2022
DOI: 10.1007/s11418-022-01666-7
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Acacetin inhibits myocardial mitochondrial dysfunction by activating PI3K/AKT in SHR rats fed with fructose

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Cited by 6 publications
(5 citation statements)
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“…Our previous studies confirmed that acacetin improved myocardial mitochondrial dysfunction by regulating the PI3 K/AKT signaling pathway-mediated oxidative stress, mitochondrial fission and fusion, and apoptosis of the mitochondrial pathway in fructose-induced SHR rats. 14 As shown in this study, AC can regulate RAAS system and endothelial cell correlated factors, activate the key protein PI3Kp85 subunit of the insulin signaling pathway, and improve SHR & IR cardiac endothelial mesenchymal conversion and myocardial fibrosis in rats. As an antagonist of PI3 K, wortmannin did not exert the expected antagonist effect on acacetin.…”
Section: Discussionmentioning
confidence: 55%
See 1 more Smart Citation
“…Our previous studies confirmed that acacetin improved myocardial mitochondrial dysfunction by regulating the PI3 K/AKT signaling pathway-mediated oxidative stress, mitochondrial fission and fusion, and apoptosis of the mitochondrial pathway in fructose-induced SHR rats. 14 As shown in this study, AC can regulate RAAS system and endothelial cell correlated factors, activate the key protein PI3Kp85 subunit of the insulin signaling pathway, and improve SHR & IR cardiac endothelial mesenchymal conversion and myocardial fibrosis in rats. As an antagonist of PI3 K, wortmannin did not exert the expected antagonist effect on acacetin.…”
Section: Discussionmentioning
confidence: 55%
“…It has been reported that acacetin (AC) has the effect of lowering blood pressure, improving myocardial damage caused by ischemia-reperfusion, 14,15 and improving lipid metabolism disorders. 16 At the same time, the previous research of our group has established the fructose-induced SHR model accompanied by metabolic syndrome successfully, and also found that acacetin improved myocardial mitochondrial dysfunction through regulating oxidative stress, mitochondrial fission and fusion, and mitochondrial pathway apoptosis mediated by PI3 K/ AKT signaling pathway in hypertensive rats with IR.…”
Section: Introductionmentioning
confidence: 99%
“…In this study, KEGG enrichment analysis indicated that 832 differentially expressed mRNAs were mainly involved in metabolic, NOD-like receptor, Wnt, PPAR, and p53 signaling pathways and in glycerophospholipid metabolism. The target genes of the differentially expressed miR-NAs were mainly involved in endocytosis, the PI3K-Akt signaling pathway, nucleocytoplasmic transport, MAPK signaling pathway, and viral carcinogenesis pathways, among these, the NOD-like receptor, Wnt, PPAR, PI3K-Akt, and MAPK signaling pathways were closely related to mitochondrial function [35][36][37]. For example, NODlike receptor family member X1 (NLRX1) localized to the mitochondrial outer membrane.…”
Section: Discussionmentioning
confidence: 99%
“…In the present study, The KEGG enrichment analysis indicated that 832 differentially expressed mRNAs were involved mainly in metabolic, NOD-like receptor, Wnt, PPAR, and p53 signaling pathways and in glycerophospholipid metabolism. The target genes of the differentially expressed miRNAs were involved mainly in endocytosis, the PI3K-Akt signaling pathway, nucleocytoplasmic transport, MAPK signaling pathway, and viral carcinogenesis pathways, among these, the NOD-like receptor, Wnt, PPAR, PI3K-Akt, and MAPK signaling pathways were closely related to mitochondrial function [35][36][37]. For example, NODlike receptor family member X1 (NLRX1) localized to the mitochondrial outer membrane.…”
Section: Discussionmentioning
confidence: 99%