国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2010年
6期
333-336
,共4页
谢衬梨%肖正伦%黎毅敏%莫红缨
謝襯梨%肖正倫%黎毅敏%莫紅纓
사츤리%초정륜%려의민%막홍영
急性肺损伤%生长素释放肽%核因子κB%纤溶酶原激活物抑制因子-1%组织型纤溶酶原激活物
急性肺損傷%生長素釋放肽%覈因子κB%纖溶酶原激活物抑製因子-1%組織型纖溶酶原激活物
급성폐손상%생장소석방태%핵인자κB%섬용매원격활물억제인자-1%조직형섬용매원격활물
Acute lung injury%Ghrelin%Nuclear factor-κB%Plasminogen activator inhibitor-1%Tissue-type plasminogen activator
目的 探讨生长素释放肽(Ghrelin)对盲肠结扎穿孔(CLP)介导的急性肺损伤小鼠早期核因子κB(NF-κB)和纤溶系统的影响.方法 将32只昆明小鼠随机分为正常组、假手术组、CLP组和Ghrelin干预组,Ghrelin干预组在CLP后5 h、10 h、15 h时间段分次腹腔注射Ghrelin(共40 nmol/kg).采用HE染色进行病理检测,免疫组织化学方法检测NF-κB表达,采用酶联免疫吸附试验方法检测血浆纤溶酶原激活物抑制因子-1(PAI-1)、组织型纤溶酶原激活物(t-PA)水平,计算t-PA/PAI-1比值.结果 ①病理结果显示:与正常组、假手术组相比,CLP组部分肺泡结构受到破坏,大量炎症细胞浸润,间质水肿明显,部分有出血,Ghrelin干预组肺组织病理损伤程度明显减轻.②免疫组织化学结果显示:与正常组、假手术组相比,CLP组肺组织NF-κB表达显著增强.Ghrelin干预组的NF-κB表达强度比CLP组弱.③与正常组、假手术组相比,CLP组PAI-1、t-PA水平明显升高(P<0.01),t-PA/PAI-1比值明显下降(P<0.01).Ghrelin干预组的血浆PAI-1水平较CLP组明显下降(P<0.01),血浆t-PA水平较CLP组轻度升高(P<0.05),t-PA/PAI-1比值较CLP组明显升高(P<0.01).结论 急性肺损伤小鼠早期纤溶系统功能抑制,Ghrelin可以降低CLP所致肺组织NF-κB的表达,Ghrelin可能通过NF-κB途径减轻CLP介导的急性肺损伤,提高纤溶活性.
目的 探討生長素釋放肽(Ghrelin)對盲腸結扎穿孔(CLP)介導的急性肺損傷小鼠早期覈因子κB(NF-κB)和纖溶繫統的影響.方法 將32隻昆明小鼠隨機分為正常組、假手術組、CLP組和Ghrelin榦預組,Ghrelin榦預組在CLP後5 h、10 h、15 h時間段分次腹腔註射Ghrelin(共40 nmol/kg).採用HE染色進行病理檢測,免疫組織化學方法檢測NF-κB錶達,採用酶聯免疫吸附試驗方法檢測血漿纖溶酶原激活物抑製因子-1(PAI-1)、組織型纖溶酶原激活物(t-PA)水平,計算t-PA/PAI-1比值.結果 ①病理結果顯示:與正常組、假手術組相比,CLP組部分肺泡結構受到破壞,大量炎癥細胞浸潤,間質水腫明顯,部分有齣血,Ghrelin榦預組肺組織病理損傷程度明顯減輕.②免疫組織化學結果顯示:與正常組、假手術組相比,CLP組肺組織NF-κB錶達顯著增彊.Ghrelin榦預組的NF-κB錶達彊度比CLP組弱.③與正常組、假手術組相比,CLP組PAI-1、t-PA水平明顯升高(P<0.01),t-PA/PAI-1比值明顯下降(P<0.01).Ghrelin榦預組的血漿PAI-1水平較CLP組明顯下降(P<0.01),血漿t-PA水平較CLP組輕度升高(P<0.05),t-PA/PAI-1比值較CLP組明顯升高(P<0.01).結論 急性肺損傷小鼠早期纖溶繫統功能抑製,Ghrelin可以降低CLP所緻肺組織NF-κB的錶達,Ghrelin可能通過NF-κB途徑減輕CLP介導的急性肺損傷,提高纖溶活性.
목적 탐토생장소석방태(Ghrelin)대맹장결찰천공(CLP)개도적급성폐손상소서조기핵인자κB(NF-κB)화섬용계통적영향.방법 장32지곤명소서수궤분위정상조、가수술조、CLP조화Ghrelin간예조,Ghrelin간예조재CLP후5 h、10 h、15 h시간단분차복강주사Ghrelin(공40 nmol/kg).채용HE염색진행병리검측,면역조직화학방법검측NF-κB표체,채용매련면역흡부시험방법검측혈장섬용매원격활물억제인자-1(PAI-1)、조직형섬용매원격활물(t-PA)수평,계산t-PA/PAI-1비치.결과 ①병리결과현시:여정상조、가수술조상비,CLP조부분폐포결구수도파배,대량염증세포침윤,간질수종명현,부분유출혈,Ghrelin간예조폐조직병리손상정도명현감경.②면역조직화학결과현시:여정상조、가수술조상비,CLP조폐조직NF-κB표체현저증강.Ghrelin간예조적NF-κB표체강도비CLP조약.③여정상조、가수술조상비,CLP조PAI-1、t-PA수평명현승고(P<0.01),t-PA/PAI-1비치명현하강(P<0.01).Ghrelin간예조적혈장PAI-1수평교CLP조명현하강(P<0.01),혈장t-PA수평교CLP조경도승고(P<0.05),t-PA/PAI-1비치교CLP조명현승고(P<0.01).결론 급성폐손상소서조기섬용계통공능억제,Ghrelin가이강저CLP소치폐조직NF-κB적표체,Ghrelin가능통과NF-κB도경감경CLP개도적급성폐손상,제고섬용활성.
Objective To investigate the effect of ghrelin on nuclear factor-κB (NF-κB) and fibrinolytic system in acute lung injury mice induced by cecal ligation and perforation (CLP) at early stage. Methods Thirty-two Kunming mice were randomly divided into normal group, sham-operated group,CLP group and ghrelin intervention group. Ghrelin intervention group received intraperitoneal injection with ghrelin at 5 h,10 h, 15 h time points after CLP (total 40 nmol/kg). HE staining was used
for pathological detection. The expression of NF-κB was detected by immunohistochemistry. Plasma plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA) were detected by enzyme linked immunosorbent assay,and the ratio of t-PA/PAI-1 was computed. Results ①Pathology results showed that compared with normal group and sham-operated group, part of alveolar cell structure was damaged,a great deal of inflammatory cell infiltrated, pulmonary interstitial edema was obvious, part had haemorrhage in CLP group. The pathologic'damage of pulmonary tissue reduced significantly in ghrelin intervention group. ②Immunohistochemistry results showed that compared with normal group and sham-operated group, NF-κB expression of pulmonary tissue markedly increased in CLP group. The expression of NF-κB in ghrelin intervention group was weaker than that in CLP group. ③Compared with normal group and sham-operated group, plasma PAI-1 and t-PA level increased significantly (P<0.01), t-PA/PAI-1 obviously decreased (P<0.01) in CLP group. Compared with CLP group, plasma PAI-1 significantly decreased (P<0.001), plasma t-PA slightly increased (P<0.05), and t-PA/PAI-1 significantly increased(P<0.01) in CLP group. Conclusions The fibrinolytic system is inhibited at the early stage of acute lung injury in mice. Ghrelin can reduce the expression of NF-κB in pulmonary tissue caused by CLP. Ghrelin may relieve acute lung injury induced by CLP and enhance fibrinolytic activity via NF-κB pathway.
