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
4期
753-757
,共5页
杨雪%王新月%景姗%杨舒
楊雪%王新月%景姍%楊舒
양설%왕신월%경산%양서
溃疡性结肠炎%从肺论治法%诱生型一氧化氮合成酶%肺损伤
潰瘍性結腸炎%從肺論治法%誘生型一氧化氮閤成酶%肺損傷
궤양성결장염%종폐론치법%유생형일양화담합성매%폐손상
Ulcerative colitis%treatment from lung%iNOS%lung injury
目的：观察从肺论治法对溃疡性结肠炎（UC）大鼠肺组织中诱生型一氧化氮合成酶（iNOS） mRNA表达的影响。方法：选取52只大鼠，采用家兔结肠黏膜组织致敏与三硝基苯磺酸（TNBS）-乙醇模型相结合的免疫复合法复制UC大鼠模型（造模成功率为78%）。从造模成功的40只大鼠及正常组大鼠中随机选出8只作为干预前（0周时间点）的模型组及正常组。剩余造模成功的32只大鼠随机分为模型组、西药组（柳氮磺胺吡啶）、从肺论治组（黄芪桔梗汤）、从肠论治组（黄芪黄连汤），每组8只，另取8只正常大鼠为对照，连续干预4周（4周时间点）后，分别于0周、4周时间点采用Real Time-PCR 法测定肺组织中iNOS mRNA表达。结果：与正常组比较，0周急性期模型组大鼠肺组织中iNOS mRNA转录水平明显上调（P<0.05）；4周治疗后，与正常组比较，模型组大鼠iNOS mRNA转录水平明显升高（P<0.05）；与模型组比较，从肺论治组大鼠iNOS mRNA转录水平显著降低（P<0.01）。结论：iNOS催化合成的NO在肺部疾病中发挥了重要作用，可引起气道炎症、水肿、肺损伤等。从肺论治法通过抑制iNOS的异常活化，进而减轻肺部损伤。
目的：觀察從肺論治法對潰瘍性結腸炎（UC）大鼠肺組織中誘生型一氧化氮閤成酶（iNOS） mRNA錶達的影響。方法：選取52隻大鼠，採用傢兔結腸黏膜組織緻敏與三硝基苯磺痠（TNBS）-乙醇模型相結閤的免疫複閤法複製UC大鼠模型（造模成功率為78%）。從造模成功的40隻大鼠及正常組大鼠中隨機選齣8隻作為榦預前（0週時間點）的模型組及正常組。剩餘造模成功的32隻大鼠隨機分為模型組、西藥組（柳氮磺胺吡啶）、從肺論治組（黃芪桔梗湯）、從腸論治組（黃芪黃連湯），每組8隻，另取8隻正常大鼠為對照，連續榦預4週（4週時間點）後，分彆于0週、4週時間點採用Real Time-PCR 法測定肺組織中iNOS mRNA錶達。結果：與正常組比較，0週急性期模型組大鼠肺組織中iNOS mRNA轉錄水平明顯上調（P<0.05）；4週治療後，與正常組比較，模型組大鼠iNOS mRNA轉錄水平明顯升高（P<0.05）；與模型組比較，從肺論治組大鼠iNOS mRNA轉錄水平顯著降低（P<0.01）。結論：iNOS催化閤成的NO在肺部疾病中髮揮瞭重要作用，可引起氣道炎癥、水腫、肺損傷等。從肺論治法通過抑製iNOS的異常活化，進而減輕肺部損傷。
목적：관찰종폐론치법대궤양성결장염（UC）대서폐조직중유생형일양화담합성매（iNOS） mRNA표체적영향。방법：선취52지대서，채용가토결장점막조직치민여삼초기분광산（TNBS）-을순모형상결합적면역복합법복제UC대서모형（조모성공솔위78%）。종조모성공적40지대서급정상조대서중수궤선출8지작위간예전（0주시간점）적모형조급정상조。잉여조모성공적32지대서수궤분위모형조、서약조（류담광알필정）、종폐론치조（황기길경탕）、종장론치조（황기황련탕），매조8지，령취8지정상대서위대조，련속간예4주（4주시간점）후，분별우0주、4주시간점채용Real Time-PCR 법측정폐조직중iNOS mRNA표체。결과：여정상조비교，0주급성기모형조대서폐조직중iNOS mRNA전록수평명현상조（P<0.05）；4주치료후，여정상조비교，모형조대서iNOS mRNA전록수평명현승고（P<0.05）；여모형조비교，종폐론치조대서iNOS mRNA전록수평현저강저（P<0.01）。결론：iNOS최화합성적NO재폐부질병중발휘료중요작용，가인기기도염증、수종、폐손상등。종폐론치법통과억제iNOS적이상활화，진이감경폐부손상。
This study was aimed to observe effects of traditional Chinese medicine (TCM) treatment from lung on mRNA expressions of iNOS in lung tissues of rats with ulcerative colitis (UC). A total of 52 rats were used to estab-lish the UC rat model by using rabbit intestinal mucosal tissue allergenic model and TNBS-ethanol model (with the model success rate of 78%). Eight rats, which were randomly selected from 40 successfully modeled rats and the normal group, were used as the model group and the normal group before intervention (time point of week zero). The rest 32 successfully modeled rats were randomly divided into the model group, the western medicine (salazosulfapyri-dine) group, treatment from lung (Huang-Qi Jie-Geng, HQJG decoction) group, and treatment from intestine (Huang-Qi Huang-Lian, HQHL decoction) group, with 8 rats in each group. Another 8 normal rats were used as the control group. The intervention was given for 4 weeks. And the mRNA expression of iNOS was detected in week ze-ro, and four weeks after the treatment using real time-PCR. The results showed that in the acute phase of week zero, the mRNA level of iNOS in lung tissues of model group was significantly increased compared with that in normal group (P < 0.05); after 4-week treatment, compared with the normal group, the mRNA level of iNOS in the model group was significantly increased (P< 0.05). Compared with the model group, the mRNA level of iNOS in the treat-ment from lung group was significantly decreased (P < 0.01). It was concluded that NO which was catalyzed and synthesized by iNOS played an important role in pulmonary diseases. It can cause airway inflammation, edema, lung injury, and etc. Treatment from lung can alleviate the lung injury by inhibiting abnormal activation of iNOS.
