山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2015年
22期
1-4
,共4页
马瑞松%李元红%江洪%胡笑容%李雪飞
馬瑞鬆%李元紅%江洪%鬍笑容%李雪飛
마서송%리원홍%강홍%호소용%리설비
心肌%缺血再灌注损伤%白介素33%细胞自噬%炎症因子
心肌%缺血再灌註損傷%白介素33%細胞自噬%炎癥因子
심기%결혈재관주손상%백개소33%세포자서%염증인자
Myocardium%ischemia-reperfusion injury%interleukin 33%autophagy%inflammatory factor
目的：探讨IL-33对心肌缺血再灌注（ I／R）损伤心肌的保护作用及机制。方法将32只大鼠随机分为假手术组（n＝10）、模型组（n＝10）、IL-33组（n＝6）及IL-33特异性受体（ST2）抑制剂组（anti-ST2组，n＝6）。除假手术组外，其余各组采用结扎冠状动脉左前降支法建立I／R心肌损伤模型。假手术组仅麻醉、开胸、穿线，但不结扎。 IL-33制模前30 min尾静脉注射IL-3310μg，anti-ST2组注射anti-ST20．2 mL（1mg／mL）。再灌注4 h后取血清或心肌组织检测各组以下指标：①血清乳酸脱氢酶（ LDH）、肌酸激酶（ CK）水平：采用分光光度法检测；②心肌组织Th1型炎症因子（ TNF-α、INF-γ、IL-6）和Th2型炎症因子（ IL-4、IL-5、IL-13）水平：采用ELISA法检测；③心肌组织自噬蛋白LC3和beclin-1相对表达量：采用Westernblot法检测。结果①LDH、CK水平：模型组均明显高于假手术组，IL-33组均明显低于模型组，P均＜0．05；anti-ST2组较模型组无统计学差异。②心肌组织炎症因子表达：Th1型炎症因子模型组及IL-33组均明显高于假手术组，IL-33组明显低于模型组，P均＜0．05；anti-ST2组与模型组比较无统计学差异。 Th2型炎症因子模型组明显低于假手术组，IL-33组明显高于模型组，anti-ST2组与模型组比较无统计学差异；③心肌组织自噬蛋白LC3和beclin-1相对表达量：模型组明显高于、IL-33组明显低于假手术组；IL-33组明显低于模型组（ P均＜0．05）；anti-ST2组与模型组比较无统计学差异。 IL-33与anti-ST2组各观察指标均有统计学差异（P均＜0．05）。结论 IL-33可通过抑制细胞过度自噬，减弱Th1型炎症反应，促进Th2型炎症反应而减轻心肌I／R损伤。
目的：探討IL-33對心肌缺血再灌註（ I／R）損傷心肌的保護作用及機製。方法將32隻大鼠隨機分為假手術組（n＝10）、模型組（n＝10）、IL-33組（n＝6）及IL-33特異性受體（ST2）抑製劑組（anti-ST2組，n＝6）。除假手術組外，其餘各組採用結扎冠狀動脈左前降支法建立I／R心肌損傷模型。假手術組僅痳醉、開胸、穿線，但不結扎。 IL-33製模前30 min尾靜脈註射IL-3310μg，anti-ST2組註射anti-ST20．2 mL（1mg／mL）。再灌註4 h後取血清或心肌組織檢測各組以下指標：①血清乳痠脫氫酶（ LDH）、肌痠激酶（ CK）水平：採用分光光度法檢測；②心肌組織Th1型炎癥因子（ TNF-α、INF-γ、IL-6）和Th2型炎癥因子（ IL-4、IL-5、IL-13）水平：採用ELISA法檢測；③心肌組織自噬蛋白LC3和beclin-1相對錶達量：採用Westernblot法檢測。結果①LDH、CK水平：模型組均明顯高于假手術組，IL-33組均明顯低于模型組，P均＜0．05；anti-ST2組較模型組無統計學差異。②心肌組織炎癥因子錶達：Th1型炎癥因子模型組及IL-33組均明顯高于假手術組，IL-33組明顯低于模型組，P均＜0．05；anti-ST2組與模型組比較無統計學差異。 Th2型炎癥因子模型組明顯低于假手術組，IL-33組明顯高于模型組，anti-ST2組與模型組比較無統計學差異；③心肌組織自噬蛋白LC3和beclin-1相對錶達量：模型組明顯高于、IL-33組明顯低于假手術組；IL-33組明顯低于模型組（ P均＜0．05）；anti-ST2組與模型組比較無統計學差異。 IL-33與anti-ST2組各觀察指標均有統計學差異（P均＜0．05）。結論 IL-33可通過抑製細胞過度自噬，減弱Th1型炎癥反應，促進Th2型炎癥反應而減輕心肌I／R損傷。
목적：탐토IL-33대심기결혈재관주（ I／R）손상심기적보호작용급궤제。방법장32지대서수궤분위가수술조（n＝10）、모형조（n＝10）、IL-33조（n＝6）급IL-33특이성수체（ST2）억제제조（anti-ST2조，n＝6）。제가수술조외，기여각조채용결찰관상동맥좌전강지법건립I／R심기손상모형。가수술조부마취、개흉、천선，단불결찰。 IL-33제모전30 min미정맥주사IL-3310μg，anti-ST2조주사anti-ST20．2 mL（1mg／mL）。재관주4 h후취혈청혹심기조직검측각조이하지표：①혈청유산탈경매（ LDH）、기산격매（ CK）수평：채용분광광도법검측；②심기조직Th1형염증인자（ TNF-α、INF-γ、IL-6）화Th2형염증인자（ IL-4、IL-5、IL-13）수평：채용ELISA법검측；③심기조직자서단백LC3화beclin-1상대표체량：채용Westernblot법검측。결과①LDH、CK수평：모형조균명현고우가수술조，IL-33조균명현저우모형조，P균＜0．05；anti-ST2조교모형조무통계학차이。②심기조직염증인자표체：Th1형염증인자모형조급IL-33조균명현고우가수술조，IL-33조명현저우모형조，P균＜0．05；anti-ST2조여모형조비교무통계학차이。 Th2형염증인자모형조명현저우가수술조，IL-33조명현고우모형조，anti-ST2조여모형조비교무통계학차이；③심기조직자서단백LC3화beclin-1상대표체량：모형조명현고우、IL-33조명현저우가수술조；IL-33조명현저우모형조（ P균＜0．05）；anti-ST2조여모형조비교무통계학차이。 IL-33여anti-ST2조각관찰지표균유통계학차이（P균＜0．05）。결론 IL-33가통과억제세포과도자서，감약Th1형염증반응，촉진Th2형염증반응이감경심기I／R손상。
Objective To investigate the protective effect of interleukin 33 (IL-33) on myocardial ischemia-reperfu-sion ( I/R) injury and the mechanism.Methods Thirty-two rats were randomly divided into 4 groups:the control group (n=10), I/R group (model group, n=10), IL-33 group (n=6) and anti-ST2 group (n=6).In addition to the control group, the left anterior descending coronary artery ligation method was adopted to establish the myocardial I/R injury model in the other groups ( the sham operation group only received anesthesia, open-chest and threading, but not ligation) .Rats in the IL-33+I/R group and anti-ST2+I/R group were separately injected to the caudal vein with 10μg IL-33 and 0.2 mL anti-ST2 (1 mg/mL) 30 min before modeling.After reperfusion for 4 h, we obtained the serum or myocardial tissues to de-tect the following indicators of each group:(1) the serum lactate dehydrogenase (LDH) and creatine kinase (CK) level:using spectrophotometry, (2) Th1 inflammation factors in the myocardial tissues (TNF-α, INF-γand IL-6) and Th2 in-flammatory cytokines (IL-4, IL-5 and IL-3):using the ELISA, (3) the relative expression of autophagy protein LC3 and beclin 1 in the myocardial tissues:using Western blotting.Results (1) LDH and CK level:the model group was signifi-cantly higher than the control group, IL-33 group was significantly lower than the model group (P<0.05), and no statisti-cal difference was found between the anti-ST2 group and the model group.(2) the inflammation factor expression in the myocardial tissues:Th1 type inflammation factor expression: the model group and IL-33 group were significantly higher than the control group, IL-33 was significantly lower than the model group (all P<0.05), and no difference was found be-tween the anti-ST2 group and the model group.Th2 type inflammation factor expression:the model group was significantly lower than the control group, IL-33 group was significantly higher than the model group, and no statistical difference was found between the anti-ST2 group and the model group.(3) The relative expression of autophagy protein LC3 and beclin-1 in the myocardial tissues:the model group was significantly higher, IL-33 group was significantly lower than the control group, IL-33 was significantly lower than the model group ( all P<0.05) , no significant difference was found between the anti-ST2 group and the model group.Statistically significant differences were found in all indexes between the IL-33 and an-ti-ST2 group.Conclusion IL-33 may attenuate myocardial I/R injury by inhibiting the excessive autophagy, weakening Th1 inflammatory response and enhancing Th2 inflammatory response.
