中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
9期
2234-2236
,共3页
腹主动脉瘤%p38丝裂原活化蛋白激酶%基质金属蛋白酶%肿瘤坏死因子-α
腹主動脈瘤%p38絲裂原活化蛋白激酶%基質金屬蛋白酶%腫瘤壞死因子-α
복주동맥류%p38사렬원활화단백격매%기질금속단백매%종류배사인자-α
Abdominal aortic aneurysm%p38 mitogen activated protein kinase%Matrix metalloproteinases%Tumor necrosis factor-α
目的 观察腹主动脉瘤(AAA)组织内磷酸化丝裂原激活蛋白激酶p38 (p38MAPK)活性表达,及其对AAA局部组织基质金属蛋白酶(MMPs)等表达的影响.方法 AAA标本取自20例AAA患者术中切除的动脉瘤组织,10例正常腹主动脉标本取自尸体供肾者之修剪供肾时所得剪下弃用的腹主动脉壁.Western blot法检测瘤壁组织磷酸化p38MAPK活性,酶联免疫吸附试验(ELlSA)法检测培养上清液中MMP-2、MMP-9、肿瘤坏死因子-α(TNF-α)含量,在体外培养条件下,观察p38MAPK特异性阻滞剂SB203580对AAA组织中MMP-2、MMP-9、TNF-α表达的影响.结果 磷酸化p38MAPK吸光度(A)值在AAA组织(3.92±0.32)明显高于正常主动脉壁组织(1.19±0.037);未经处理的AAA组织与经SB203580共培养处理过的AAA组织比较,培养上清液中TNF-α、MMP-9、MMP-2含量明显升高,浓度分别为(375.11±87.33)、(69.37±13.44) ng/L;(87.09±8.89)、(38.33 ±6.78) μg/L;(630.25±37.03)、(403.14±36.90) μg/L.结论 阻断p38MAPK转导通路,可减少AAA组织炎性反应及MMP-2、MMP-9的表达.
目的 觀察腹主動脈瘤(AAA)組織內燐痠化絲裂原激活蛋白激酶p38 (p38MAPK)活性錶達,及其對AAA跼部組織基質金屬蛋白酶(MMPs)等錶達的影響.方法 AAA標本取自20例AAA患者術中切除的動脈瘤組織,10例正常腹主動脈標本取自尸體供腎者之脩剪供腎時所得剪下棄用的腹主動脈壁.Western blot法檢測瘤壁組織燐痠化p38MAPK活性,酶聯免疫吸附試驗(ELlSA)法檢測培養上清液中MMP-2、MMP-9、腫瘤壞死因子-α(TNF-α)含量,在體外培養條件下,觀察p38MAPK特異性阻滯劑SB203580對AAA組織中MMP-2、MMP-9、TNF-α錶達的影響.結果 燐痠化p38MAPK吸光度(A)值在AAA組織(3.92±0.32)明顯高于正常主動脈壁組織(1.19±0.037);未經處理的AAA組織與經SB203580共培養處理過的AAA組織比較,培養上清液中TNF-α、MMP-9、MMP-2含量明顯升高,濃度分彆為(375.11±87.33)、(69.37±13.44) ng/L;(87.09±8.89)、(38.33 ±6.78) μg/L;(630.25±37.03)、(403.14±36.90) μg/L.結論 阻斷p38MAPK轉導通路,可減少AAA組織炎性反應及MMP-2、MMP-9的錶達.
목적 관찰복주동맥류(AAA)조직내린산화사렬원격활단백격매p38 (p38MAPK)활성표체,급기대AAA국부조직기질금속단백매(MMPs)등표체적영향.방법 AAA표본취자20례AAA환자술중절제적동맥류조직,10례정상복주동맥표본취자시체공신자지수전공신시소득전하기용적복주동맥벽.Western blot법검측류벽조직린산화p38MAPK활성,매련면역흡부시험(ELlSA)법검측배양상청액중MMP-2、MMP-9、종류배사인자-α(TNF-α)함량,재체외배양조건하,관찰p38MAPK특이성조체제SB203580대AAA조직중MMP-2、MMP-9、TNF-α표체적영향.결과 린산화p38MAPK흡광도(A)치재AAA조직(3.92±0.32)명현고우정상주동맥벽조직(1.19±0.037);미경처리적AAA조직여경SB203580공배양처리과적AAA조직비교,배양상청액중TNF-α、MMP-9、MMP-2함량명현승고,농도분별위(375.11±87.33)、(69.37±13.44) ng/L;(87.09±8.89)、(38.33 ±6.78) μg/L;(630.25±37.03)、(403.14±36.90) μg/L.결론 조단p38MAPK전도통로,가감소AAA조직염성반응급MMP-2、MMP-9적표체.
Objective To reaserch the relationship between the activity of p38 mitogen activated protein kinase (p38MAPK) and the expression of matrix metalloproteinases (MMPs) in tissue of abdominal aortic aneurysm (AAA).Methods AAA specimens were taken from AAA tissues of 20 patients with AAA in surgical procedure of resection of the aneurysm,and 10 cases of normal abdominal aorta specimens were taken from abdominal aortic wall cut by cadaveric donor kidney.Western blotting was used to detect the activity of phosphorylated p38MAPK in AAA wall,and enzyme linked immunosorbent assay (ELISA) to determine the contents of MMP-2,MMP-9 and tumor necrosis factor-α (TNF-α) in the culture supernatant.The efffect of SB203580 on the expression of MMP-2,MMP-9 and TNF-α in AAA group was observed.Results As compared with the normal abdominal aortic wall,the activity of p38MAPK was significantly increased in AAA group (3.92 ± 0.32 vs.1.19 ± 0.037);The levels of TNF-α,MMP-9 and MMP-2 in the supernatant were remarkablely increased in the untreated group [(375.11 ± 87.33) ng/L,(87.09 ± 8.89) μg/L,and (630.25 ± 37.03) μg/L] as compared with the group treated with SB203580 [(69.37 ± 13.44) ng/L,(38.33 ±6.78) μg/L,and (403.14 ±36.90) μg/L].Conclusion Blocking p38MAPK transduction pathway can reduce the inflammatory response and the expression of MMP-2 and MMP-9 in AAA groups.
