CAJ | 학술논문

目的探讨过氧化物酶体增殖物活化受体γ(peroxisome proliferator activated receptorγ,PPARγ)激动剂罗格列酮(rosiglita-zone,RSG)舒张大鼠气道平滑肌的部分机制.方法 SD大鼠40只,按随机数字表法分为正常对照组(A组)、哮喘组(B组),每组20只,制备各组大鼠离体去上皮气管环.观察RSG对乙酰胆碱(acetycholine,ACh)预收缩气管环的舒张作用,观察前列环素合成酶抑制剂吲哚美辛、胞浆可溶性鸟甘酸环化酶抑制剂亚甲基蓝、β2受体阻断剂普萘洛尔、一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(NG-Nitro-L-arginine Methyl Ester,L-NAME)、大电导钙激活钾通道(Large-conductance calcium-activated potassium channels,BKCa)抑制剂伊比蝎毒素(Iberiotoxin,IbTX)对RSG舒张气管环作用的影响.结果吲哚美辛、亚甲基蓝、普萘洛尔分别对三种浓度RSG作用于两组气管环的舒张效应均无阻断作用(P值均＞0.05,n=20),L-NAME对三种浓度RSG所引起B组气管环的舒张效应均有阻断作用(RSG浓度从低到高对B组气管环舒张作用与加L-NAME前比较tD值分别为6.00、4.84、4.47,P值均＜0.01,n=20),而对A组无作用(P值均＞0.05,n=20).IbTX对三种浓度RSG分别作用于A、B两组气管环的舒张效应均有阻断作用(RSG浓度从低到高对A组气管环舒张作用与加IbTX前比较,其tD值分别为:7.03、9.91、17.1,P值均＜0.01；对B组气管环舒张作用与加IbTX前比较,tD值分别为8.00、6.76、11.7,P值均＜0.01,n=20),并且IbTX对A组的阻断作用大于对B组的阻断作用,差异有统计学意义(RSG浓度由低到高f值分别为-3.604,-4.469,-4.724,P值均＜0.01,n =20).结论 RSG对ACh预收缩的大鼠气管环的舒张作用可能与前列环素、胞浆可溶性鸟苷酸环化酶、β2肾上腺素受体无关,与BKCa、一氧化氮有关.
목적 탐토과양화물매체증식물활화수체γ(peroxisome proliferator activated receptorγ,PPARγ)격동제라격렬동(rosiglita-zone,RSG)서장대서기도평활기적부분궤제.방법 SD대서40지,안수궤수자표법분위정상대조조(A조)、효천조(B조),매조20지,제비각조대서리체거상피기관배.관찰RSG대을선담감(acetycholine,ACh)예수축기관배적서장작용,관찰전렬배소합성매억제제신타미신、포장가용성조감산배화매억제제아갑기람、β2수체조단제보내락이、일양화담합매억제제좌선초기정안산갑지(NG-Nitro-L-arginine Methyl Ester,L-NAME)、대전도개격활갑통도(Large-conductance calcium-activated potassium channels,BKCa)억제제이비갈독소(Iberiotoxin,IbTX)대RSG서장기관배작용적영향.결과 신타미신、아갑기람、보내락이분별대삼충농도RSG작용우량조기관배적서장효응균무조단작용(P치균＞0.05,n=20),L-NAME대삼충농도RSG소인기B조기관배적서장효응균유조단작용(RSG농도종저도고대B조기관배서장작용여가L-NAME전비교tD치분별위6.00、4.84、4.47,P치균＜0.01,n=20),이대A조무작용(P치균＞0.05,n=20).IbTX대삼충농도RSG분별작용우A、B량조기관배적서장효응균유조단작용(RSG농도종저도고대A조기관배서장작용여가IbTX전비교,기tD치분별위:7.03、9.91、17.1,P치균＜0.01；대B조기관배서장작용여가IbTX전비교,tD치분별위8.00、6.76、11.7,P치균＜0.01,n=20),병차IbTX대A조적조단작용대우대B조적조단작용,차이유통계학의의(RSG농도유저도고f치분별위-3.604,-4.469,-4.724,P치균＜0.01,n =20).결론 RSG대ACh예수축적대서기관배적서장작용가능여전렬배소、포장가용성조감산배화매、β2신상선소수체무관,여BKCa、일양화담유관.
Objective To evaluate a part of the mechanism of the rosiglitazone,an agonist of peroxisome proliferator-activated receptor γ (PPARγ),diastoling airway smooth muscle in rats.Methods 40 SD rats were randomly divided into control group(group A),asthma group (group B),n =20,isolated rats tracheal rings without epithelium in each group were prepared.To evaluate the relaxing effect on isolated rings in rats from group A and group B,which were precontracted by Acetycholine (ACh).The effect of Indomethacin which was the Prostacyclin synthesis inhibitors,Methylene blue which was the Cytosolic soluble birds adenosine cyclase inhibitor,Propranolol which was the β2 receptor blocker,L-NAME which was the Nitric oxide synthase inhibitor and IbTX which is the The large conductance calcium-activated potassium channel inhibitor on the relaxation of tracheal rings caused by the RSG were observed.Results Indomethacin,Methylene blue and Propranolol were no effect on the relaxation which was induced by the concentration gradient of RSG to tracheal rings in both groups (all P ＞0.05,n =20).L-NAME was blocking effect on the relaxation which was induced by the three concentrations of RSG in group B (compare of the relaxation which was induced by the three concentrations of RSG in group B tracheal rings,added in L-NAME before and after,the difference was statistically significant,tD values were 6.00,4.84,4.47 respectively,all P ＜ 0.01,n =20.But was no blocking effect on the relaxation in group A.all P ＞ 0.05,n =20.) IbTX was blocking effect on the relaxation which was induced by RSG in two groups (compare of the relaxation which was induced by the three concentrations of RSG in group A tracheal rings,added in IbTX before and after,the difference was statistically significant.tD were 7.03,9.91,17.1,respectively,all P ＜0.01.That was in group B,tD were 8.00,6.76,11.7,respectively,all P ＜0.01,n =20),and the blocking effect of IbTX on group A tracheal rings was greater than that on group B,the difference was statistically significant (the concentrations of RSG from low to high,the t values were-3.604,-4.469,-4.724,respectively,All P ＜0.01,n =20).Conclusions RSG could relax tracheal rings of rats induced by ACh pretreatment,it might be independent of Prostacyclin,cyclase and β-adrenergic receptor,but it might be dependent on the Largeconductance calcium activated potassium channels and NO.