1.辽宁中医药大学附属医院,辽宁省沈阳市皇姑区北陵大街33号,110032
2.辽宁中医药大学
linda1795@sina.com
收稿:2022-03-27,
修回:2022-06-20,
纸质出版:2022-12-02
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肖福龙,宫丽鸿,吴启华等.祛痰化瘀中药复方对心房颤动模型大鼠心肌超微结构及氧化应激的影响[J].中医杂志,2022,63(23):2266-2271.
XIAO Fulong,GONG Lihong,WU Qihua,et al.Effect of Compound Qutan Huayu Formula (祛痰化瘀中药复方) on Myocardial Ultrastructure and Oxidative Stress in Atrial Fibrillation Model Rats[J].Journal of Traditional Chinese Medicine,2022,63(23):2266-2271.
肖福龙,宫丽鸿,吴启华等.祛痰化瘀中药复方对心房颤动模型大鼠心肌超微结构及氧化应激的影响[J].中医杂志,2022,63(23):2266-2271. DOI: 10.13288/j.11-2166/r.2022.23.012.
XIAO Fulong,GONG Lihong,WU Qihua,et al.Effect of Compound Qutan Huayu Formula (祛痰化瘀中药复方) on Myocardial Ultrastructure and Oxidative Stress in Atrial Fibrillation Model Rats[J].Journal of Traditional Chinese Medicine,2022,63(23):2266-2271. DOI: 10.13288/j.11-2166/r.2022.23.012.
目的
2
探讨祛痰化瘀中药复方治疗心房颤动(AF)的可能作用机制。
方法
2
60只雄性SD大鼠随机分为空白组,模型组,维拉帕米组及祛痰化瘀高、中、低剂量组,每组10只。除空白组外其余各组大鼠采用尾静脉注射乙酰胆碱(Ach,66 μg/ml)-氯化钙(CaCl
2
,10 mg/ml)混合液连续7天建立AF大鼠模型。从造模第2天起,祛痰化瘀高、中、低剂量组大鼠分别给予祛痰化瘀中药复方41.25、20.63、10.31 g/(kg·d)灌胃,维拉帕米组给予维拉帕米溶液25 mg/(kg·d)灌胃,空白组和模型组灌服8.93 ml/(kg·d)生理盐水,连续灌胃2周。最后一次灌胃后12 h记录各组大鼠肢体Ⅱ导联心电图,监测AF持续时间;透射电镜下观察各组大鼠心肌超微结构变化;ELISA法检测大鼠血清中晚期氧化蛋白产物(AOPP)、丙二醛(MDA)、活性氧(ROS)、超氧化物歧化酶(SOD)含量。
结果
2
空白组大鼠为正常心电图,心房肌细胞的肌小节完整清晰,线粒体结构正常。与空白组相比,模型组大鼠心电图显示为AF心律,血清中AOPP、MDA、ROS含量升高,SOD含量降低(
P
<0.05或
P<
0.01),心房肌细胞的肌小节断裂,“Z”带不连续,排列混乱,“I”带模糊不清,线粒体肿胀、增多。与模型组比较,各给药组大鼠AF持续时间明显缩短;祛痰化瘀高、中剂量组大鼠血清AOPP、ROS、MDA含量降低,SOD含量升高(
P
<0.05或
P
<0.01),维拉帕米组大鼠血清AOPP、ROS含量降低,SOD含量升高(
P
<0.05);祛痰化瘀高、中剂量组和维拉帕米组大鼠心房肌细胞的肌小节轻微断裂,排列相对整齐,线粒体稍有肿胀、增多,结构相对完整,而祛痰化瘀低剂量组大鼠心肌超微结果改善不明显。
结论
2
祛痰化瘀中药复方可以缩短心房颤动持续时间,改善心肌损伤,其机制可能与抑制氧化应激有关,且以高中剂量效果为佳。
Objective
2
To explore the mechanism of
Compound Qutan Huayu Formula
(祛痰化瘀中药复方, CQHF) in the treatment of atrial fibrillation (AF).
Methods
2
Sixty male SD rats were randomly divided into blank group, model group, verapamil group, and low-, medium- and high-dose CQHF groups, with 10 rats in each group. Except for the blank group, the rats were injected with acetylcholine (Ach, 66 μg/ml)-calcium chloride (CaCl
2
, 10 mg/ml) mixture through tail vein for 7 days to establish the AF rat model. From the second day of modeling, the rats in the high-, medium-, and low-dose CQHF groups were given 41.25, 20.63, and 10.31 g/(kg·d) of CQHF by gavage, respectively, while those in the verapamil group were given 25 mg/(kg·d) of verapamil solution by gavage, and those in the blank group and the model group were administered with 8.93 ml/(kg·d) of normal saline by gavage, all treated for two weeks. Twelve hours after the last intragastric administration, the electrocardiogram in lead Ⅱ of the limbs was recorded, and the duration of AF was monitored. The changes of myocardial ultrastructure of the rats in each group were observed under transmission electron microscope. Contents of advanced oxidation protein products (AOPP), malondialde-hyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) in serum were detected by ELISA.
Results
2
The rats in the blank group had a normal electrocardiogram, and the sarcomere of the atrial myocytes were intact and clear, with normal mitochondrial structure. Compared to those in the blank group, the ECG of the rats in the model group showed AF rhythm, while serum AOPP, MDA, ROS levels increased, and SOD level decreased (
P
<0.05 or
P
<0.01); moreover, the sarcomere of atrial myocytes was broken, with discontinuous “Z” band, disordered arrangement, blurred “I” band, and swollen and increased mitochondria. Compared to those in the model group, the AF duration of the rats in each treatment group was significantly reduced; serum AOPP, ROS, and MDA levels in the low-, medium- and high-dose
CQHF groups increased (
P
<0.05 or
P
< 0.01); serum AOPP and ROS levels in the verapamil group decreased, while the SOD level increased (
P
<0.05); the sarcomere of the atrial myocytes of the rats in the high- and medium-dose CQHF groups were slightly broken, with relatively neat arrangement, slightly swollen and increased mitochondria, and relatively complete structure, while the myocardial ultrasonography in the low-dose CQHF group was not significantly improved.
Conclusion
2
CQHF can shorten the AF duration and improve myocardial injury. The mechanism may be related to the inhibition of oxidative stress, and the effect is better in terms of the medium- and high-dose CQHF.
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