杧果叶中杧果苷的提取与鉴定

目的 :探讨从本地漆树科植物果树叶中提取鉴定果苷的方法。方法 :使用乙醇渗漉等一系列步骤从果树叶中提取和纯化果苷 ,用聚酰胺薄层色谱、吸收光谱检测、红外光谱测定、高效液相色谱、高效毛细管电泳等方法进行鉴定。结果 :提取的果苷外观呈金黄色 ,显微镜下呈针状结晶 ;熔点 (mp)为 2 71～ 2 73℃ ;三氯化铁、二氯化锶反应阳性 ;聚酰胺薄层色谱Rf=0 .4 6 ;吸收光谱扫描、高效液相色谱、高效毛细管电泳、红外光谱分析结果等均与对照品相似。结论 :从果树叶中提取的果苷经上述方法鉴定后证明其纯度已和对照品相同 ,可用于药理实验     

In vivo acute toxicological studies of an antioxidant extract from Mangifera indica L. (Vimang)

Mango (Mangifera indica L.) stem bark aqueous extract (MSBE) is a natural product with antioxidant, anti-inflammatory, analgesic, and immunomodulatory effects. Its formulations (e.g., tablets, capsules, syrup, vaginal oval, and suppositories) are known by the brand name of Vimang®. In view of the ethnomedical, preclinical, and clinical uses of this extract and the necessity to assess its possible toxicological effect on man, a toxicological analysis of a standard extract is reported in this paper. Acute toxicity was evaluated in mice and rats by oral, dermal, and intraperitoneal (i.p.) administration. The extract, by oral or dermal administration, showed no lethality at the limit doses of 2,000 mg/kg body weight and no adverse effects were found. Deaths occurred with the i.p. administration at 200, but not 20 mg/kg in mice. MSBE was also studied on irritant tests in rabbits, and the results showed that it was nonirritating on skin, ocular, or rectal mucosa. The extract had minimal irritancy following vaginal application.     

芒果树皮的化学成分研究

目的 对芒果(Mangifera indica L.)树皮的化学成分进行研究。方法 用色谱法分离,并用波谱法对化合物的结构进行鉴定。结果 从芒果树皮中分离鉴定了7个化合物,分别为芒果苷(1)、西瑞香素(2)、杨梅素(3)、杨梅苷(4)、芦丁(5)、槲皮素(6)和β-谷甾醇(7)。结论 芒果苷为芒果树皮的主要化学成分;杨梅素和杨梅苷为首次从该植物中分离得到。     

Vascular effects of the Mangifera indica L. extract (Vimang)

The effects of the Mangiferia indica L. (Vimang) extract, and mangiferin (a C-glucosylxanthone of Vimang) on the inducible isoforms of cyclooxygenase (cyclooxygenase-2) and nitric oxide synthase (iNOS) expression and on vasoconstrictor responses were investigated in vascular smooth muscle cells and mesenteric resistance arteries, respectively, from Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Vimang (0.5-0.1 mg/ml) and mangiferin (0.025 mg/ml) inhibited the interleukin-1beta (1 ng/ml)-induced iNOS expression more in SHR than in WKY, and cyclooxygenase-2 expression more in WKY than in SHR. Vimang (0.25-1 mg/ml) reduced noradrenaline (0.1-30 microM)- and U46619 (1 nM-30 microM)- but not KCl (15-70 mM)-induced contractions. Mangiferin (0.05 mg/ml) did not affect noradrenaline-induced contraction. In conclusion, the antiinflammatory action of Vimang would be related with the inhibition of iNOS and cyclooxygenase-2 expression, but not with its effect on vasoconstrictor responses. Alterations in the regulation of both enzymes in hypertension would explain the differences observed in the Vimang effect.     

Anti-allergic properties of Mangifera indica L. extract (Vimang) and contribution of its glucosylxanthone mangiferin

Vimang is the brand name of formulations containing an extract of Mangifera indica L., ethnopharmacologically used in Cuba for the treatment of some immunopathological disorders, including bronchial asthma, atopic dermatitis and other allergic diseases. However, the effects of Vimang on allergic response have not been reported until now. In this study, the effects of Vimang and mangiferin, a C-glucosylxanthone isolated from the extract, on different parameters of allergic response are reported. Vimang and mangiferin showed a significant dose-dependent inhibition of IgE production in mice and anaphylaxis reaction in rats, histamine-induced vascular permeability and the histamine release induced by compound 48/80 from rat mast cells, and of lymphocyte proliferative response as evidence of the reduction of the amount of B and T lymphocytes able to contribute to allergic response. In these experiments, ketotifen, promethazine and disodium cromoglicate were used as reference drugs. Furthermore, we demonstrated that Vimang had an effect on an in-vivo model of inflammatory allergy mediated by mast cells. These results constitute the first report of the anti-allergic properties of Vimang on allergic models, as well as suggesting that this natural extract could be successfully used in the treatment of allergic disorders. Mangiferin, the major compound of Vimang, contributes to the anti-allergic effects of the extract.     

Kochia scoparia fruit attenuates allergic airway inflammation in ovalbumin (OVA)-induced murine asthma model

Kochia scoparia fruit has been used in Asia for a long time. It possesses anti-inflammatory, antiallergic, and antipruritic actions. We investigated the role of a K. scoparia fruit ethanolic extract (KSEE) in allergic airway inflammation in a mouse asthma model. BALB/c mice were sensitized with ovalbumin (OVA) and, upon OVA aerosol challenge, developed airway eosinophilia, mucus hypersecretion, elevations in cytokine, chemokine, and immunoglobulin levels, and upregulation of MMP-9, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression. Intragastric administration of KSEE significantly attenuated OVA-induced influx of total leukocytes, eosinophils, neutrophils, macrophages, and lymphocytes into lungs, as well as attenuating levels of interleukin (IL)-4 and IL-5 in a dose-dependent manner. KSEE also significantly reduced the serum levels of total and OVA-specific immunoglobulin (Ig)E and OVA-specific IgG1 release into the airspace. Histological studies showed that KSEE inhibited OVA-induced lung tissue eosinophilia and airway mucus production. Moreover, in whole lung tissue lysates, immunoreactivity showed that KSEE markedly attenuated the OVA-induced increase in expression of ICAM-1, VCAM-1, and MMP-9. These results show that KSEE possesses protective effects against allergic airway inflammation, acts as an MMP-9 inhibitor, and induces a reduction in ICAM-1 and VCAM-1 expression.     

Modulation of eosinophil generation and migration by Mangifera indica L. extract (Vimang)

The effects of Vimang, an aqueous extract of the stem bark of Mangifera indica L. (Anacardiaceae), on cell migration in an experimental model of asthma was investigated. In vivo treatment of Toxocara canis-infected BALB/c mice for 18 days with 50 mg/kg Vimang reduced eosinophil migration into the bronchoalveolar space and peritoneal cavity. Also, eosinophil generation in bone marrow and blood eosinophilia were inhibited in infected mice treated with Vimang. This reduction was associated with inhibition of IL-5 production in serum and eotaxin in lung homogenates. In all these cases the effects of Vimang were more selective than those observed with dexamethasone. Moreover, Vimang treatment is not toxic for the animals, as demonstrated by the normal body weight increase during infection. These data confirm the potent anti-inflammatory effect of Vimang and support its potential use as an alternative therapeutic drug to the treatment of eosinophilic disorders including those caused by nematodes and allergic diseases.     

Effects of Mangifera indica L. aqueous extract (Vimang) on primary culture of rat hepatocytes

Vimang is an aqueous extract from stem bark of Mangifera indica L. (Mango) with pharmacological properties. It is a mixture of polyphenols (as main components), terpenoids, steroids, fatty acids and microelements. In the present work we studied the cytotoxic effects of Vimang on rat hepatocytes, possible interactions of the extract with drug-metabolizing enzymes and its effects on GSH levels and lipid peroxidation. No cytotoxic effects were observed after 24 h exposure to Vimang of up to 1000 μg/mL, while a moderate cytotoxicity was observed after 48 and 72 h of exposure at higher concentrations (500 and 1000 μg/mL). The effect of the extract (50–400 μg/mL) on several P450 isozymes was evaluated. Exposure of hepatocytes to Vimang at concentrations of up to 100 μg/mL produced a significant reduction (60%) in 7-methoxyresorufin-O-demethylase (MROD; CYP1A2) activity, an increase (50%) in 7-penthoxyresorufin-O-depentylase (PROD; CYP2B1) activity, while no significant effect was observed with other isozymes. To our knowledge, this is the first report regarding the modulation of the activity of the P450 system by an extract of Mangifera indica L. The antioxidant properties of Vimang were also evaluated in t-butyl-hydroperoxide-treated hepatocytes. A 36-h pre-treatment of cells with Vimang (25–200 μg/mL) strongly inhibited the decrease of GSH levels and lipid peroxidation induced by t-butyl-hydroperoxide dose- and time-dependently.     

Modulation of rat macrophage function by the Mangifera indica L. extracts Vimang and mangiferin

Vimang is an aqueous extract of Mangiferia indica L., traditionally used in Cuba as an anti-inflammatory, analgesic and antioxidant. In the present study, we investigated the effects of Vimang and of mangiferin (a C-glucosylxanthone present in the extract) on rat macrophage functions including phagocytic activity and the respiratory burst. Both Vimang and mangiferin showed inhibitory effects on macrophage activity: (a) intraperitoneal doses of only 50-250 mg/kg markedly reduced the number of macrophages in peritoneal exudate following intraperitoneal injection of thioglycollate 5 days previously (though there was no significant effect on the proportion of macrophages in the peritoneal-exudate cell population); (b) in vitro concentrations of 0.1-100 microg/ml reduced the phagocytosis of yeasts cells by resident peritoneal and thioglycollate-elicited macrophages; (c) in vitro concentrations of 1-50 microg/ml reduced nitric oxide (NO) production by thioglycollate-elicited macrophages stimulated in vitro with lipopolysaccharide (LPS) and IFNgamma; and (d) in vitro concentrations of 1-50 microg/ml reduced the extracellular production of reactive oxygen species (ROS) by resident and thioglycollate-elicited macrophages stimulated in vitro with phorbol myristate acetate (PMA). These results suggest that components of Vimang, including the polyphenol mangiferin, have depressor effects on the phagocytic and ROS production activities of rat macrophages and, thus, that they may be of value in the treatment of diseases of immunopathological origin characterized by the hyperactivation of phagocytic cells such as certain autoimmune disorders.     

Lack of in vivo embryotoxic and genotoxic activities of orally administered stem bark aqueous extract of Mangifera indica L. (Vimang)

Mango (Mangifera indica L.) stem bark aqueous extract (MSBE) is a new natural product with antioxidant, anti-inflammatory and immunomodulatory effects known by the brand name of its formulations as Vimang^®. Previously, the oral toxicity studies of the extract showed a low toxicity potential up to 2000 mg/kg. This work reports the results about teratogenic and genotoxicologic studies of MSBE. For embryotoxicity study, MSBE (20, 200, or 2000 mg/kg/day) was given to Sprague–Dawley rats by gavage on days 6–15 of gestation. For genotoxicity, MSBE was administered three times during 48 h to NMRI mice. Cyclophosphamide (50 mg/kg) was used as a positive control. No maternal or developmental toxicities were observed when the rats were killed on day 20th. The maternal body-weight gain was not affected. No dose-related effects were observed in implantations, fetal viability or external fetal development. Skeletal and visceral development was similar among fetuses from all groups. No genotoxicity was observed in bone marrow erythrocytes and liver cells after administration. MSBE appears to be neither embryotoxic nor genotoxic as measured by bone marrow cytogenetics in rodents.     

Mangifera indica. Stem Bark Effect on the Rat Trachea Contracted by Acetylcholine and Histamine

Abstract

Experiments were designed to determine the effect of Mangifera indica. Linn stem bark aqueous extract on rat trachea previously incubated in presence of indomethacin, propranolol, and atropine or promethazine with histamine or acetylcholine as agonist. The strips of trachea were suspended for isometric tension recording at 37°C. M. indica. aqueous extract at 2 mg/ml impair the contraction induced both by histamine and acetylcholine in all three experimental conditions. The contractile responses (% maximum effect) induced by histamine at 12 × 10^?4 g/ml, in the presence of extract, were respectively 69.18 ± 3.05% (indomethacin), 74.18 ± 1.03% (indomethacin + propranolol), and 45.54 ± 1.7% (indomethacin + propranolol + atropine) versus 100 ± 5.15% for control. The extract also reduced the contraction induced by acetylcholine, but this inhibitory effect is lightly decreased when the tissues were contracted by acetylcholine after incubation in presence of indomethacin + propranolol. These experiments suggest that the aqueous extract of M. indica. could block both the histaminic and muscarinic receptors on rat trachea; and the results corroborate with the traditional use of M. indica. stem bark in the treatment of asthma.     

Mangifera indica L. extract (Vimang) inhibits Fe2+-citrate-induced lipoperoxidation in isolated rat liver mitochondria.

The extract of Mangifera indica L. (Vimang) is able to prevent iron mediated mitochondrial damage by means of oxidation of reduced transition metals required for the production of superoxide and hydroxyl radicals and direct free radical scavenging activity. In this study we report for the first time the iron-complexing ability of Vimang as a primary mechanism for protection of rat liver mitochondria against Fe2+ -citrate-induced lipoperoxidation. Thiobarbituric acid reactive substances (TBARS) and antimycin A-insensitive oxygen consumption were used as quantitative measures of lipoperoxidation. Vimang at 10 microM mangiferin concentration equivalent induced near-full protection against 50 microM Fe2+ -citrate-induced mitochondrial swelling and loss of mitochondrial transmembrane potential (DeltaPsi). The IC50 value for Vimang protection against Fe2+ -citrate-induced mitochondrial TBARS formation (7.89+/-1.19 microM) was around 10 times lower than that for tert-butylhydroperoxide mitochondrial induction of TBARS formation. The extract also inhibited the iron citrate induction of mitochondrial antimycin A-insensitive oxygen consumption, stimulated oxygen consumption due to Fe2+ autoxidation and prevented Fe3+ ascorbate reduction. The extracted polyphenolic compound, mainly mangiferin, could form a complex with Fe2+, accelerating Fe2+ oxidation and the formation of more stable Fe3+ -polyphenol complexes, unable to participate in Fenton-type reactions and lipoperoxidation propagation phase. The strong DPPH radical scavenging activity with an apparent IC50 of 2.45+/-0.08 microM suggests that besides its iron-complexing capacity, Vimang could also protect mitochondria from Fe2+ -citrate lipoperoxidation through direct free radical scavenging ability, mainly lipoperoxyl and alcoxyl radicals, acting as both a chain-breaking and iron-complexing antioxidant. These results are of pharmacological relevance since Vimang could be a potential candidate for antioxidant therapy in diseases related to abnormal intracellular iron distribution or iron overload.     

Interaction of Vimang (Mangifera indica L. extract) with Fe(III) improves its antioxidant and cytoprotecting activity.

A standard aqueous stem bark extract from selected species of Mangifera indica L. (Anacardiaceae)--Vimang, whose major polyphenolic component is mangiferin, displays potent in vitro and in vivo antioxidant activity. The present study provides evidence that the Vimang-Fe(III) mixture is more effective at scavenging 2,2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide radicals, as well as in protecting against t-butyl hydroperoxide-induced mitochondrial lipid peroxidation and hypoxia/reoxygenation-induced hepatocytes injury, compared to Vimang alone. Voltammetric assays demonstrated that Vimang, in line with the high mangiferin content of the extract, behaves electrochemically like mangiferin, as well as interacts with Fe(III) in close similarity with mangiferin's interaction with the cation. These results justify the high efficiency of Vimang as an agent protecting from iron-induced oxidative damage. We propose Vimang as a potential therapy against the deleterious action of reactive oxygen species generated during iron-overload, such as that occurring in diseases like beta-thalassemia, Friedreich's ataxia and haemochromatosis.     

Protective effects of Mangifera indica L extract (Vimang), and its major component mangiferin, on iron-induced oxidative damage to rat serum and liver.

In vivo preventive effects of a Mangifera indica L extract (Vimang) or its major component mangiferin on iron overload injury have been studied in rats given respectively, 50, 100, 250 mg kg(-1) body weight of Vimang, or 40 mg kg(-1) body weight of mangiferin, for 7 days prior to, and for 7 days following the administration of toxic amounts of iron-dextran. Both Vimang or mangiferin treatment prevented iron overload in serum as well as liver oxidative stress, decreased serum and liver lipid peroxidation, serum GPx activity, and increased serum and liver GSH, serum SOD and the animals overall antioxidant condition. Serum iron concentration was decreased although at higher doses, Vimang tended to increase it; percent tranferrin saturation, liver weight/body mass ratios, liver iron content was decreased. Treatment increased serum iron-binding capacity and decreased serum levels of aspartate-amine transferase (ASAT) and alanine-amine transferase (ALAT), as well as the number of abnormal Kupffer cells in iron-loaded livers. It is suggested that besides acting as antioxidants, Vimang extract or its mangiferin component decrease liver iron by increasing its excretion. Complementing earlier in vitro results from our group, it appears possible to support the hypothesis that Vimang and mangiferin present therapeutically useful effects in iron overload related diseases.     

Shikonin inhibits maturation of bone marrow-derived dendritic cells and suppresses allergic airway inflammation in a murine model of asthma

BACKGROUND AND PURPOSE

Shikonin exhibits a wide range of anti-inflammatory actions. Here, we assessed its effects on maturation of murine bone marrow-derived dendritic cells (BM-DCs) and on allergic reactions in a murine model of asthma.

EXPERIMENTAL APPROACH

Cultured murine BM-DCs were used to investigate the effects of shikonin on expression of cell surface markers and their stimulation of T-cell proliferation and cytokine production. The therapeutic potential of shikonin was evaluated in a model of allergic airway disease.

KEY RESULTS

Shikonin dose-dependently inhibited expression of major histocompatibility complex class II, CD80, CD86, CCR7 and OX40L on BM-DCs, induced by a mixture of ovalbumin (OVA; 100 µg·mL⁻¹) and thymic stromal lymphopoietin (TSLP; 20 ng·mL⁻¹). Shikonin-treated BM-DCs were poor stimulators of CD4⁺ T lymphocyte and induced lower levels of interleukin (IL)-4, IL-5, IL-13 and tumour necrosis factor (TNF)-α release by responding T-cells. After intratracheal instillation of shikonin in OVA-immunized mice, OVA challenge induced lower IL-4, IL-5, IL-13, TNF-α and eotaxin release in bronchial alveolar lavage fluid, lower IL-4 and IL-5 production in lung cells and mediastinal lymph node cells and attenuated OVA-induced lung eosinophilia and airway hyperresponsiveness.

CONCLUSION AND IMPLICATIONS

Shikonin effectively suppressed OVA + TSLP-induced BM-DC maturation in vitro and inhibited allergic inflammation and airway hyperresponsiveness in a murine model of asthma, showing good potential as a treatment for allergic asthma. Also, our model provides a novel platform for screening drugs for allergic diseases.     

Kochia scoparia fruit attenuates allergic airway inflammation in ovalbumin (OVA)-induced murine asthma model

Kochia scoparia fruit has been used in Asia for a long time. It possesses anti-inflammatory, antiallergic, and antipruritic actions. We investigated the role of a K. scoparia fruit ethanolic extract (KSEE) in allergic airway inflammation in a mouse asthma model. BALB/c mice were sensitized with ovalbumin (OVA) and, upon OVA aerosol challenge, developed airway eosinophilia, mucus hypersecretion, elevations in cytokine, chemokine, and immunoglobulin levels, and upregulation of MMP-9, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression. Intragastric administration of KSEE significantly attenuated OVA-induced influx of total leukocytes, eosinophils, neutrophils, macrophages, and lymphocytes into lungs, as well as attenuating levels of interleukin (IL)-4 and IL-5 in a dose-dependent manner. KSEE also significantly reduced the serum levels of total and OVA-specific immunoglobulin (Ig)E and OVA-specific IgG1 release into the airspace. Histological studies showed that KSEE inhibited OVA-induced lung tissue eosinophilia and airway mucus production. Moreover, in whole lung tissue lysates, immunoreactivity showed that KSEE markedly attenuated the OVA-induced increase in expression of ICAM-1, VCAM-1, and MMP-9. These results show that KSEE possesses protective effects against allergic airway inflammation, acts as an MMP-9 inhibitor, and induces a reduction in ICAM-1 and VCAM-1 expression.     

Flavonone treatment reverses airway inflammation and remodelling in an asthma murine model

Background and Purpose

Asthma is an inflammatory disease that involves airway hyperresponsiveness and remodelling. Flavonoids have been associated to anti-inflammatory and antioxidant activities and may represent a potential therapeutic treatment of asthma. Our aim was to evaluate the effects of the sakuranetin treatment in several aspects of experimental asthma model in mice.

Experimental Approach

Male BALB/c mice received ovalbumin (i.p.) on days 0 and 14, and were challenged with aerolized ovalbumin 1% on days 24, 26 and 28. Ovalbumin-sensitized animals received vehicle (saline and dimethyl sulfoxide, DMSO), sakuranetin (20 mg kg^–1 per mice) or dexamethasone (5 mg kg^–1 per mice) daily beginning from 24th to 29th day. Control group received saline inhalation and nasal drop vehicle. On day 29, we determined the airway hyperresponsiveness, inflammation and remodelling as well as specific IgE antibody. RANTES, IL-5, IL-4, Eotaxin, IL-10, TNF-α, IFN-γ and GMC-SF content in lung homogenate was performed by Bioplex assay, and 8-isoprostane and NF-kB activations were visualized in inflammatory cells by immunohistochemistry.

Key Results

We have demonstrated that sakuranetin treatment attenuated airway hyperresponsiveness, inflammation and remodelling; and these effects could be attributed to Th2 pro-inflammatory cytokines and oxidative stress reduction as well as control of NF-kB activation.

Conclusions and Implications

These results highlighted the importance of counteracting oxidative stress by flavonoids in this asthma model and suggest sakuranetin as a potential candidate for studies of treatment of asthma.     

Obesity enhances eosinophilic inflammation in a murine model of allergic asthma

Background and purpose:

Obesity is associated with deterioration in asthma outcomes. Although airways eosinophil accumulation is characteristic of lung allergic diseases, little is known about the influence of obesity on the allergic eosinophil trafficking from bone marrow to lung tissues, and recruitment to airways lumen. Here, we have assessed the effects of diet-induced obesity on allergic eosinophilic inflammation in mice, examining eosinophil trafficking from bone marrow to airways, and production of T_H1/T_H2 cytokines.

Experimental approach:

C57BL/6 mice fed for 10 weeks with standard chow or high-fat diet were sensitized and challenged with ovalbumin. At 24–96 h post-ovalbumin challenge, bronchoalveolar lavage (BAL) fluid, lung tissue and bone marrow were examined.

Key results:

The high-fat-fed mice exhibited increased body weight and epididymal fat, glucose intolerance and alterations in lipid profile compared with the lean mice. Obesity markedly elevated serum leptin and lowered adiponectin levels. Ovalbumin challenge in obese mice promoted a markedly higher eosinophil accumulation in bone marrow and connective tissue surrounding the bronchial and bronchiolar segments. Eosinophil number in BAL fluid of obese mice was lower at 24 and 48 h. Levels of interleukin (IL)-5, eotaxin, tumour necrosis factor-α and IL-10 in BAL fluid of obese mice were significantly higher than in lean mice.

Conclusions and implications:

Diet-induced obesity enhanced eosinophil trafficking from bone marrow to lung tissues, and delayed their transit through the airway epithelium into the airway lumen. Consequently, eosinophils remain longer in lung peribronchiolar segments due to overproduction of T_H1/T_H2 cytokines and chemokines.     

舌下特异性免疫治疗对过敏性哮喘患儿Th1／Th2细胞因子平衡的调控

目的：探讨舌下特异性免疫治疗（SLIT）对过敏性哮喘患儿T淋巴细胞表达Th1／Th2细胞因子（IL-2、IL4、IFN-γ）之间的平衡以及血清IgE水平调控的作用。方法：选择粉尘螨变应原皮试阳性的过敏性支气管哮喘患儿95例作为观察对象，根据随机化原则分为两组，使用SUT（粉尘螨滴剂）48例（治疗组），未使用SLIT47例（对照组），在研究前、后分别取血，测定Th1、Th2细胞因子IFN-γ、IL-2、IL-4的表达及血清IgE水平。结果：SLIT疗程（1年）结束后，治疗组Th1细胞因子IFN-γ、IL-2表达分别增加了30．76％、33．23％，而Th2细胞因子IL-4表达及血清IgE的水平分别降低了31．07％、33．60％；与对照组相比各种细胞因子表达的差异均有统计学意义。结论：舌下特异性免疫治疗对于过敏性支气管哮喘，可显著纠正Th1／Th2表达细胞因子功能的失衡，减轻患者的变态反应性炎症。