Epigallocatechin gallate prevents mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis

Zhang, Chan; Liao, Ping; Liang, Ronggan; Zheng, Xiaojia; Jian, Jie

doi:10.1016/j.phymed.2019.152845

Cited by 32 publications

(32 citation statements)

References 30 publications

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“…Yang et al discovered for the first time that miR30a is highly expressed in the myocardium and efficiently transferred via exosomes between hypoxic cardiomyocytes (Yang et al, 2016). Coincidently, our preliminary results demonstrated that miR30a is a key regulator of EGCG action in ischemic reperfusion injury (Zhang C. et al, 2019). Based on previous studies, we proposed that EGCG achieved an improved effect on cardiac recovery following AMI by specifically targeting the regulatory exosomal miR30a.…”

Section: Discussionsupporting

confidence: 70%

“…Coincidentally, our previous study confirmed that EGCG alleviated I/R injury in myocardial cells by regulating apoptosis and autophagy (Xuan and Jian, 2016). Furthermore, the beneficial effect of EGCG on attenuating mitochondrial impairment and myocardial apoptosis was associated with miR-30a levels (Zhang C. et al, 2019). Accordingly, we hypothesized that exosomal miR-30a could be a target of EGCG.…”

Section: Introductionmentioning

confidence: 71%

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Exosomes Derived From Epigallocatechin Gallate-Treated Cardiomyocytes Attenuated Acute Myocardial Infarction by Modulating MicroRNA-30a

et al. 2020

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Background: Ischemia-derived exosomes can restrict excessive autophagy by transferring microRNA-30a (miR30a) to cells. Reports have confirmed that epigallocatechin gallate (EGCG) alleviates acute myocardial infarction (AMI) by regulating autophagy; however, research evaluating the communication with cardiomyocytes and exosomes is lacking. This study aimed to explore whether exosomes derived from EGCGtreated cardiomyocytes mitigated AMI by adjusting miR30a to inactivate apoptosis and autophagy. Methods: Exosomes were extracted from cardiomyocytes, cultured either in control or AMI condition, with or without EGCG pretreatment. The exosome characteristics were analyzed by nanoparticle tracking analyses and transmission electron microscopy. The change in miR30a in cells and exosomes was demonstrated by qRT-PCR. H9c2 or stable miR30a knockdown (miR30a KD) cell lines were incubated with exosomes derived from EGCG-treated cardiomyocytes in vitro or in vivo. The effect of EGCG and exosomes on I/ R-induced cardiomyocyte apoptosis and autophagy was assessed. Results: EGCG improved the activity of cardiomyocytes, and increased average diameter, concentration, miR30a mRNA level, and specific protein expression in AMIderived exosomes produced by cardiomyocytes. Moreover, the coincubation of AMI cells with EGCG or exosomes derived from EGCG-treated cardiomyocytes attenuated cardiomyocyte apoptosis and autophagy. Conclusions: The findings showed that EGCG upregulates miR30a, which was efficiently transferred via exosomes between cardiomyocytes, thereby contributing to the suppression of apoptosis and autophagy. By focusing on the cardiomyocyte microenvironment, we identified a new target of EGCG alleviating AMI by regulating apoptosis and autophagy.

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 71%

Exosomes Derived From Epigallocatechin Gallate-Treated Cardiomyocytes Attenuated Acute Myocardial Infarction by Modulating MicroRNA-30a

et al. 2020

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“…The transcription factor p53 is the main p53 family member in the apoptotic signaling pathway [ 88 , 89 ]. Activation of NF-κB or p53 plays a role in inducing inflammation, oxidative stress, and apoptosis in tissue injuries [ 90 – 92 ]. Myocardial I/R injuries are found to induce inflammation, oxidative stress, and apoptosis via the NF-κB pathway [ 93 ].…”

Section: Discussionmentioning

confidence: 99%

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

Almoiliqy

Wen

et al. 2020

Acta Pharmacol Sin

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Our preliminary study shows that cinnamaldehyde (CA) could protect against intestinal ischemia/reperfusion (I/R) injuries, in which p53 and NF-κB p65 play a synergistic role. In this study, we conducted in vivo and in vitro experiments to verify this proposal. SD rats were pretreated with CA (10 or 40 mg · kg −1 · d −1 , ig) for 3 days, then subjected to 1 h mesenteric ischemia followed by 2 h reperfusion. CA pretreatment dose-dependently ameliorated morphological damage and reduced inflammation evidenced by decreased TNF-α, IL-1β, and IL-6 levels and MPO activity in I/R-treated intestinal tissues. CA pretreatment also attenuated oxidative stress through restoring SOD, GSH, LDH, and MDA levels in I/R-treated intestinal tissues. Furthermore, CA pretreatment significantly reduced the expression of inflammation/apoptosis-related NF-κB p65, IKKβ, IK-α, and NF-κB p50, and downregulated apoptotic protein expression including p53, Bax, caspase-9 and caspase-3, and restoring Bcl-2, in I/R-treated intestinal tissues. We pretreated IEC-6 cells in vitro with CA for 24 h, followed by 4 h hypoxia and 3 h reoxygenation (H/R) incubation. Pretreatment with CA (3.125, 6.25, and 12.5 μmol · L −1 ) significantly reversed H/R-induced reduction of IEC-6 cell viability. CA pretreatment significantly suppressed oxidative stress, NF-κB activation and apoptosis in H/R-treated IEC-6 cells. Moreover, CA pretreatment significantly reversed mitochondrial dysfunction in H/R-treated IEC-6 cells. CA pretreatment inhibited the nuclear translocation of p53 and NF-κB p65 in H/R-treated IEC-6 cells. Double knockdown or overexpression of p53 and NF-κB p65 caused a synergistic reduction or elevation of p53 compared with knockdown or overexpression of p53 or NF-κB p65 alone. In H/R-treated IEC-6 cells with double knockdown or overexpression of NF-κB p65 and p53, CA pretreatment caused neither further decrease nor increase of NF-κB p65 or p53 expression, suggesting that CA-induced synergistic inhibition on both NF-κB and p53 played a key role in ameliorating intestinal I/R injuries. Finally, we used immunoprecipitation assay to demonstrate an interaction between p53 and NF-κB p65, showing the basis for CA-induced synergistic inhibition. Our results provide valuable information for further studies.

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“…Therefore, in the present study the safest maximum concentration (100 µM) was used in the present experiments. Recent studies on the optimum concentrations have since been conducted, the cell viability and Actin-Tracker Green technique in these recent studies demonstrated that the optimal range of concentration for the protective effects of EGCG was 50-100 µM (35,36).…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin‑3‑gallate ameliorates LPS‑induced inflammation by inhibiting the phosphorylation of Akt and ERK signaling molecules in rat H9c2 cells

Shi

Tang

et al. 2020

Exp Ther Med

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T he inf lam mator y response has been implicated in various cardiac and systemic diseases. Epigallocatechin-3-gallate (EGCG), the major polyphenol extracted from green tea, has various biological and pharmacological properties, such as anti-inflammation, anti-oxidative and anti-tumorigenesis. To some extent, the mechanism of EGCG in the inflammatory response that characterizes myocardial dysfunction is not fully understood. The present study aimed to investigate the inhibiting effect of EGCG on lipopolysaccharide (LPS)-induced inflammation in vitro. Treatment with LPS affected rat H9c2 cardiomyocytes and induced an inflammatory response. However, the LPS-induced effects were attenuated after treatment with EGCG. The present results demonstrated that EGCG treatment repressed several inflammatory mediators, such as vascular endothelial growth factor, chemokine ligand 5, chemokine ligand 2, intercellular adhesion molecule-1, matrix metalloproteinase-2, tumor necrosis factor-α and nitric oxide (induced by LPS), and the repressing effect of EGCG on inflammatory response was dose-dependent in the range of 6.25-100 µM. EGCG inhibited these marked inflammatory key signaling molecules by reducing the expression of phospho-nuclear factor-κB p65,-Akt,-ERK and-MAPK p38 while the total protein level of these signal proteins were not affected. In conclusion, the present findings suggested that EGCG possesses cardiomyocyte-protective action in reducing the LPS-induced inflammatory response due to the inhibition of the phosphorylation of Akt and ERK signaling molecules.

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Epigallocatechin gallate prevents mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis

Cited by 32 publications

References 30 publications

Exosomes Derived From Epigallocatechin Gallate-Treated Cardiomyocytes Attenuated Acute Myocardial Infarction by Modulating MicroRNA-30a

Exosomes Derived From Epigallocatechin Gallate-Treated Cardiomyocytes Attenuated Acute Myocardial Infarction by Modulating MicroRNA-30a

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

Epigallocatechin‑3‑gallate ameliorates LPS‑induced inflammation by inhibiting the phosphorylation of Akt and ERK signaling molecules in rat H9c2 cells

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