Salidroside inhibits oxygen glucose deprivation (OGD)/re-oxygenation-induced H9c2 cell necrosis through activating of Akt–Nrf2 signaling

Zheng, Koulong; Sheng, Zhenqiang; Li, Yefei; Lu, Hongzhou

doi:10.1016/j.bbrc.2014.07.072

Cited by 51 publications

(89 citation statements)

References 34 publications

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“…However, few studies have reported the impact of hyperglycemia on Akt signaling in H9c2 cells. Consistent with previous reports [16], our results showed that myricitrin increased HO-1 and NQO-1 expression, activated Akt, as a classical signaling pathway, has been reported to be tightly related to cell apoptosis, the latter of which has been confirmed to regulate Nrf2 activation [18,21]. However, few studies have reported the impact of hyperglycemia on Akt signaling in H9c2 cells.…”

Section: Discussionsupporting

confidence: 92%

“…Collectively, myricitrin exerted its anti-apoptotic effect by eliminating ROS production and restoring MMP. Akt, as a classical signaling pathway, has been reported to be tightly related to cell apoptosis, the latter of which has been confirmed to regulate Nrf2 activation [21,18]. However, few studies have reported the impact of hyperglycemia on Akt signaling in H9c2 cells.…”

Section: Discussionmentioning

confidence: 99%

“…The antioxidant-responsive element (ARE) regulates the transcription of many anti-oxidant genes (i.e., heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1)) and phase II detoxification enzymes [21]. Nrf2 regulates the transcriptional activation of HO-1 and NQO-1 by binding to ARE [22].…”

Section: Myricitrin Exerts Its Effects By Activating the Pi3k/akt Patmentioning

confidence: 99%

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Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Myricitrin Exerts Its Effects By Activating the Pi3k/akt Patmentioning

confidence: 99%

See 1 more Smart Citation

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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“…It has been reported that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is an amenable pharmacological target for CVD protection, and it achieves its effect mainly through regulating caspase activation, Bcl-2 family activity, and so on (Wang J. et al, 2015). In the past few years, many traditional Chinese medicines have been claimed to be useful for controlling CVD, particularly for the injury induced by ischemia (Quan et al, 2014;Zheng et al, 2014). Therefore, searching for anti-necrosis and anti-apoptotic compounds with minimal side effects from traditional Chinese medicines probably is an ideal way for CVD patients, and to help create a much safer and more effective treatment.…”

Section: Introductionmentioning

confidence: 99%

Protective mechanisms of hypaconitine and glycyrrhetinic acid compatibility in oxygen and glucose deprivation injury

Wang

Wan

Zhou

et al. 2017

J. Zhejiang Univ. Sci. B

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This study investigated the protective effect of the compatibility of hypaconitine (HA) and glycyrrhetinic acid (GA) on H9c2 cells under oxygen and glucose deprivation (OGD)-induced injury, and the possible mechanisms. We found that HA+GA significantly improved pathology and morphology of the nucleus and ultrastructure of H9c2 cells under OGD as determined by Hoechst 33342 staining and transmission electron microscopy (TEM) tests. It also reduced the releases of lactate dehydrogenase (LDH), creatine kinase-myocardial band isoenzyme (CK-MB), and aspartate transaminase (AST) from the cultured supernatant of H9c2 cells, which were tested by enzyme-linked immune sorbent assay (ELISA) kits. In addition, it lessened the apoptotic rate as determined by a fluorescein isothiocyanate-annexin V/propidium iodide (FITC-AV/PI) double staining assay. It was also found that HA+GA might regulate the protein expression associated with the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Overall, the study demonstrated that HA+GA protected H9c2 cells against OGD-induced injury, and the signaling mechanism might be related to the PI3K/Akt signaling pathway.

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“…However, it is noteworthy that salidroside was recently found to inhibit pulmonary fibrosis in rats treated with bleomycin, and that this inhibition was accompanied by stabilization of NRF2 and increased levels of its downstream target proteins NAD(P)H:quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HMOX1), and suppression of pro-inflammatory responses (Tang et al 2015). In addition, salidroside protects H9c2 cardiomyocytes against ischemic damage caused by oxygen and glucose deprivation/re-oxygenation (Zheng et al 2014). …”

Section: Phytochemical Composition Of Rhodiola Roseamentioning

confidence: 99%

Rhodiola rosea L.: from golden root to green cell factories

et al. 2016

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Salidroside inhibits oxygen glucose deprivation (OGD)/re-oxygenation-induced H9c2 cell necrosis through activating of Akt–Nrf2 signaling

Cited by 51 publications

References 34 publications

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Protective mechanisms of hypaconitine and glycyrrhetinic acid compatibility in oxygen and glucose deprivation injury

Rhodiola rosea L.: from golden root to green cell factories

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