[1]施洋,候宝林,陈晓黎,等.基于氧化应激损伤探究参麦注射液对急性心肌梗死大鼠的干预作用[J].西部中医药,2024,37(10):6-9.[doi:10.12174/j.issn.2096-9600.2024.10.02]
　SHI Yang,HOU Baolin,CHEN Xiaoli,et al.Intervention Effects of Shenmai Injection on Rats with Acute Myocardial Infarction Based on Oxidative Stress Injury[J].Western Journal of Traditional Chinese Medicine,2024,37(10):6-9.[doi:10.12174/j.issn.2096-9600.2024.10.02]
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基于氧化应激损伤探究参麦注射液对急性心肌梗死大鼠的干预作用
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《西部中医药》[ISSN:2096-9600/CN:62-1204/R]

卷:
37
期数:
2024年10期
页码:
6-9
栏目:
基础研究
出版日期:
2024-10-15

文章信息/Info

Title:
Intervention Effects of Shenmai Injection on Rats with Acute Myocardial Infarction Based on Oxidative Stress Injury
作者:
施洋1, 候宝林2, 陈晓黎1, 吴胜利1
1.克拉玛依市中西医结合医院/市人民医院，新疆 克拉玛依 834000
2.克拉玛依市第二人民医院/康复医院，新疆 克拉玛依 834000
Author(s):
SHI Yang1, HOU Baolin2, CHEN Xiaoli1, WU Shengli1
1.Karamay City Hospital of Integrated Traditional Chinese and Western Medicine/City People's Hospital, Karamay 834000, China
2.Karamay City Second People's Hospital/Rehabilitation Hospital, Karamay 834000, China
关键词:
急性心肌梗死; 氧化应激损伤; 心脏保护; 参麦注射液
Keywords:
acute myocardial infarction; oxidative stress injury; cardiac protection; injection
分类号:
R285.5
DOI:
10.12174/j.issn.2096-9600.2024.10.02
文献标志码:
A
摘要:
目的探究参麦注射液（Shenmai injection，SMI）对急性心肌梗死（acute myocardial infarc-tion，AMI）模型大鼠心脏保护作用的机制。 方法将40只SPF级雄性SD大鼠随机分为假手术组、模型组、缬沙坦组和SMI组各10只，假手术组不造模，其余各组采用左冠状动脉前降支结扎法建立AMI模型，造模成功后，假手术组和模型组均予生理盐水0.38 mL/kg肌内注射，缬沙坦组予缬沙坦胶囊溶液10 mg/kg灌胃，SMI组予SMI 0.38 mL/kg肌内注射；连续干预14天后测定各组大鼠血清超氧化物歧化酶（superoxide dismutase，SOD）及丙二醛（malonaldehyde，MDA）水平；逆转录聚合酶链式反应检测心肌核因子E2相关因子2（nuclear factor erythroid 2 related factor 2，Nrf-2）、血红素氧合酶（heme oxygenase 1，HO-1）、过氧化氢酶（catalase，CAT）、超氧化物歧化酶（superoxide dismutase，SOD）mRNA水平；蛋白质印迹法测定心肌组织磷酸化蛋白激酶B（phosphorylated protein kinase B，p-Akt）、Akt和Nrf-2蛋白表达。 结果与假手术组比较，模型组大鼠血清SOD水平降低（P＜0.01），MDA水平升高（P＜0.05），Nrf-2、HO-1、CAT、SOD mRNA表达均降低，其中CAT、SOD mRNA表达差异有统计学意义（P＜0.01），p-Akt/Akt及Nrf-2蛋白表达降低，其中p-Akt/Akt蛋白表达差异有统计学意义（P＜0.05）；与模型组比较，缬沙坦组和SMI组血清SOD水平升高（P＜0.01），缬沙坦组CAT mRNA水平升高（P＜0.01），SMI组CAT、SOD mRNA水平均升高（P＜0.01），缬沙坦组和SMI组p-Akt/Akt及Nrf-2蛋白表达均升高（P＜0.05），SMI组与缬沙坦组以上各指标比较差异无统计学意义（P＞0.05）。 结论SMI对AMI模型大鼠心脏具有保护作用，其机制可能与SMI调节抗氧化酶，促进Akt磷酸化，调控Nrf-2表达，从而抑制AMI引起的氧化应激损伤有关。
Abstract:
ObjectiveTo investigate the mechanism of Shenmai injection (SMI) on cardiac protection in rats with acute myocardial infarction (AMI). MethodsAll 40 SPF grade male SD rats were randomly allocated to sham operation group, the model group and valsartan group and SMI group with ten rats in each, sham operation group remained unhandled, the other groups adopted ligation of the anterior descending branch of the left coronary artery to establish AMI models, after successfully modeling, sham operation group and the model group accepted muscular injection of physiological saline,0.38 mL/kg valsartan capsules solution, 10 mg/kg, was administered to the rats in valsartan group, and muscular injection of SMI, 0.38 mL/kg, was given to SMI group; to detect the levels of SOD and MDA in the rats of different groups after 14 days of intervention; reverse transcription-polymerase chain reaction (RT-PCR) was applied to detect the levels of Nrf-2, HO-1, CAT and SOD mRNA; Western blotting was used to measure the expressions of p-Akt, Akt and Nrf-2 protein in myocardium. ResultsCompared with sham operation group, the level of SOD was reduced in the model group (P<0.01), the level of MDA was hoisted (P<0.05), the expressions of Nrf-2, HO-1, CAT and SOD mRNA were lowered, while the difference had statistical meaning in the expressions of CAT and SOD mRNA (P<0.01), the expressions of p-Akt/Akt and Nrf-2 protein were reduced, while the difference had statistical meaning in the expressions of p-Akt/Akt protein (P<0.05). Compared with the model group, the levels of SOD were increased in valsartan group and SMI group (P<0.01), the levels of CAT mRNA were increased in valsartan group (P<0.01), the levels of CAT and SOD mRNA in SMI group went up (P<0.01), the expressions of p-Akt/Akt and Nrf-2 protein were elevated in valsartan group and SMI group (P<0.05); there was no significant difference between SMI group and valsartan group (P>0.05). ConclusionSMI could protect the heart of AMI rat models, and its mechanism may involve SMI regulating antioxidant enzymes, promoting Akt phosphorylation and and modulating Nrf-2 expressions, thereby inhibiting AMI-induced oxidative stress damage.

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备注/Memo

备注/Memo:
施洋（1990—），男，硕士学位，主管药师。研究方向：临床药学及心血管药理学。国家自然科学基金（81774050）；国家重点研发计划“重大慢性非传染性疾病防控研究”重点专项定向项目（2018YFC1311800）；克拉玛依市首届科技创新人才培养项目（克科发〔2023〕1号）。
更新日期/Last Update: 2024-10-15