我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

NLRP3炎症小体在大鼠严重烫伤早期心肌内的表达及意义

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第5期
页码:
508-511,522
栏目:
基础研究
出版日期:
2016-04-25

文章信息/Info

Title:
Severe burn induces NLRP3 inflammasome activation in rat myocardium
作者:
赵 欢1; 2; 4; 傅 豪1; 解营利1; 杨 涛1; 张 明1; 张海燕3; 徐 晖1
（第四军医大学:1.神经生物学教研室，陕西 西安710032，2.唐都医院疼痛生物医学研究所，陕西 西安710038；
3.菏泽医学专科学校科教科，4.菏泽市立医院麻醉科，山东 菏泽 274000）
Author(s):
ZHAO Huan1; 2; 4;  FU Hao1;  XIE Ying-li1;  YANG Tao1;  ZHANG Ming1;  ZHANG Hai-yan3;  XU Hui1
(1.Department of Neurobiology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China, 2.Institute for Biomedical Sciences of Pain and Institute for Functional Brain Disorders, Tangdu Hospital, Fourth Military Medical University, Xi’an 710038, Shaanxi, China；
3.Department of Science and Education, He’ze Medical College, 4.Department of Anesthesia, He’ze Municipal Hospital, He’ze 274000, Shandong, China)
关键词:
烫伤; 心肌; 炎症小体; NLRP3; 白细胞介素-1β
Keywords:
burn;  heart;  inflammasome;  NLRP3;  IL-1β
分类号:
R722.14
DOI:
-
文献标识码:
A
摘要:
目的 探讨严重烫伤大鼠早期心肌组织内NLRP3炎症小体信号通路的表达及意义。方法 采用大鼠95℃热水浴18 s，制成40%总体表面积Ⅲ度烫伤模型，将24只健康雄性SD大鼠按随机数表法分为对照组、烫伤组、干预组。烫伤组大鼠立即腹腔注射10 ml生理盐水补液；干预组大鼠注射10 ml生理盐水+(BAY11-7082) 10 μl(0.2 mg/ml,10 mg/kg)；对照组动物背部置于25℃温水浴18 s模拟烫伤过程。伤后8 h分别取各组大鼠心肌组织及血清，采用蛋白免疫印迹法和实时荧光定量RT-PCR法检测心肌组织中NLRP3、半胱氨酸天冬氨酸蛋白酶（caspase）-1蛋白表达水平和NLRP3、caspase-1、IL-1β、TNF-α mRNA表达水平，同时观察HE染色组织大体形态，酶联免疫吸附试验法检测血清肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）含量。结果 ①烫伤组大鼠心肌组织内NLRP3、caspase-1蛋白表达量显著高于对照组（P<0.01）；与烫伤组比较，干预组大鼠心肌组织内NLRP3、caspase-1明显降低（P<0.01）；②烫伤组大鼠心肌组织中NLRP3、caspase-1、IL-1β和TNF-α的mRNA表达量分别为3.15±0.46，2.47±0.24，3.26±0.22和2.17±0.32，显著高于对照组的1.00±0.09，1.00±0.06，1.00±0.08和1.00±0.07（均P<0.01）；干预组大鼠心肌组织中NLRP3、caspase-1、IL-1β和TNF-α的mRNA表达量分别为1.68±0.37，1.55±0.17，1.21±0.15和1.38±0.23，显著低于烫伤组（均P<0.01）；③对照组大鼠心肌组织呈不规则圆柱形、排列整齐、横纹清晰，结构完整。烫伤组大鼠部分心肌纤维排列紊乱，细胞和间质可见水肿，见点片状溶解灶及炎性细胞浸润。BAY11-7082干预组部分心肌纤维排列紊乱，心肌细胞和间质水肿、心肌纤维溶解及炎细胞浸润程度均较烫伤组减轻；④烫伤组大鼠血清CK-MB、LDH含量分别为(2753±825)U/L，(2618±238)U/L，显著高于对照组的(247±76)U/L，(721±59)U/L（均P<0.01）；干预组大鼠血清CK-MB、LDH含量分别为(1267±248)U/L，(1982±183)U/L，显著低于单纯烫伤组（均P<0.01）。结论 NLRP3炎症小体在严重烫伤大鼠早期心肌组织内活性增高，使用BAY11-7082干预后，可抑制NLRP3炎症小体的活化，减轻心肌组织损伤，降低心肌炎症反应。
Abstract:
AIM To study the expression and effect of NLRP3 inflammasome in severely burned rat myocardium. METHODSTwenty-four rats were randomly divided into three groups: sham group, burn group and BAY11-7082 treatment group. Animals were subjected to full-thickness burn injury of a 40% total body surface area via exposure to water maintained at 95°C for 18 sec. Rats in burn group received an intraperitoneal injection of 10 ml normal saline for resuscitation and rats in treatment group received 10 ml normal saline and 10 μl BAY11-7082 (0.2 mg/ml, 10 mg/kg). Rats in the sham group were immersed in room temperature water for 18 sec. Rats were sacrificed 8 h after burn and myocardial tissues and serums were sampled. Protein expressions of NLRP3 and caspase-1 were examined by Western blot and mRNA levels of NLRP3, caspase-1, IL-1β and TNF-α were tested by RT-PCR. Histomorphological images were also observed by H&E staining and levels of CK-MB and LDH were detected by ELISA. RESULTSProtein expressions of myocardial NLRP3 and caspase-1 in the burn group were significantly higher than in the sham group (P<0.01). When treated with BAY11-7082, expressions of NLRP3 and caspase-1 were significantly decreased (P<0.01). mRNA values of myocardial NLRP3, caspase-1, IL-1β and TNF-α in the burn group were 3.15±0.46, 2.47±0.24, 3.26±0.22 and 2.17±0.32, respectively, much higher than 1.00±0.09, 1.00±0.06, 1.00±0.08 and 1.00±0.07 in the sham group (P<0.01). When treated with BAY11-7082, mRNA values changed to 1.68±0.37, 1.55±0.17, 1.21±0.15 and 1.38±0.23, respectively, significantly lower compared with those in the burn group (P<0.01). In the sham group, myocardial fibers were in a well-arranged irregular stripe shape and the transverse striation was distinct. In the burn group, part of the myocardial fibers were arranged in a disordered manner with edema of the myocardial interstitium. Part of the myocardial fibers dissolved and inflammatory cells were infiltrated. In the treatment group, myocardial fibers were disordered and myocardial interstitial edema and inflammatory cell infiltration were alleviated. The values of CK-MB and LDH in serum of in burned rats were (2753±825) U/L and (2618±238) U/L, respectively, much higher than (247±76) U/L and (721±59) U/L in the sham rats (P<0.01). When treated with BAY11-7082, the values changed to (1267±248) U/L and 1982±183 U/L, respectively, significantly lower compared to those in the burn group (P<0.01). CONCLUSIONNLRP3 inflammasome is activated in severely burned rat myocardium. When treated with BAY11-7082, the activity of NLRP3 is inhibited, with myocardial injury alleviated and myocardial inflammatory response relieved.

参考文献/References

[1]黄跃生,杨宗城,迟路湘,等.烧伤后“休克心”的研究[J].中华烧伤杂志,2000,16(5):19-22.
[2]杨宗诚.烧伤早期脏器损害发病机制的探讨[J].解放军医学杂志,1998,23(2):84-87.
[3]黄跃生,李志清,吴庆云,等.缺血缺氧在大鼠烧伤后“休克心”中的作用及其机制探讨［J］. 中华创伤杂志, 2002, 18(4):204-209.
[4] De Nardo D, De Nardo C M, Latz E. New insights into mechanisms controlling the NLRP3 inflammasome and its role in lung disease[J].Am J Pathol,2014,184(1):42-54.
[5] Liu Y,Lian K,Zhang L,et al.TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury[J].Basic Res Cardiol,2014,109(5):415.
[6]Strowig T,Henao-Mejia J,Elinav E,et al.Inflammasomes in health and disease[J].Nature,2012,481(7381):278-286.
[7]Tao K,Bai X,Jia W,et al.Effects of resveratrol on the treatment of inflammatory response induced by severe burn[J].Inflammation,2015,38(3):1273-1280.
[8]Sahoo M,Ceballos-Olvera I,Del Barrio L,et al.Role of the inflammasome,IL-1beta,and IL-18 in bacterial infections[J].Scientific World Journal,2011,11:2037-2050.
[9]Ipaktchi K,Mattar A,Niederbichler AD,et al.Attenuating burn wound inflammatory signaling reduces systemic inflammation and acute lung injury[J].J Immunol,2006,177(11):8065-8071.

备注/Memo

备注/Memo:
收稿日期：2015-11-02.
基金项目：国家自然科学基金项目资助（31371120）
通讯作者：徐晖，教授，主要从事慢性痛研究 Email: xubz@fmmu.edu.cn
作者简介：赵欢，硕士生 Email:zhaohuanjiyi1@163.com
更新日期/Last Update: 2016-04-13