中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2009年
12期
2390-2393
,共4页
黄新莉%周晓红%周君琳%羡晓辉%丁春华
黃新莉%週曉紅%週君琳%羨曉輝%丁春華
황신리%주효홍%주군림%이효휘%정춘화
脂多糖类%胆囊收缩素%血红素氧合酶-1%信号转导
脂多糖類%膽囊收縮素%血紅素氧閤酶-1%信號轉導
지다당류%담낭수축소%혈홍소양합매-1%신호전도
Lipopolysaccharides%Cholecystokinin%Heme oxygenase-1%Signal transduction
目的:旨在研究八肽胆囊收缩素(CCK-8)上调脂多糖(LPS)诱导的大鼠肺组织中血红素氧合酶(HO)-1表达的信号转导机制.方法: 将42只雄性SD大鼠随机分为7组(每组6只),即对照组、LPS组、LPS+SP600125(JNK特异性抑制剂)组、CCK-8+LPS组、CCK-8+LPS+SP600125组、CCK-8组、CCK-8+SP600125组.注药后6 h放血处死动物留取肺组织,应用RT-PCR、Western blotting和免疫荧光流式细胞术(FCM)等技术分别检测各组肺组织HO-1 mRNA和蛋白表达.结果: 与正常对照组相比,LPS组可见肺组织中出现明显的HO-1 mRNA表达的阳性信号,CCK-8可使LPS诱导的阳性表达信号进一步增强,CCK单独作用也可上调HO-1表达.信号密度扫描结果显示,LPS组、CCK-8+LPS组和CCK-8组HO-1 mRNA表达强度分别是正常对照组3.01(P<0.01)、5.88(P<0.01)和3.45倍(P<0.01);JNK特异性抑制剂SP600125抑制了CCK-8和(或)LPS诱导的HO-1 mRNA表达;Western blotting、免疫荧光FCM检测结果显示,肺组织HO-1蛋白表达变化与其mRNA表达一致.结论: JNK/c-Jun通路在CCK-8上调LPS诱导肺组织HO-1表达过程中发挥重要作用.
目的:旨在研究八肽膽囊收縮素(CCK-8)上調脂多糖(LPS)誘導的大鼠肺組織中血紅素氧閤酶(HO)-1錶達的信號轉導機製.方法: 將42隻雄性SD大鼠隨機分為7組(每組6隻),即對照組、LPS組、LPS+SP600125(JNK特異性抑製劑)組、CCK-8+LPS組、CCK-8+LPS+SP600125組、CCK-8組、CCK-8+SP600125組.註藥後6 h放血處死動物留取肺組織,應用RT-PCR、Western blotting和免疫熒光流式細胞術(FCM)等技術分彆檢測各組肺組織HO-1 mRNA和蛋白錶達.結果: 與正常對照組相比,LPS組可見肺組織中齣現明顯的HO-1 mRNA錶達的暘性信號,CCK-8可使LPS誘導的暘性錶達信號進一步增彊,CCK單獨作用也可上調HO-1錶達.信號密度掃描結果顯示,LPS組、CCK-8+LPS組和CCK-8組HO-1 mRNA錶達彊度分彆是正常對照組3.01(P<0.01)、5.88(P<0.01)和3.45倍(P<0.01);JNK特異性抑製劑SP600125抑製瞭CCK-8和(或)LPS誘導的HO-1 mRNA錶達;Western blotting、免疫熒光FCM檢測結果顯示,肺組織HO-1蛋白錶達變化與其mRNA錶達一緻.結論: JNK/c-Jun通路在CCK-8上調LPS誘導肺組織HO-1錶達過程中髮揮重要作用.
목적:지재연구팔태담낭수축소(CCK-8)상조지다당(LPS)유도적대서폐조직중혈홍소양합매(HO)-1표체적신호전도궤제.방법: 장42지웅성SD대서수궤분위7조(매조6지),즉대조조、LPS조、LPS+SP600125(JNK특이성억제제)조、CCK-8+LPS조、CCK-8+LPS+SP600125조、CCK-8조、CCK-8+SP600125조.주약후6 h방혈처사동물류취폐조직,응용RT-PCR、Western blotting화면역형광류식세포술(FCM)등기술분별검측각조폐조직HO-1 mRNA화단백표체.결과: 여정상대조조상비,LPS조가견폐조직중출현명현적HO-1 mRNA표체적양성신호,CCK-8가사LPS유도적양성표체신호진일보증강,CCK단독작용야가상조HO-1표체.신호밀도소묘결과현시,LPS조、CCK-8+LPS조화CCK-8조HO-1 mRNA표체강도분별시정상대조조3.01(P<0.01)、5.88(P<0.01)화3.45배(P<0.01);JNK특이성억제제SP600125억제료CCK-8화(혹)LPS유도적HO-1 mRNA표체;Western blotting、면역형광FCM검측결과현시,폐조직HO-1단백표체변화여기mRNA표체일치.결론: JNK/c-Jun통로재CCK-8상조LPS유도폐조직HO-1표체과정중발휘중요작용.
AIM: To study the signal pathway involved in up-regulation of LPS-induced HO-1 expression by CCK-8. METHODS: Forty-two SD rats were divided into 7 groups (six rats each) randomly as follows: control group, LPS group, LPS+SP600125 (JNK-specific inhibitor) group, CCK-8+LPS group, CCK-8+LPS+SP600125 group, CCK-8 group and CCK-8 +SP600125 group. Lungs from the rats in these 7 groups were excised 6 h after the agents were administered. HO-1 mRNA expression was examined by RT-PCR. The protein expression of HO-1 was detected by Western blotting and immunofluorescence flow cytometry (FCM). RESULTS: There were significant positive expression of HO-1 mRNA in LPS group compared to control group. CCK-8 enhanced LPS-induced HO-1 mRNA expression and CCK-8 alone induced HO-1 mRNA expression as well. The mRNA expressions of HO-1 in LPS group, CCK-8+LPS group and CCK-8 group were 3.01 (P<0.01), 5.88 (P<0.01) and 3.45 (P<0.01) times as many as that in control group, respectively. SP600125 inhibited the mRNA expression of HO-1 induced by CCK-8 and (or) LPS. The change of HO-1 protein expression was in accordance with that of HO-1 mRNA expression by Western blotting and immunofluorescence FCM. CONCLUSION: These results suggest that JNK/c-Jun signal pathway plays an important role in the up-regulation of LPS-induced HO-1 expression by CCK-8.