世界科学技术-中医药现代化
世界科學技術-中醫藥現代化
세계과학기술-중의약현대화
WORLD SCIENCE AND TECHNOLOGY-MODERNIZATION OF TRADITIONAL CHINESE MEDICINE
2014年
1期
98-102
,共5页
鼻渊舒%慢性鼻原鼻窦炎%鼻窦黏膜上皮%糖皮质激素受体%IκBα
鼻淵舒%慢性鼻原鼻竇炎%鼻竇黏膜上皮%糖皮質激素受體%IκBα
비연서%만성비원비두염%비두점막상피%당피질격소수체%IκBα
Bi-Yuan-Shu%chronic rhinosinusitis%nasal sinuses mucosa epithelium%glucocorticoid receptors%IκBα
观察鼻渊舒口服液对慢性鼻原鼻窦炎（CRS）模型鼻窦黏膜上皮糖皮质激素受体（GR）及核因子资B抑制蛋白（I资Bα）表达的影响，从抑炎机制角度，探索鼻渊舒对CRS的治疗机制。方法：选取新西兰大白兔100只，按每组20只，随机分为正常组、假手术组、模型组、鼻渊舒组、克拉霉素组后，建立CRS模型，正常组、假手术组、模型组不干预，鼻渊舒、克拉霉素组分别给予鼻渊舒（1.5 mL·kg-1·d-1）、克拉霉素（25 mg·kg-1·d-1）灌胃14天，治疗结束后取鼻窦黏膜，HE染色观察其病理改变，Western Blotting法检测鼻窦黏膜上皮细胞胞浆糖皮质激素受体（GR）及核因子资B抑制蛋白（I资Bα）蛋白表达。结果：模型组鼻窦黏膜炎细胞明显浸润，呈慢性炎症病变，腺体及杯状细胞明显增生；与正常组比较，GR表达显著降低（P约0.01），I资Bα表达显著增高（P约0.01）。鼻渊舒灌胃治疗后，鼻窦黏膜上皮得到较好修复，炎细胞浸润不明显，腺体和杯状细胞增生亦不明显；与模型组比较，GR表达显著增高（P约0.01），I资Bα表达显著降低（P约0.01）。结论：鼻渊舒在促进抑炎途径的GR表达的同时，通过抑制I资Bα表达，防止I资Bα对NF-资B促炎途径的过度抑制，动态调控了鼻窦黏膜上皮炎症的平衡。
觀察鼻淵舒口服液對慢性鼻原鼻竇炎（CRS）模型鼻竇黏膜上皮糖皮質激素受體（GR）及覈因子資B抑製蛋白（I資Bα）錶達的影響，從抑炎機製角度，探索鼻淵舒對CRS的治療機製。方法：選取新西蘭大白兔100隻，按每組20隻，隨機分為正常組、假手術組、模型組、鼻淵舒組、剋拉黴素組後，建立CRS模型，正常組、假手術組、模型組不榦預，鼻淵舒、剋拉黴素組分彆給予鼻淵舒（1.5 mL·kg-1·d-1）、剋拉黴素（25 mg·kg-1·d-1）灌胃14天，治療結束後取鼻竇黏膜，HE染色觀察其病理改變，Western Blotting法檢測鼻竇黏膜上皮細胞胞漿糖皮質激素受體（GR）及覈因子資B抑製蛋白（I資Bα）蛋白錶達。結果：模型組鼻竇黏膜炎細胞明顯浸潤，呈慢性炎癥病變，腺體及杯狀細胞明顯增生；與正常組比較，GR錶達顯著降低（P約0.01），I資Bα錶達顯著增高（P約0.01）。鼻淵舒灌胃治療後，鼻竇黏膜上皮得到較好脩複，炎細胞浸潤不明顯，腺體和杯狀細胞增生亦不明顯；與模型組比較，GR錶達顯著增高（P約0.01），I資Bα錶達顯著降低（P約0.01）。結論：鼻淵舒在促進抑炎途徑的GR錶達的同時，通過抑製I資Bα錶達，防止I資Bα對NF-資B促炎途徑的過度抑製，動態調控瞭鼻竇黏膜上皮炎癥的平衡。
관찰비연서구복액대만성비원비두염（CRS）모형비두점막상피당피질격소수체（GR）급핵인자자B억제단백（I자Bα）표체적영향，종억염궤제각도，탐색비연서대CRS적치료궤제。방법：선취신서란대백토100지，안매조20지，수궤분위정상조、가수술조、모형조、비연서조、극랍매소조후，건립CRS모형，정상조、가수술조、모형조불간예，비연서、극랍매소조분별급여비연서（1.5 mL·kg-1·d-1）、극랍매소（25 mg·kg-1·d-1）관위14천，치료결속후취비두점막，HE염색관찰기병리개변，Western Blotting법검측비두점막상피세포포장당피질격소수체（GR）급핵인자자B억제단백（I자Bα）단백표체。결과：모형조비두점막염세포명현침윤，정만성염증병변，선체급배상세포명현증생；여정상조비교，GR표체현저강저（P약0.01），I자Bα표체현저증고（P약0.01）。비연서관위치료후，비두점막상피득도교호수복，염세포침윤불명현，선체화배상세포증생역불명현；여모형조비교，GR표체현저증고（P약0.01），I자Bα표체현저강저（P약0.01）。결론：비연서재촉진억염도경적GR표체적동시，통과억제I자Bα표체，방지I자Bα대NF-자B촉염도경적과도억제，동태조공료비두점막상피염증적평형。
This study was aimed to investigate the influence of Bi-Y uan-Shu (BYS) Oral Liquid on glucocorticoid re-ceptor (GR) and nuclear factor IκBα expression of nasal sinuses mucosa epithelium among chronic rhinosinusitis (CRS) models in order to explore its therapeutic mechanism for CRS from the anti-inflammatory reaction aspect. One hundred New Zealand rabbits were selected and randomly divided into the normal group, sham operation group, model group, BYS group, and clarithromycin group, with 20 rabbits in each group. After the CRS model was established, no intervention was given to the normal group, sham operation group, or model group. The intragastric administrations of BYS (1.5 mL·kg-1·d-1) and clarithromycin (25 mg·kg-1·d-1) were given for 14 days, respectively. The nasal sinuses mucosa was taken after the treatment. And HE stain was used to observe its pathological changes. Western Blotting was used in the detection of nasal sinuses mucosal epithelium cytoplasm GR and IκBα expression. The results showed that there were obvious nasal sinuses mucosa inflammatory cell infiltration, chronic inflammation changes, and obvious hyperplasia of glandular organs and goblet cells. Compared with the normal group, the GR expression was obviously reduced (P< 0.01). And the IκBα expression was obviously increased (P< 0.01). After the intragastric administration of BYS, the nasal sinuses mucosal epithelium was repaired with no obvious inflammatory cell infiltration, glandular organs, or goblet cells. Compared with the model group, the GR expression was obviously increased (P< 0.01). The IκBα expression was obviously decreased (P<0.01). It was concluded that BYS can promote GR expression to inhibit inflammation. Meanwhile, it can restrain IκBα expression to prevent the over inhabitation of IκBα on NF-κB. It can dynamically regulate the balance of the nasal sinuses mucosa epithelium inflammation.
