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何娜祯, 贝雪怡, 陈光宇, 李亮, 瞿昊宇, 谢梦洲.益气活血方对冠心病气虚血瘀证大鼠PI3K/Akt/mTOR信号通路及自噬的影响[J].湖南中医药大学学报英文版,2025,45(11):2035-2043.[Click to copy
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| 益气活血方对冠心病气虚血瘀证大鼠PI3K/Akt/mTOR信号通路及自噬的影响 |
| 何娜祯,贝雪怡,陈光宇,李亮,瞿昊宇,谢梦洲 |
| (湖南中医药大学, 湖南 长沙 410208;湖南省药食同源功能性食品工程技术研究中心, 湖南 长沙 410208;湖南中医药大学中医心肺病证辨证与药膳食疗重点研究室, 湖南 长沙 410208;湖南中医药大学中医诊断学湖南省重点实验室, 湖南 长沙 410208;湖南中医药大学信息科学与工程学院, 湖南 长沙 410208) |
| 摘要: |
| 目的 探讨益气活血方对冠心病气虚血瘀证大鼠自噬及磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（Akt）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路的影响，阐明其作用机制。方法 48只SPF级SD雄性大鼠，随机分为假手术组、模型组、益气活血方组(17.1 g·kg-1)、西药组(单硝酸异山梨酯3.6 mg·kg-1)，每组12只。除假手术组外，其余各组均用结扎冠状动脉左前降支合并游泳力竭法制备冠心病气虚血瘀证大鼠模型，而假手术组只穿线不结扎。灌胃给药14 d后取材，观察各组大鼠一般情况、心电图变化情况，超声心动图检测大鼠心功能，血液流变学检测大鼠的全血黏度，HE染色观察心肌组织病理形态，透射电子显微镜观察心肌组织超微结构，RT-PCR检测Beclin-1、微管相关蛋白1轻链3-Ⅱ（LC3-Ⅱ）、Akt、m TOR的mRNA表达水平，Western blot检测大鼠心肌组织中Beclin-1、LC3-Ⅱ、Akt、mTOR的蛋白表达。结果 与假手术组比较，模型组大鼠一般状态变差；心电图ST段抬高（P<0.01）；射血分数（EF）、短轴缩短率（FS）值降低（P<0.01），左室舒张末期内径（LVIDd）、左室收缩末期内径（LVIDs）值升高（P<0.01）；全血黏度升高（P<0.01）；心肌组织排列紊乱，心肌损伤严重；心肌超微结构受损严重；Akt、mTOR的mRNA及蛋白表达上调（P<0.01）,Beclin-1、LC3-Ⅱ的mRNA及蛋白表达下调（P<0.01）。与模型组比较，益气活血方组及西药组一般状态改善；心电图ST段降低（P<0.01）;EF、FS值升高（P<0.01）,LVIDd、LVIDs值降低（P<0.05,P<0.01）；全血黏度下降（P<0.01）；心肌纤维排列整齐，心肌细胞结构及形态改善；心肌超微结构损伤改善；Akt、mTOR的mRNA及蛋白表达下调（P<0.05,P<0.01）,Beclin-1、LC3-Ⅱ的mRNA及蛋白表达上调（P<0.05,P<0.01）。结论 益气活血方可改善冠心病气虚血瘀证大鼠心功能，减轻心肌损伤，有效治疗冠心病气虚血瘀证，其作用机制可能与调节PI3K/Akt/mTOR信号通路，激活自噬有关。 |
| 关键词: 冠心病 益气活血方 气虚血瘀证 PI3K/Akt/mTOR信号通路 自噬 |
| DOI：10.3969/j.issn.1674-070X.2025.11.003 |
| Received:June 19, 2025 |
| 基金项目:国家自然科学基金面上项目(82374323); 湖南省重点领域研发计划项目(2022SK2124); 湖南省教育厅科研项目(19A380); 湖南省中医药科研计划项目(202004)。 |
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| Effects of Yiqi Huoxue Formula on PI3K/Akt/mTOR signaling pathway and autophagy in coronary heart disease rats with qi deficiency induced blood stasis pattern |
| HE Nazhen, BEI Xueyi, CHEN Guangyu, LI Liang, QU Haoyu, XIE Mengzhou |
| (Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Hunan Engineering Technology Research Center for Medicine & Food Homology of Functional Food, Changsha, Hunan 410208, China;Key Laboratory of Chinese Medicine Heart and Lung Syndrom Differentiation, Medicated Diet & Dietotherapy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Hunan Key Laboratory of Chinese Medicine Diagnostics, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;School of Informatics, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To investigate the effects of the Yiqi Huoxue Formula（YQHXF） on autophagy and phosphatidylinositol3-kinase/protein kinase B/mammalian target of rapamycin（PI3K/Akt/mTOR） signaling pathway in coronary heart disease（CHD） rats with qi deficiency induced blood stasis pattern, and to clarify its mechanism of action. Methods Forty-eight male SPF-grade SD rats were randomly divided into sham-operated group, model group, YQHXF group(17.1 g·kg-1), and western medicine group(isosorbide mononitrate 3.6 mg·kg-1), with 12 rats in each group. Except the rats of the sham-operated group, models of CHD rats with qi deficiency induced blood stasis pattern were prepared by ligation of left anterior descending coronary artery combined with swimming exhaustion method in the other groups. For the sham-operated group, only threading without ligation was performed. After14 days of gavage intervention, samples were collected. The general state and changes of electrocardiogram were observed among different groups of rats. The cardiac function was measured by echocardiography, whole blood viscosity by hemorheography,pathological morphology of myocardial tissue by HE staining, myocardial ultrastructure by transmission electron microscopy, mRNA expression levels of Beclin-1, LC3-II, Akt, and mTOR by RT-PCR, protein expressions of Beclin-1, LC3-II, Akt, and m TOR in myocardial tissue by Western blot. Results Compared with the sham-operated group, the model group exhibited worsened general state: elevated ST segment of electrocardiograms（P＜0.01）, decreased ejection fraction（EF） and fractional shortening（FS） values（P＜0.01）, increased left ventricular internal end-diastolic diameter（LVIDd） and left ventricular internal end-systolic diameter（LVIDs）（P＜0.01）, increased whole blood viscosity（P＜0.01）, disorganized myocardial tissue arrangement, severe myocardial injury, significantly impaired myocardial ultrastructure, up-regulated mRNA and protein expressions of Akt and m TOR（P＜0.01）, and down-regulated mRNA and protein expressions of Beclin-1 and LC3-Ⅱ（P ＜0.01）. Compared with the model group, the YQHXF group and western medicine group both showed improved general state: decreased ST segment of electrocardiogram（P ＜0.01）, increased EF and FS values（P＜0.01）, decreased LVIDd and LVIDs（P＜0.05, P＜0.01）, decreased whole blood viscosity（P＜0.01）, aligned myocardial fibers,improved myocardial cell structure and morphology, ameliorated myocardial ultrastructure impairment, down-regulated m RNA and protein expressions of Akt and mTOR（P＜0.05, P＜0.01）, and up-regulated m RNA and protein expressions of Beclin-1 and LC3-Ⅱ（P ＜0.05, P ＜0.01）. Conclusion YQHXF can improve cardiac function and ameliorate myocardial injury in CHD rats with qi deficiency induced blood stasis pattern, effectively treating CHD with qi deficiency induced blood stasis pattern. Its mechanism of action may be related to the regulation of PI3K/Akt/mTOR signaling pathway and the activation of autophagy. |
| Key words: coronary heart disease Yiqi Huoxue Formula qi deficiency induced blood stasis pattern PI3K/Akt/mTOR signaling pathway autophagy |
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