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纸质出版日期:2012
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郭宏伟, 邓家刚, 运晨霞, 等. 芒果苷抑制哮喘小鼠气道炎症的机制[J]. 中国实验方剂学杂志, 2012,18(9):187-190.
GUO Hong-wei, DENG Jia-gang, YUN Chen-xia, et al. Mechanism of Mangiferin Inhibiting the Airway Inflammation in a Murine Model of Asthma[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(9): 187-190.
郭宏伟, 邓家刚, 运晨霞, 等. 芒果苷抑制哮喘小鼠气道炎症的机制[J]. 中国实验方剂学杂志, 2012,18(9):187-190. DOI:
GUO Hong-wei, DENG Jia-gang, YUN Chen-xia, et al. Mechanism of Mangiferin Inhibiting the Airway Inflammation in a Murine Model of Asthma[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(9): 187-190. DOI:
目的: 观察芒果苷对哮喘小鼠气道炎症的影响
探讨芒果苷平喘的作用机制。 方法: 将72只4~5周SPF级BALB/c雌性小鼠随机分为正常对照组、模型对照组、地塞米松阳性对照组(0.001 25 g·kg-1)、芒果苷高、中、低剂量组(0.4
0.2
0.1 g·kg-1)。采用卵白蛋白(OVA)致敏和激发构建小鼠哮喘模型
收集支气管肺泡灌洗液(BALF)进行细胞计数及分类;肺组织病理切片HE染色观察炎性细胞浸润情况;采用 ELISA 法检测小鼠血清中OVA特异性IgE(OVA-sIgE)和BALF中白三烯C4(LTC4)
前列腺素D2(PGD2)的含量。 结果: 芒果苷高、中、低剂量组BALF中嗜酸性粒细胞(EOS)比例由模型组(6.57±1.44)%降低为 (1.63±0.43
2.72±0.83
4.11±1.08)%(P<0.01~P<0.05);芒果苷高、中剂量组BALF中白细胞总数由模型组(83.25±10.19)×105/mL减少为(25.66±6.16
53.38±9.19)×105/mL(P<0.01);芒果苷各剂量均可不同程度的改善肺组织的病理学改变
减轻气道炎症;芒果苷高、中、低剂量组血清中OVA-sIgE含量由模型组(0.26±0.04)ng·mL-1降低为(0.10±0.04
0.12±0.02
0.18±0.03) ng·mL-1(P<0.01);芒果苷高剂量组BALF中PGD2水平由模型组(74.36±22.72)ng·mL-1降低为(60.30±12.19)ng·mL-1(P<0.05)
而芒果苷中、低剂量组对PGD2的降低无统计学差异;芒果苷各剂量对LTC4水平有降低趋势。 结论: 芒果苷可通过减少EOS浸润、小鼠体内OVA-sIgE和PGD2含量
抑制哮喘小鼠的气道炎症
在治疗哮喘方面有潜在的应用前景。
Objective: To investigate the inhibitory effect and mechanism of mangiferin on the airway inflammation in BALB/c mice model of asthma. Method : Seventy-two BALB/c mice
aged 4-5 weeks
were randomly divided into 6 groups: normal control group
model control group
dexamethasone group (0.001 25 g·kg-1)
mangiferin high-dose group (0.4 g·kg-1)
mangiferin middle-dose group (0.2 g·kg-1) and mangiferin low-dose group (0.1 g·kg-1). The mice were sensitized and challenged with ovalbumin (OVA) to establish a murine model of asthma.Bronchoalveolar lavage fluid (BALF) was collected for total and differential cell count. HE staining was used to observe airway inflammation in lung tissue. Quantification of leukotriene C4(LTC4)
prostaglandin D2(PGD2) in BALF and OVA special immunoglobulin E (OVA-sIgE) in serum were detected by ELISA. Result: The number of eosinophil(EOS) in BALF
compared with model group (6.57±1.44)%
could obviously be reduced by three mangiferin groups (1.63±0.43
2.72±0.83
4.11±1.08)% (P<0.01-P<0.05). The total number of white cells in BALF
compared with model group (83.25±10.19)×105/mL
could be cut down by mangiferin high-dose and middle-dose group (25.66±6.16
53.38±9.19) ×105/mL(P<0.01); HE staining showed that three mangiferin groups could improve
to some extent
the histological changes of lung and bronchus and reduce airway inflammation. The level of OVA-sIgE in serum
compared with the model group (0.26±0.04) ng·mL-1
could significantly be decreased by three mangiferin groups (0.10±0.04
0.12±0.02
0.18±0.03) ng·mL-1 (P<0.01). And the level of PGD2 in BALF
compared with model group (74.36±22.72) ng·mL-1
could be reduced by mangiferin high-dose group (60.30±12.19) ng·mL-1 (P<0.05). For the level of LTC4
there was a reduce tendency in every mangiferin group
but no statistical significance. Conclusion: Mangiferin
through reducing the number of EOS
decreasing the level of OVA-sIgE and PGD2 in mice
could obviously inhibit the airway inflammation in mice model of asthma
which promises to be a potential drug in the treatment of allergic asthma.
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