中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2009年
4期
230-233
,共4页
曲政海%谢宁%车淑玉%林荣军%胡素娟
麯政海%謝寧%車淑玉%林榮軍%鬍素娟
곡정해%사저%차숙옥%림영군%호소연
昆布多糖%支气管哮喘%气道炎症%气道重塑%卵清蛋白%小鼠
昆佈多糖%支氣管哮喘%氣道炎癥%氣道重塑%卵清蛋白%小鼠
곤포다당%지기관효천%기도염증%기도중소%란청단백%소서
okam%bronchial asthma%inflammation of airway%remodeling of airway%ovalbumin%mouse
目的 观察昆布多糖对卵清蛋白(OVA)致敏激发哮喘小鼠气道炎症及重塑的影响.方法 将32只昆明系小鼠被随机分为模型组、激素吸入组、昆布多糖组和对照组4组,每组8只.经OVA致敏激发制模成功后,模型组用生理盐水0.3 ml灌胃干预,激素吸入组雾化吸入布地奈德混悬液0.4 ml(200 μg)+生理盐水3.6 ml干预,昆布多糖组采用昆布多糖50 mg/kg灌胃干预,均每日1次.对照组采用生理盐水代替OVA致敏激发和灌胃干预.各组动物于42 d后麻醉,行右肺支气管肺泡灌洗留取灌洗液(BALF),并取右肺组织进行病理学观察.在光镜下计数BALF中细胞总数及分类;采用酶联免疫吸附法(ELISA)检测BALF中γ-干扰素(IFN-γ)、白细胞介素-4(IL-4)水平;肺组织病理学改变程度在苏木素-伊红(HE)染色后于光镜下进行评价;肺组织基质金属蛋白酶-9(MMP-9)及金属蛋白酶组织抑制剂-1(TIMP-1)的表达采用免疫组化法检测.结果 与模型组比较,昆布多糖组及激素吸入组BALF中细胞总数及分类计数、IL-4、肺组织病理学评分均显著降低,IFN-γ显著升高(P均<0.01);激素吸入组MMP-9、TIMP-1及昆布多糖组TIMP-1均显著下降(P<0.05或P<0.01);与对照组比较,昆布多糖组各指标差异仍有统计学意义(P<0.05或P<0.01);与昆布多糖组比较,激素吸入组细胞总数及分类计数、IFN-γ、病理学评分、MMP-9、TIMP-1差异均有统计学意义(P<0.05或P<0.01).结论 昆布多糖在一定程度上能抑制急性哮喘小鼠的气道炎症,减轻气道重塑的发生,可能是一种新的治疗哮喘的辅助药物.
目的 觀察昆佈多糖對卵清蛋白(OVA)緻敏激髮哮喘小鼠氣道炎癥及重塑的影響.方法 將32隻昆明繫小鼠被隨機分為模型組、激素吸入組、昆佈多糖組和對照組4組,每組8隻.經OVA緻敏激髮製模成功後,模型組用生理鹽水0.3 ml灌胃榦預,激素吸入組霧化吸入佈地奈德混懸液0.4 ml(200 μg)+生理鹽水3.6 ml榦預,昆佈多糖組採用昆佈多糖50 mg/kg灌胃榦預,均每日1次.對照組採用生理鹽水代替OVA緻敏激髮和灌胃榦預.各組動物于42 d後痳醉,行右肺支氣管肺泡灌洗留取灌洗液(BALF),併取右肺組織進行病理學觀察.在光鏡下計數BALF中細胞總數及分類;採用酶聯免疫吸附法(ELISA)檢測BALF中γ-榦擾素(IFN-γ)、白細胞介素-4(IL-4)水平;肺組織病理學改變程度在囌木素-伊紅(HE)染色後于光鏡下進行評價;肺組織基質金屬蛋白酶-9(MMP-9)及金屬蛋白酶組織抑製劑-1(TIMP-1)的錶達採用免疫組化法檢測.結果 與模型組比較,昆佈多糖組及激素吸入組BALF中細胞總數及分類計數、IL-4、肺組織病理學評分均顯著降低,IFN-γ顯著升高(P均<0.01);激素吸入組MMP-9、TIMP-1及昆佈多糖組TIMP-1均顯著下降(P<0.05或P<0.01);與對照組比較,昆佈多糖組各指標差異仍有統計學意義(P<0.05或P<0.01);與昆佈多糖組比較,激素吸入組細胞總數及分類計數、IFN-γ、病理學評分、MMP-9、TIMP-1差異均有統計學意義(P<0.05或P<0.01).結論 昆佈多糖在一定程度上能抑製急性哮喘小鼠的氣道炎癥,減輕氣道重塑的髮生,可能是一種新的治療哮喘的輔助藥物.
목적 관찰곤포다당대란청단백(OVA)치민격발효천소서기도염증급중소적영향.방법 장32지곤명계소서피수궤분위모형조、격소흡입조、곤포다당조화대조조4조,매조8지.경OVA치민격발제모성공후,모형조용생리염수0.3 ml관위간예,격소흡입조무화흡입포지내덕혼현액0.4 ml(200 μg)+생리염수3.6 ml간예,곤포다당조채용곤포다당50 mg/kg관위간예,균매일1차.대조조채용생리염수대체OVA치민격발화관위간예.각조동물우42 d후마취,행우폐지기관폐포관세류취관세액(BALF),병취우폐조직진행병이학관찰.재광경하계수BALF중세포총수급분류;채용매련면역흡부법(ELISA)검측BALF중γ-간우소(IFN-γ)、백세포개소-4(IL-4)수평;폐조직병이학개변정도재소목소-이홍(HE)염색후우광경하진행평개;폐조직기질금속단백매-9(MMP-9)급금속단백매조직억제제-1(TIMP-1)적표체채용면역조화법검측.결과 여모형조비교,곤포다당조급격소흡입조BALF중세포총수급분류계수、IL-4、폐조직병이학평분균현저강저,IFN-γ현저승고(P균<0.01);격소흡입조MMP-9、TIMP-1급곤포다당조TIMP-1균현저하강(P<0.05혹P<0.01);여대조조비교,곤포다당조각지표차이잉유통계학의의(P<0.05혹P<0.01);여곤포다당조비교,격소흡입조세포총수급분류계수、IFN-γ、병이학평분、MMP-9、TIMP-1차이균유통계학의의(P<0.05혹P<0.01).결론 곤포다당재일정정도상능억제급성효천소서적기도염증,감경기도중소적발생,가능시일충신적치료효천적보조약물.
Objective To investigate the effect of okam (昆布) on inflammation and remodeling of airway in mice with ovalbumin (OVA) induced asthma. Methods Thirty-two mice of Kunming strain were divided into four groups randomly: model group, glucocorticoid inhalation group, okam group and control group, with 8 mice in each group. The asthmatic mice model was reproduced by combined injection and aerosol inhalation of OVA. The mice in model group received normal saline (0. 3 ml) gavage daily. The mice in glucocorticoid inhalation group received budesonide (0. 4 ml, 200 μg) and normal saline (3.6 ml) inhalation. The mice in okam group were gavaged with okam daily (50 mg/kg). The controls were given normal saline instead of OVA sensitization. All mice were sacrificed 42 days later, followed by lavage of tracheo-bronchial tree of the right lung, and the right lung was saved for pathological examination. The total cell number and differentiation in bronchoalveolar lavage fluid (BALF) were counted under microscope. The expression of interferon-γ (IFN-γ), interleukin-4 (IL-4) in BALF were assessed by enzyme linked immunosorbent asay (ELISA). The histological changes in the bronchi and alveoli were evaluated after hematoxylin and eosin (HE) staining. The expression of matrix metalloproteinase-9 (MMP-9) as well as the tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by immunohistochemistry. Results Compared with the model group, the total cell count and IL-4 level in BALF, and the score of pathological changes in the broncho-alveolar tissue in okam group or glucocorticoid inhalation group were lower significantly, and the IFN-γ level elevated markedly (all P <0.01). The MMP-9, TIMP-1 expression in glucocorticoid inhalation group and the TIMP-1 expression in okam group were decreased greatly (P<0. 05 or P<0. 01). All of above indexes showed marked differences between control group and okam group (P< 0. 05 or P<0. 01). There were significant changes in the total cell count, IFN-γ, pathological changes, MMP-9 and TIMP-1 between the glucocorticoid inhalation group and the okam group (P<0. 05 or P< 0. 01). Conclusion Okam may alleviate inflammation of the bronchia and degrade the development of airway remodeling to some degree.