临床肺科杂志
臨床肺科雜誌
림상폐과잡지
Journal of Clinical Pulmonary Medicine
2015年
10期
1797-1801
,共5页
低分子肝素%黏液高分泌%炎症%哮喘
低分子肝素%黏液高分泌%炎癥%哮喘
저분자간소%점액고분비%염증%효천
low molecular weight heparin%mucus hypersecretion%inflammation%asthma
目的 探讨低分子肝素对哮喘小鼠气道黏液高分泌和炎症反应的影响. 方法 30只健康雄性C57BL/6小鼠,按随机数字表法分为正常对照组、哮喘组和低分子肝素干预组,每组10只,检测三组小鼠气道上皮细胞黏液分泌量、气道内炎症细胞浸润、黏蛋白基因MUC5AC的表达、细胞因子IL-13、IL-4和IL-5的表达. 结果 (1)哮喘小鼠气道黏液细胞化生、黏液过度分泌,气道内炎症细胞浸润增多,经鼻腔滴入低分子肝素后,黏液过度分泌受抑制,气道内炎症细胞浸润减少. (2)哮喘组小鼠气道黏液细胞MUC5AC mRNA相对表达量(26. 43 ±0. 47)及气道内炎症因子IL-13[(16. 03 ±0. 53)ng/ml]、IL-4[(603. 68 ±50. 32)pg/ml]和IL-5 [(1308.80 ±224.84)pg/ml]表达的水平均高于正常组[(1.17 ±0.18)ng/ml、(17.56 ±3.01)pg/ml和(33.09 ±5.92)pg/ml];经鼻腔滴入低分子肝素后,上述指标[16.26 ±2.07,(11.50 ±0.89)ng/ml,(409.56 ±46.25) pg/ml,(874. 65 ± 32. 833)pg/ml] 均下降,P<0. 05,差异有统计学意义. 结论 低分子肝素抑制哮喘小鼠气道黏液高分泌和气道炎症反应. 经鼻滴入的低分子肝素可能为哮喘过敏性炎症的治疗提供新的方法.
目的 探討低分子肝素對哮喘小鼠氣道黏液高分泌和炎癥反應的影響. 方法 30隻健康雄性C57BL/6小鼠,按隨機數字錶法分為正常對照組、哮喘組和低分子肝素榦預組,每組10隻,檢測三組小鼠氣道上皮細胞黏液分泌量、氣道內炎癥細胞浸潤、黏蛋白基因MUC5AC的錶達、細胞因子IL-13、IL-4和IL-5的錶達. 結果 (1)哮喘小鼠氣道黏液細胞化生、黏液過度分泌,氣道內炎癥細胞浸潤增多,經鼻腔滴入低分子肝素後,黏液過度分泌受抑製,氣道內炎癥細胞浸潤減少. (2)哮喘組小鼠氣道黏液細胞MUC5AC mRNA相對錶達量(26. 43 ±0. 47)及氣道內炎癥因子IL-13[(16. 03 ±0. 53)ng/ml]、IL-4[(603. 68 ±50. 32)pg/ml]和IL-5 [(1308.80 ±224.84)pg/ml]錶達的水平均高于正常組[(1.17 ±0.18)ng/ml、(17.56 ±3.01)pg/ml和(33.09 ±5.92)pg/ml];經鼻腔滴入低分子肝素後,上述指標[16.26 ±2.07,(11.50 ±0.89)ng/ml,(409.56 ±46.25) pg/ml,(874. 65 ± 32. 833)pg/ml] 均下降,P<0. 05,差異有統計學意義. 結論 低分子肝素抑製哮喘小鼠氣道黏液高分泌和氣道炎癥反應. 經鼻滴入的低分子肝素可能為哮喘過敏性炎癥的治療提供新的方法.
목적 탐토저분자간소대효천소서기도점액고분비화염증반응적영향. 방법 30지건강웅성C57BL/6소서,안수궤수자표법분위정상대조조、효천조화저분자간소간예조,매조10지,검측삼조소서기도상피세포점액분비량、기도내염증세포침윤、점단백기인MUC5AC적표체、세포인자IL-13、IL-4화IL-5적표체. 결과 (1)효천소서기도점액세포화생、점액과도분비,기도내염증세포침윤증다,경비강적입저분자간소후,점액과도분비수억제,기도내염증세포침윤감소. (2)효천조소서기도점액세포MUC5AC mRNA상대표체량(26. 43 ±0. 47)급기도내염증인자IL-13[(16. 03 ±0. 53)ng/ml]、IL-4[(603. 68 ±50. 32)pg/ml]화IL-5 [(1308.80 ±224.84)pg/ml]표체적수평균고우정상조[(1.17 ±0.18)ng/ml、(17.56 ±3.01)pg/ml화(33.09 ±5.92)pg/ml];경비강적입저분자간소후,상술지표[16.26 ±2.07,(11.50 ±0.89)ng/ml,(409.56 ±46.25) pg/ml,(874. 65 ± 32. 833)pg/ml] 균하강,P<0. 05,차이유통계학의의. 결론 저분자간소억제효천소서기도점액고분비화기도염증반응. 경비적입적저분자간소가능위효천과민성염증적치료제공신적방법.
Objective To investigate the effect of low molecular weight heparin on mucus hypersecretion and airway inflammation in asthmatic mice. Methods 30 healthy male C57BL/6 mice were randomly divided into the control group, the asthmatic group and the low molecular weight heparin group. The mucus production, inflammatory cells, MUC5AC, and the levels of cytokines such as IL-13, IL-4 and IL-5 were examined in the three groups. Re-sults (1) Their mucous cells manufactured, slime over secreted, and inflammatory cell infiltration increased before treatment. After the treatment, slime secretion inhibited and inflammatory cell infiltration decreased. ( 2 ) The ex-pression of MUC5AC mRNA in the airway mucous cells, IL-13, IL-4 and IL-5 in the asthmatic group was (26. 43 ± 0. 47) ng/ml, (16. 03 ± 0. 53) ng/ml, (603. 68 ± 50. 32) pg/ml and (1308. 80 ± 224. 84) pg/ml, which were all significantly higher than those in the control group [(1. 17 ± 0. 18) ng/ml, (17. 56 ± 3. 01) pg/ml and (33. 09 ± 5. 92) pg/ml], and all of them decreased to (16. 26 ± 2. 07) ng/ml, (11. 50 ± 0. 89) ng/ml, (409. 56 ± 46. 25) pg/ml and ( 874. 65 ± 32. 833 ) pg/ml respectively after treating with low molecular weight heparin ( P <0. 05 ) . Conclusion Low molecular weight heparin could inhibit mucus hypersecretion and airway inflammation in asthmatic mice. Intranasal instillation with low molecular weight heparin might be a novel approach for asthma treatment.
