Cardioprotective Effect of Stem-Leaf Saponins From Panax notoginseng on Mice With Sleep Derivation by Inhibiting Abnormal Autophagy Through PI3K/Akt/mTOR Pathway.
Cardioprotective Effect of Stem-Leaf Saponins From Panax notoginseng on Mice With Sleep Derivation by Inhibiting Abnormal Autophagy Through PI3K/Akt/mTOR Pathway.
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DOI：
10.3389/fcvm.2021.694219
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发表时间：
2021
影响因子：
3.6
通讯作者：
Wu X
中科院分区：
文献类型：
--
作者：
Cao Y;Li Q;Yang Y;Ke Z;Chen S;Li M;Fan W;Wu H;Yuan J;Wang Z;Wu X
睡眠剥夺（SD）可能会导致心血管疾病中严重的心肌损伤。三七皂苷是从三七根中提取的一种具有活血止血作用的中药，是治疗心律失常、缺血再灌注损伤、心肌肥厚等心血管疾病的主要活性成分。目的探讨三七茎叶皂苷（SLSP）对SD小鼠心肌损伤的保护作用。SD通过改良的多平台方法诱导。苏木精-伊红（H&E）染色观察心脏形态学改变。用专用仪器检测心率和射血分数。用生化试剂盒测定血清心钠素（ANP）和乳酸脱氢酶（LDH）水平。应用透射电镜、免疫荧光和Western blotting等方法观察SD小鼠心脏组织自噬和凋亡的过程和途径。在体外，采用吖啶橙子染色、瞬时转染、流式细胞术和Western blotting分析等方法，观察雷帕霉素预处理的H9 c2细胞及SLSP的作用。SLSP对SD大鼠心肌细胞形态学损伤、自噬体在心肌组织中的积聚、异常高心率、血清ANP、血清LDH均有保护作用。此外，它还逆转了自噬和凋亡相关蛋白的表达，激活了SD干扰的PI 3 K/Akt/mTOR信号通路。SLSP能明显恢复雷帕霉素诱导的H9 c2细胞异常自噬和凋亡。SLSP可能通过激活PI 3 K/Akt/mTOR信号通路，抑制SD大鼠心肌细胞过度自噬和凋亡。
Sleep deprivation (SD) may lead to serious myocardial injury in cardiovascular diseases. Saponins extracted from the roots of Panax notoginseng, a traditional Chinese medicine beneficial to blood circulation and hemostasis, are the main bioactive components exerting cardiovascular protection in the treatment of heart disorders, such as arrhythmia, ischemia and reperfusion injury, and cardiac hypertrophy. This study aimed to explore the protective effect of stem-leaf saponins from Panax notoginseng (SLSP) on myocardial injury in SD mice. SD was induced by a modified multi-platform method. Cardiac morphological changes were assessed by hematoxylin and eosin (H&E) staining. Heart rate and ejection fraction were detected by specific instruments. Serum levels of atrial natriuretic peptide (ANP) and lactate dehydrogenase (LDH) were measured with biochemical kits. Transmission electron microscopy (TEM), immunofluorescent, and Western blotting analysis were used to observe the process and pathway of autophagy and apoptosis in heart tissue of SD mice. In vitro, rat H9c2 cells pretreated with rapamycin and the effect of SLSP were explored by acridine orange staining, transient transfection, flow cytometry, and Western blotting analysis. SLSP prevented myocardial injury, such as morphological damage, accumulation of autophagosomes in heart tissue, abnormal high heart rate, serum ANP, and serum LDH induced by SD. In addition, it reversed the expressions of proteins involved in the autophagy and apoptosis and activated PI3K/Akt/mTOR signaling pathway that is disturbed by SD. On H9c2 cells induced by rapamycin, SLSP could markedly resume the abnormal autophagy and apoptosis. Collectively, SLSP attenuated excessive autophagy and apoptosis in myocardial cells in heart tissue induced by SD, which might be acted through activating PI3K/Akt/mTOR signaling pathway.
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影响因子：
4
作者：
Huo, Jun-Feng;Chen, Xiao-Bing
通讯作者：
Chen, Xiao-Bing
DOI：
10.1253/jcj.63.447
发表时间：
1999-06-01
期刊：
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
影响因子：
--
作者：
Tanabe, K;Yamamoto, A;Murayama, M
通讯作者：
Murayama, M
影响因子：
2.6
作者：
Jeddi S;Asl AN;Asgari A;Ghasemi A
通讯作者：
Ghasemi A
影响因子：
2.9
作者：
Suchecki, D;Tufik, S
通讯作者：
Tufik, S
影响因子：
11.7
作者：
Liu Z;Nie R;Liu Y;Li Z;Yang C;Xiong Z
通讯作者：
Xiong Z