[1]张冬青,潘 飞,胡梦婷,等.炎性细胞因子在射频导管消融术治疗房颤大鼠中的表达及对心肌损伤的影响[J].陕西医学杂志,2024,(7):900-904,909.[doi:DOI:10.3969/j.issn.1000-7377.2024.07.007]
　ZHANG Dongqing,PAN Fei,HU Mengting,et al.Expression of inflammatory cytokines in rats with atrial fibrillation treated by radiofrequency catheter ablation and its effect on myocardial injury[J].,2024,(7):900-904,909.[doi:DOI:10.3969/j.issn.1000-7377.2024.07.007]
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炎性细胞因子在射频导管消融术治疗房颤大鼠中的表达及对心肌损伤的影响
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
期数:
2024年7期
页码:
900-904,909
栏目:
基础研究
出版日期:
2024-07-05

文章信息/Info

Title:
Expression of inflammatory cytokines in rats with atrial fibrillation treated by radiofrequency catheter ablation and its effect on myocardial injury
作者:
张冬青; 潘 飞; 胡梦婷; 干佳琦; 邵金炎
(复旦大学附属闵行医院全科医学科,上海 201199)
Author(s):
ZHANG Dongqing; PAN Fei; HU Mengting; GAN Jiaqi; SHAO Jinyan
(Department of General Medicine,Minhang Hospital,Fudan University,Shanghai 201199,China)
关键词:
白细胞介素-1β;  白细胞介素-6;  肿瘤坏死因子-α;  血清肌酸激酶同工酶;  一氧化氮;  一氧化氮合酶;  半胱氨酸天冬氨酸蛋白酶-3;  房颤;  心肌损伤
Keywords:
IL-1β;  IL-6;  TNF-α;  CK-MB;  NO;  iNOS;  Caspase-3;  Atrial fibrillation;  Myocardial injury
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2024.07.007
文献标志码:
A
摘要:
目的:本研究旨在探讨炎性细胞因子在射频导管消融术治疗房颤大鼠中的表达及对心肌损伤的影响。方法:选择60只6周龄SPF级雄性SD大鼠,体重为180～200 g,随机将其分为空白组、模型组及射频导管消融术组各20只。其中空白组正常饲养1周; 模型组及射频导管消融术组均建立房颤动物模型,空白组饲养1周后,经鼠尾注射50 μg/100 g生理盐水; 模型组造模成功后,将氯化钙(10 mg/ml)与乙酰胆碱(66 μg/ml)混合后经鼠尾静脉注射; 射频导管消融术组房颤造模方法与模型组相同,造模成功后3 d给予射频导管消融术,术后根据心肌肌钙蛋白T(CTnT)的水平超过0.08 ng/L则为心肌损伤组(7只),未超过则为未发生心肌损伤组(12只)。结果:模型组及射频导管消融术组造模后,40只大鼠中2只大鼠死亡,造模成功率为95.00%(38/40)。最终模型组19只大鼠、射频导管消融术组19只大鼠造模成功。空白组大鼠皮毛有光泽,饮食、水正常,呼吸均匀,活动灵敏; 模型组大鼠毛色无光泽,眼睛充血,饮食、水减少,呼吸、心率加快,动作迟缓,乏力,目光呆滞; 射频导管消融术组大鼠无明显食欲减退,心率、呼吸稍加快,眼睛充血,喜倦卧。模型组的房颤持续时间及房颤诱发时间均高于未发生心肌损伤组及心肌损伤组,心肌损伤组的房颤持续时间及房颤诱发时间均高于未发生心肌损伤组,差异具有统计学意义(均P<0.05)。空白组大鼠心肌细胞正常,排列整齐、致密,细胞形态正常; 模型组大鼠心肌细胞间质增多,间隙增大,排列紊乱,存在大量炎症浸润; 未发生心肌损伤组大鼠心肌组织间质稍增多,排列尚整齐,不存在明显的炎症细胞浸润; 心肌损伤组:大鼠心肌细胞间质明显增多,间隙稍增加,排列稍乱,存在炎症浸润。心肌损伤组的白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)均高于空白组、未发生心肌损伤组,模型组、未发生心肌损伤组的IL-1β、IL-6、TNF-α均高于空白组,模型组的IL-1β、IL-6、TNF-α均高于未发生心肌损伤组,差异具有统计学意义(均P<0.05)。心肌损伤组的血清肌酸激酶同工酶(CK-MB)、一氧化氮(NO)、一氧化氮合酶(iNOS)、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)水平均高于空白组、未发生心肌损伤组,模型组、未发生心肌损伤组的CK-MB、NO、iNOS、Caspase-3水平均高于空白组,模型组的CK-MB、NO、iNOS、Caspase-3水平均高于未发生心肌损伤组,差异具有统计学意义(均P<0.05)。结论:IL-1β、IL-6、TNF-α在房颤心肌损伤大鼠中呈高表达,其机制为上述炎性细胞因子能够调节心肌细胞功能及心肌细胞凋亡。
Abstract:
Objective:To investigate the expression of inflammatory cytokines in rats with atrial fibrillation treated by radiofrequency catheter ablation and its effect on myocardial injury.Methods:Sixty 6-week-old SPF male SD rats with a body weight of 180 to 200 g were purchased and randomly divided into blank group,model group and RF catheter ablation group with 20 rats each.The blank group was fed normally for 1 week.Atrial fibrillation animal models were established in both model group and RF catheter ablation group.After feeding the blank group for 1 week,50 μg/100 g 0.9% sodium chloride was injected through the rat tail.After successful modeling in the model group,calcium chloride(10 mg/ml)was mixed with acetylcholine(66 μg/ml)and injected through rat tail vein.RF catheter ablation group had the same method of atrial fibrillation modeling as the model group,and 3 days after successful modeling,radiofrequency catheter ablation was given.According to the level of cardiac troponin T(CTnT)after operation,the rats were divided into myocardial injury group(7 rats,more than 0.08 ng/L)and non-myocardial injury group(12 rats,less than 0.08 ng/L).Results:After modeling in the model group and the RF catheter ablation group,2 of 40 rats died,resulting in a success rate of 95.00%(38/40).Finally,19 rats in the model group and 19 rats in the RF catheter ablation group were successfully modeled.The rats in the blank group had glossy fur,normal diet and water,even breathing and sensitive activity.The rats in the model group had dull hair color,bloodshot eyes,reduced diet and water,accelerated respiration and heart rate,slow movement,fatigue and dull eyes.The rats in the radio frequency catheter ablation group had no obvious loss of appetite,slightly accelerated heart rate and breathing,bloodshot eyes,and sleepy.The duration and induction time of atrial fibrillation in the model group were higher than those in the non-myocardial injury group and the myocardial injury group,and the duration and induction time of atrial fibrillation in the myocardium injury group were higher than those in the non-myocardial injury group(all P<0.05).In the blank group,the myocardial cells were normal,neatly arranged and dense,and the cell morphology was normal.In the model group,the interstitium of myocardial cells increased,the space increased,the arrangement was disordered,and there was a lot of inflammatory infiltration.In the non-myocardial injury group,the interstitial tissue of myocardium increased slightly,the arrangement was orderly,and there was no obvious inflammatory cell infiltration.In the myocardial injury group,the interstitium of myocardium increased significantly,the space increased slightly,the arrangement was slightly disordered,and there was inflammatory infiltration.The levels of interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in myocardial injury group were higher than those in blank group and non-myocardial injury group,and the levels of IL-1β,IL-6 and TNF-α in model group and non-myocardial injury group were higher than those in blank group.The levels of IL-1β,IL-6 and TNF-α in the model group were higher than those in the non-myocardial injury group(all P<0.05).Serum creatine kinase isoenzyme(CK-MB),nitric oxide(NO),nitric oxide synthase(iNOS)and cysteine aspartic protease-3(Caspase-3)levels in myocardial injury group were higher than those in blank group and non-myocardial injury group.The levels of CK-MB,NO,iNOS and Caspase-3 in model group and non-myocardial injury group were higher than those in blank group,and the levels of CK-MB,NO,iNOS and Caspase-3 in model group were higher than those in non-myocardial injury group(all P<0.05).Conclusion:IL-1β,IL-6 and TNF-α are highly expressed in rats with atrial fibrillation myocardial injury,and the mechanism is that these inflammatory cytokines can regulate the function and apoptosis of cardiomyocytes.

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备注/Memo

备注/Memo:
基金项目:上海市闵行区卫生健康委员会临床研究类科研立项课题(2021MW67); 上海市中西医结合学会科研基金资助项目(2021-13); 上海市闵行区中心医院扶持学科-医联体慢病管理项目(YJXK-2021-15)
更新日期/Last Update: 2024-07-04