黄表华 刘燕 黄兰松 黄照河

【摘要】 目的 通過检测心肌缺血再灌注损伤大鼠血清肿瘤坏死因子α（TNFα）、白介素6（IL6）含量以及显微镜观察心肌细胞病理学结构，探讨龙血竭总黄酮对大鼠心肌缺血再灌注损伤的影响。

方法 将40只SD大鼠随机分为4组：空白对照组（control组）、假手术组（sham组）、缺血再灌注组（I/R组）、缺血再灌注+龙血竭总黄酮干预组（SDFI/R组），每组10只。I/R组及SDFI/R组进行心肌缺血再灌注损伤造模。所有大鼠均在相应处理后通过腹主动脉采血留取血清标本，通过ELISA法测定TNFα和IL6含量;留取结扎梗死相应部位心肌组织进行HE染色，显微镜下观察其病理变化，并行qPCR检测心肌组织TNFα和IL6的mRNA含量。

结果 大鼠心肌组织病理HE染色示：I/R组的心肌肌纤维有大范围断裂，结构最为紊乱，炎症、水肿最明显;SDFI/R组心肌细胞排列较规整，断裂较少，组织间隙水肿较轻;control组及sham组差异不大，心肌组织无明显变性，心肌纤维排列基本规整，组织间隙水肿最轻，损伤最小。不同组间的TNFα、IL6水平比较差异均有统计学意义（P<0.01）;sham组、I/R组及SDFI/R组的TNFα、IL6水平均高于control组（P<0.05），SDFI/R组TNFα、IL6水平均低于I/R组（P<0.05）。不同组间的TNFα、IL6 mRNA 表达量比较差异均有统计学意义（P<0.001）;sham组、I/R组及SDFI/R组的TNFα、IL6 mRNA水平高于control组（P<0.05），SDFI/R组、I/R组的TNFα、IL6 mRNA水平高于sham组（P<0.05），SDFI/R组的TNFα、IL6 mRNA水平低于I/R组（P<0.05）。

结论 龙血竭总黄酮可减少心肌缺血再灌注损伤大鼠血清中的炎症因子TNFα和IL6的释放，从而保护心肌细胞组织。

【关键词】 心肌缺血再灌注损伤;龙血竭总黄酮;TNFα;IL6

中图分类号：R542. 文献标志码： DOI：10.3969/j.issn.10031383.2021.06.002

Effects of Sanguis Draconis flavones on serum inflammatory cytokines TNFα and IL6 in myocardial ischemiareperfusion injury rats

HUANG Biaohua1， 2， LIU Yan1， HUNAG Lansong1， 2， HUANG Zhaohe1▲

（1. Department of Cardiology of Affiliated Hospital， 2. Graduate School， Youjiang Medical University for Nationalities， Baise 533000， Guangxi， China）

【Abstract】 Objective To discuss the influence of Sanguis Draconis flavones （SDF） on myocardial ischemiareperfusion injury （MIRI） by detecting the content of serum tumor necrosis factorα （TNFα） and interleukin6 （IL6） in MIRI rats， and by observing pathological structure of cardiomyocytes of them under microscope.

Methods 40 SD rats were randomly divided into four groups： control group， sham group， ischemiareperfusion（I/R）group， and I/R + Sanguis Draconis flavones （SDFI/R） group， with 10 rats in each group. MIRI models were made in the I/R group and the SDFI/R group. Blood sample were collected from the abdominal aorta， and their serum TNFα and IL6 were detected by ELISA. Finally， the rats were sacrificed and their hearts were immediately taken out， the corresponding myocardial tissues were ligated for HE staining， the pathological changes were observed under microscope， and the mRNA content of TNFα and IL6 in myocardial tissues were detected by qPCR.

Results Pathological HE staining of the myocardial tissue of rats showed that myocardial muscle fibers in the I/R group had a wide range of breakage， the most disordered structure， and the most obvious inflammation and edema. In the SDFI/R group， the arrangement of myocardial cells was more regular， the rupture was less， and the interstitial edema was milder. There was no significant difference between the control group and the sham group， no obvious degeneration of the myocardial tissue was found， the arrangement of myocardial fibers was basically regular， the intertissue edema was the mildest， and the injury was the least. Difference of the TNFα and IL6 levels among groups was statistically significant （P < 0.01）， the TNFα and IL6 levels of the sham group， the I/R group， and the SDFI/R group were higher than those of the control group （P < 0.05）， and those in the SDFI/R group were lower than those in the I/R group （P <0.05）. There was statistically significant difference in TNFα and IL6 mRNA expression levels （P < 0.001）. The TNFα and IL6 mRNA levels of the sham group， the I/R group and the SDFI/R group were higher than those of the control group （P <0.05）， those of the SDFI/R group and the I/R group were higher than those of the sham group （P < 0.05）， and those of the SDFI/R group were lower than those of the I/R group （P <0.05）.

Conclusion SDF can reduce the release of inflammatory cytokines TNFα and IL6 in serum of rats with myocardial ischemiareperfusion injury， so as to protect myocardial tissue.

【Key words】 MIRI; SDF; TNFα; IL6

心肌缺血再灌注损伤（myocardial ischemiareperfusion injury，MIRI）是指缺血心肌在恢复血流再灌注后，反而加重其结构破坏，引起心肌细胞死亡，导致梗死范围扩大，造成心功能的进一步损害并影响急性心肌梗死（AMI）患者的预后[1]。MIRI是AMI再灌注治疗中最棘手的问题，严重影响AMI患者的预后，是当前国内外学者研究的热点。……