| 刘海燕,于晶晶,师志云,张 华,徐清斌.基于PI3K-AKT-mTOR信号通路探讨参附注射液对心力衰竭大鼠的作用及其机制[J].,2023,(22):4218-4222 |
| 基于PI3K-AKT-mTOR信号通路探讨参附注射液对心力衰竭大鼠的作用及其机制 |
| Exploring the Effect and Mechanism of Shenfu Injection on Heart Failure Rats Based on the PI3K-AKT-mTOR Signaling Pathway |
| 投稿时间：2023-06-06 修订日期：2023-06-28 |
| DOI：10.13241/j.cnki.pmb.2023.22.004 |
| 中文关键词: 心力衰竭 参附注射液 P13KAktmTOR信号通路 作用机制 |
| 英文关键词: Heart failure Shenfu Injection P13KAktmTOR signaling pathway Mechanism of action |
| 基金项目:宁夏回族自治区自然科学基金项目（2019AAC03216） |
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| 中文摘要: |
| 摘要 目的：基于PI3K-AKT-mTOR信号通路探讨参附注射液对心力衰竭大鼠的作用及其机制。方法：60只SD大鼠随机分为正常对照组（n=20）、心力衰竭模型组（n=20）、参附注射液治疗组（n=20），正常对照组不做任何处理，其余两组采取腹主动脉缩窄法构建心力衰竭模型，给予心力衰竭模型组氯化钠溶液，参附注射液治疗组给予参附注射液。比较各组大鼠心脏功能、氧化应激、炎症因子、P13K-Akt-mTOR表达。结果：与正常对照组相比，参附注射液治疗组、心力衰竭模型组左心室舒张末期内径（LVEDD）、左心室收缩末期内径（LVESD）水平依次升高，而左心室射血分数（LVEF）水平依次下降（P<0.05）。与正常对照组相比，参附注射液治疗组、心力衰竭模型组血清丙二醛（MDA）水平依次升高，血清超氧化物歧化酶（SOD）水平依次下降（P<0.05）。与正常对照组相比，参附注射液治疗组、心力衰竭模型组血清白介素6（IL-6）、白介素1β（IL-1β）、肿瘤坏死因子-α（TNF-α）水平依次升高（P<0.05）。与正常对照组相比，参附注射液治疗组、心力衰竭模型组P13K-Akt-mTOR表达依次下降（P<0.05）。结论：参附注射液能够保护心力衰竭大鼠心脏功能，并可减轻氧化应激反应、抑制炎症因子表达，其作用机制可能与激活P13K-Akt-mTOR信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the effect and mechanism of Shenfu Injection on heart failure rats based on the PI3K-AKT-mTOR signaling pathway. Methods: Sixty SD rats were randomly divided into a normal control group (n=20), a heart failure model group (n=20), and a Shenfu injection treatment group (n=20). The normal control group did not receive any treatment, while the other two groups were treated with abdominal aortic constriction to construct a heart failure model. The heart failure model group was given sodium chloride solution, and the Shenfu injection treatment group was given Shenfu injection. Compare the cardiac function, oxidative stress, inflammatory factors, and P13K Akt mTOR expression of rats in each group. Results: Compared to the normal control group, the levels of left ventricular end diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) in the Shenfu injection treatment group and heart failure model group increased sequentially, while the levels of left ventricular ejection fraction (LVEF) decreased sequentially (P<0.05). Compared to the normal control group, the level of serum malondialdehyde (MDA) in the Shenfu injection treatment group and the heart failure model group increased in turn, and the level of serum superoxide dismutase (SOD) decreased in turn(P<0.05). Compared to the normal control group, the Shenfu Injection treatment group and the heart failure model group had serum interleukin-6 (IL-6) and interleukin-1 levels β (IL-1 β), Tumor Necrosis Factor-α (TNF-α) The levels increased sequentially (P<0.05). Compared to the normal control group, the expression of P13K-Akt-mTOR in the Shenfu Injection treatment group and heart failure model group decreased sequentially (P<0.05). Conclusion: Shenfu Injection can protect the cardiac function of heart failure rats, alleviate oxidative stress response, and inhibit the expression of inflammatory factors. Its mechanism of action may be related to the activation of the P13K-Akt-mTOR signaling pathway. |
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