bioRxivGeneticsPreprint
Protective Effects of Matrine on Acute Myocardial Hypertrophy Induced by Isoproterenol via Akt/mTOR/p70S6K/eIF4E Signaling Pathway in Rats
Hui MaiD, Hongwan Dang, Shijie WeiiD, Xiaoying YangiD, Wenping ZhangiD
Abstract
This study aimed to investigate whether matrine (Ma) attenuates isoproterenol (ISO)-induced acute myocardial hypertrophy via activating Akt/mTOR/p70S6K/eIF4E signaling pathway in rats. We collected 42 male Sprague-Dawley rats weighing 300{+/-}20g, randomly divided into seven groups (n=6). The myocardial hypertrophy (MH) model was well established by 85 mg/kg ISO. Changes in hemodynamic parameters were recorded using electrocardiogram after 24h with ISO injection. Western blot and real-time polymerase chain reaction were used to evaluate the expression of Akt, mechanistic target of rapamycin (mTOR), p70S6K, and eIF4E. Tissue arrangement of the 200 and 100 mg/kg Ma+ISO groups was regularly smaller than that of the ISO group. For the protein expression, Akt values in the 200 and 100 mg/kg Ma+ISO groups were 1.57- and 1.81-fold higher than in the ISO group, respectively. Moreover, compared with the ISO group, the expression trends of mTOR in the 200, 100, and 50 mg/kg Ma+ISO groups significantly downregulated. The levels of p70S6K and eIF4E reduced in the 200, 100, and 50 mg/kg Ma+ISO groups according to the ISO group (P<0.05). MRNA expression of p70S6K and eIF4E in the ISO group were 1.90- and 6.38-fold higher compared with that in the 100 mg/kg Ma+ISO group. Ma exerted neuroprotective effects against pachyntic injury. Akt activity was accelerated, but activities of mTOR, p70S6K, and eIF4E were inhibited by Ma. Activation of the Akt/mTOR/p70S6K/eIF4E signaling pathway might be the targets for the protective effects of Ma on acute myocardial hypertrophy in rats.
- Citations
- 1
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Effects of calorie restriction on reactive oxygen species production by mitochondrial reverse electron transport, mitochondrial permeability transition pore, and beta-adrenergic stimulation during cardiac hypertrophy
A. M. B. Lucas, P. B. Palacio, … H. T. Facundo·bioRxiv·Feb 2, 2022
- Oral administration of Angiotensin-(1-7) included in hydroxypropyl β-cyclodextrin attenuates cardiac hypertrophy and inflammation in a mouse model of Takotsubo cardiomyopathy
Maria Luiza Dias-Pinto, Bruno Sanches, … Thiago Verano‐Braga·bioRxiv·Oct 9, 2026
- Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptors
M. Iveth Garcia, Anja Karlstaedt, … Darren Boehning·bioRxiv·Sep 13, 2016
- Myocardial damage induced by a single high dose of isoproterenol in C57BL/6J mice triggers a persistent adaptive immune response against the heart.
E. Forte, M. Panahi, … S. Sattler·bioRxiv·Feb 27, 2020
- Anacardic acid protects against phenylephrine-induced mouse cardiac hypertrophy through JNK signaling-dependent regulation of histone acetylation
- Metallothionein-2A protect Cardiomyocytes from Ischemia/ Reperfusion through inhibiting p38