑制) 및 면역조절효과(免疫調節效果)에 대(對) 실험적(實驗的) 연구(硏究)

Objectives : The purpose of this study was to confirm the suppressive effect against asthma and immune regulatory effect of Perillae Fractusher Herbal-acupuncture at Chok-samni(ST36) on ovalbumin-induced asthma in mice. Methods : C57BL/6 mice were sensitized and challenged with OVA(ovalbumin) for 12 weeks. The mice in the PF-HA group were treated with PF-HA at ST36 for the later 8 weeks(3 times a weeks). The mice in the OVA-Needle-Prink(NP) group were treated with single prick with an injection needle at ST36 for the later 8 weeks(3 times a weeks). Results : 1. The lung weight of the mice treated with PF-HA at St36 were decreased significantly compared with that of the control group. 2. The total leukocytes and eosinophils in BALF of the group treated with PF-HA were decreased significantly compared with those of the control group. 3. Eosinophils in BALF and the collagen accumulation in lung of the mice treated with PF-HA were decreased significantly compared with those of the control group. 4. The Concentrations of IgE, IL-4 and IL-5 in BALF, and IL-4, IL-5 and IL-13 in serum of the PF-HA group were decreased significantly compared with those of the control group. 5. The numbers of CD3-/CCR3+, Gr-1+/CD11b+,CD4+, and CD3e+/CD69+cells in lung of the mice group treated with PF-HA at St36 were decreased significantly compared with those of the control group. 6. The mRNA expressions of TNF-, IL-4, IL-5, IL-13 in lung of the mice group treated with PF-HA at St36 were decreased significantly compared with those of the control group.