Pretreatment with Tilianin improves mitochondrial energy metabolism and oxidative stress in rats with myocardial ischemia/reperfusion injury via AMPK/SIRT1/PGC-1 alpha signaling pathway

Tian, Li; Cao, Wenjiang; Yue, Rujing; Yang, Yuan; Guo, Xing; Dong-mei, Qin; Xing, Jianguo; Wang, Xinchun

doi:10.1016/j.jphs.2019.02.008

Cited by 163 publications

(120 citation statements)

References 20 publications

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“…As activated AMPK could monitor mitochondrial energy metabolism and cellular energy status, the relative mRNA and protein expression of upstream and downstream of the AMPK signalling pathway were detected. Thus, the relative mRNA and protein expression levels of the LKB1/AMPKα/Sirt1 pathway were measured by RT‐PCR and Western blotting, respectively (Figure ).…”

Section: Resultsmentioning

confidence: 99%

Therapeutic effects of higenamine combined with [6]‐gingerol on chronic heart failure induced by doxorubicin via ameliorating mitochondrial function

Wen

Zhang

Wang

et al. 2020

J Cellular Molecular Medi

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Higenamine (HG) is a natural benzylisoquinoline alkaloid isolated from Aconitum with positive inotropic and chronotropic effects. This study aimed to investigate the possible cardioprotective effects of HG combined with [6]-gingerol (HG/[6]-GR) against DOXinduced chronic heart failure (CHF) by comprehensive approaches. DOX-induced cardiotoxicity model in rats and H9c2 cells was established. Therapeutic effects of HG/[6]-GR on haemodynamics, serum indices and histopathology of cardiac tissue were analysed. Cell mitochondrial energy phenotype and cell mitochondrial fuel flex were measured by a Seahorse XFp analyser. Moreover, UHPLC-Q-TOF/MS was performed to explore the potential metabolites affecting the therapeutic effects and pathological process of CHF. To further investigate the potential mechanism of HG/[6]-GR, mRNA and protein expression levels of RAAS and LKB1/AMPK/Sirt1-related pathways were detected. The present data demonstrated that the therapeutic effects of HG/[6]-GR combination on CHF were presented in ameliorating heart function, down-regulation serum indices and alleviating histological damage of heart tissue. Besides, HG/[6]-GR has an effect on increasing cell viability of H9c2 cells, ameliorating DOX-induced mitochondrial dysfunction and elevating mitochondrial OCR and ECAR value. Metabolomics analyses showed that the therapeutic effect of HG/[6]-GR combination is mainly associated with the regulation of fatty acid metabolites and energy metabolism pathways. Furthermore, HG/ [6]-GR has an effect on down-regulating RAAS pathway-related molecules and up-regulating LKB1/AMPKα/Sirt1-related pathway. The present work demonstrates that HG/ [6]-GR prevented DOX-induced cardiotoxicity via the cardiotonic effect and promoting myocardial energy metabolism through the LKB1/AMPKα/Sirt1 signalling pathway, which promotes mitochondrial energy metabolism and protects against CHF. K E Y W O R D S [6]-gingerol, Aconiti Lateralis Radix Praeparata, chronic heart failure, doxorubicin, energy metabolism, higenamine | 4037 WEN Et al.

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Section: Resultsmentioning

confidence: 99%

Therapeutic effects of higenamine combined with [6]‐gingerol on chronic heart failure induced by doxorubicin via ameliorating mitochondrial function

Wen

Zhang

Wang

et al. 2020

J Cellular Molecular Medi

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“…In addition, the reported study showed that TST can protect the acute liver injury by inhibiting NF-κB expression [46,47]. More importantly, it was reported that the activation of AMPK/Sirt1 could inhibited MIRI through alleviate in ammation reaction [32][33][34][35], which is very important for MIRI therapy in clinic. Thus, in this study, we further evaluated that whether TST plays an antiin ammatory role by stimulating AMPK/Sirt1/NF-κB signaling pathway [48].…”

Section: Discussionmentioning

confidence: 94%

“…Furthermore, it was reported that the activation of adenosine 5'-mono phosphate activated protein kinase (AMPK) / silent information regulator 1 (Sirt1) signaling pathway could inhibited MIRI through alleviate in ammation reaction [32][33][34][35]. Thus, in this study, we attempted to explore and evaluate the protective effect and potential mechanisms of TST in MIRI in rat.…”

Section: Trillium Tschonoskii Maxim (Ttm) a Plant From Trillocerosamentioning

confidence: 99%

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Zhang

Wang

Tang

et al. 2020

Preprint

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BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

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“…To investigate the potential mechanisms underlying the effects of sufentanil on myocardial I/R injury, we examined the expression of the AMPK signalling pathway. It has been well documented that the AMPK pathway is closely implicated in I/R injury [26]. For instance, ghrelin pretreatment protects against I/Rinduced H9c2 cell injury via the AMPK pathway [27].…”

Section: Sufentanil Protected Against Myocardial I/r Injury In H9c2 Vmentioning

confidence: 99%

Sufentanil attenuates inflammation and oxidative stress in myocardial ischemia reperfusion injury via upregulating Sestrin 2 expression and activating AMPK signalling pathway

Jiang

Zou

et al. 2020

Biotechnology & Biotechnological Equipment

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This study explored whether sufentanil, a lipophilic opioid, can protect against myocardial ischemia-reperfusion (I/R) injury via regulating Sestrin 2 (Sesn2) expression. The expression of Sesn2 was measured in the blood of patients with myocardial I/R after sufentanil administration. H9c2 cells were applied to establish I/R injury by oxygen-glucose deprivation and reoxygenation (OGD/R). After treatment with 5, 10 and 20 lmol/L sufentanil, the expression of Sesn2 was examined. Then, shRNA-Sesn2 was transfected into H9c2 cells. The concentrations of creatine kinase (CK), CK isoenzymes (CK-MB), cardiac troponin I (cTnI), inflammation-related factors and oxidative-related factors were sequentially determined by kits. Western blotting was exploited to determine the expression of AMP-activated protein kinase (AMPK) pathway proteins. The results revealed that the expression of Sesn2 was increased in patients after administration with sufentanil. OGD/R intervention upregulated the expression of Sesn2, which continued to increase in a dose-dependent manner following treatment with sufentanil. Moreover, sufentanil attenuated the concentrations of CK, CK-MB and cTnl induced by OGD/R in H9c2 cells. This effect was reversed after Sesn2 silencing. Meanwhile, the levels of inflammatory factors and oxidative stress were notably decreased when cells were treated with sufentanil, and these inhibitory effects were alleviated after transfection with shRNA-Sesn2. Furthermore, sufentanil enhanced the phosphorylation of AMPK and its downstream acetyl CoA carboxylase (ACC), whereas Sesn2 silencing inhibited the expression of the above proteins. These findings demonstrated that sufentanil could attenuate inflammation and oxidative stress in myocardial I/R injury via upregulating Sesn2 expression and activating the AMPK pathway.

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Pretreatment with Tilianin improves mitochondrial energy metabolism and oxidative stress in rats with myocardial ischemia/reperfusion injury via AMPK/SIRT1/PGC-1 alpha signaling pathway

Cited by 163 publications

References 20 publications

Therapeutic effects of higenamine combined with [6]‐gingerol on chronic heart failure induced by doxorubicin via ameliorating mitochondrial function

Therapeutic effects of higenamine combined with [6]‐gingerol on chronic heart failure induced by doxorubicin via ameliorating mitochondrial function

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Sufentanil attenuates inflammation and oxidative stress in myocardial ischemia reperfusion injury via upregulating Sestrin 2 expression and activating AMPK signalling pathway

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