Tetramethylpyrazine attenuates lipopolysaccharide-induced cardiomyocyte injury via improving mitochondrial function mediated by 14-3-3γ

Huang, Bowei; You, Jiegeng; Qiao, Yi; Wu, Zelong; Liu, Dan; Yin, Dong; He, Huan; He, Ming

doi:10.1016/j.ejphar.2018.05.019

Cited by 29 publications

(20 citation statements)

References 48 publications

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“…14-3-3 is the molecular target of many active ingredients of plants. We have confirmed that 14-3-3 assists PKCε, Bcl-2, and other functional proteins to locate to mitochondria and protect cardiomyocytes and vascular endothelial cells against multiple injuries [7,9,[40][41][42][43]. Further studies are needed to define specific mechanism(s) of action for Cap-activated 14-3-3η in anoxia and A/R injured cardiomyocytes.…”

Section: Discussionsupporting

confidence: 53%

Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3η in Anoxic or Anoxic/Reoxygenated Cardiomyocytes

Qiao

Yang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Reactive oxygen species (ROS) are byproducts of a defective electron transport chain (ETC). The redox couples, GSH/GSSG and NAD+/NADH, play an essential role in physiology as internal defenses against excessive ROS generation by facilitating intracellular/mitochondrial (mt) redox homeostasis. Anoxia alone and anoxia/reoxygenation (A/R) are dissimilar pathological processes. In this study, we measured the impact of capsaicin (Cap) on these pathological processes using a primary cultured neonatal rat cardiomyocyte in vitro model. The results showed that overproduction of ROS was tightly associated with disturbed GSH/GSSG and NAD+/NADH suppressed mt complex I and III activities, decreased oxygen consumption rates, and elevated extracellular acidification rates. During anoxia or A/R period, these indices interact with each other causing the mitochondrial function to worsen. Cap protected cardiomyocytes against the different stages of A/R injury by rescuing NAD+/NADH, GSH/GSSG, and mt complex I/III activities and cellular energy metabolism. Importantly, Cap-mediated upregulation of 14-3-3η, a protective phosphoserine-binding protein in cardiomyocytes, ameliorated mt function caused by a disruptive redox status and an impaired ETC. In conclusion, redox pair, mt complex I/III, and metabolic equilibrium were significantly different in anoxia alone and A/R injury; Cap through upregulating 14-3-3η plays a protection against the above injury in cardiomyocyte.

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Section: Discussionsupporting

confidence: 53%

Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3η in Anoxic or Anoxic/Reoxygenated Cardiomyocytes

Qiao

Yang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Several natural and synthetic compounds have been introduced in previous studies for protecting cardiomyocytes against injury [8][9][10]. 6-Gingerol (6 G) is a natural chemical compound isolated from ginger (Zingiber officinale).…”

Section: Introductionmentioning

confidence: 99%

6-Gingerol protects cardiocytes H9c2 against hypoxia-induced injury by suppressing BNIP3 expression

Ren¹,

Zhao²,

Ren³

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Cardiomyocytes loss is the predominant pathogenic characteristic in the hypoxia-induced injury. Meanwhile, it has been corroborated that Bcl-2 E1B 19-KDa interacting protein 3 (BNIP3) provokes apoptosis and autophagy. For moderating cardiomyocytes loss, we initially probed the cyto-protection effects of 6-Gingerol (6 G), meanwhile, its potential mechanisms associated with BNIP3 were elucidated in our studies. Methods: We pretreated cardiomyocytes H9c2 cells with 6 G at different concentrations (0-100 lM) before exposure to hypoxia. Thereafter, the cell viability, lactate dehydrogenase (LDH), apoptosis and protein expression were respectively assessed using cell counting kit-8 and methyl thiazolyl tetrazolium (MTT) assay, LDH assay kit, Annexin V-fluorescein isothiocyannate/propidium iodide (Annexin V-FITC/PI) apoptosis detection kit and Western blotting analysis. In addition, we also analyzed BNIP3 level after treatment. Moreover, we enforced the exogenous overexpression of BNIP3 and then evaluated the cell viability, apoptosis, and protein level again. Results: In our present work, we observed that the cell viability was promoted by 6 G in the hypoxiainduced H9c2 cells in a dose-dependent manner. Moreover, hypoxia-induced LDH release, apoptosis and autophagy were inhibited by 6 G pretreatment through promoting phosphorylation of PI3K, AKT and mTOR. Remarkably, accumulation of BNIP3 protein was significantly reduced by 6 G in hypoxia-induced H9c2 cells. Mechanistically, 6 G initiated the phosphorylated expression of PI3K, AKT and mTOR by down-regulating BNIP3 with reducing cardiomyocytes apoptosis and autophagy. Conclusion: Hypoxia-induced cardiomyocytes injury was ameliorated by 6 G through suppressing BNIP3 expression with triggering PI3K/AKT/mTOR signalling pathway.

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“…Recently, researches were set out to investigate the protective activities of TMP against lipopolysaccharide (LPS)-evoked injury of cells and the protection mechanisms. For example, Huang et al reported that TMP represses LPS-induced damages through promoting the production of 14-3-3c [8]. In addition, it has been found that TMP treatment can significantly improve blood glucose and renal function in the streptozotocin-induced diabetic nephropathy rat model compared to the untreated diabetic rats [9].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Tetramethylpyrazine relieves LPS-induced pancreatic β-cell Min6 injury via regulation of miR-101/MKP-1

Chen

Cao

Sui

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Tetramethylpyrazine (TMP) is a traditional Chinese medicine with anti-inflammation and immunomodulatory effects. In this context, our purpose was to investigate the associated regulatory mechanisms of TMP against lipopolysaccharide (LPS)-caused pancreatic b cell Min6 injury. The injury of Min6 cells was induced by 10 lg/mL of LPS. Viability of Min6 cells was detected through CCK-8 assay, apoptosis process through flow cytometry, and the proteins involved in apoptosis through western blot. Insulin secretion was valued through the glucose-stimulated insulin secretion (GSIS) assay. microRNA-101 (miR-101) was measured through qRT-PCR. Mitogen-activated protein kinase phosphatase 1 (MKP-1) and signaling regulators was measured through western blot. We found that, TMP treatment effectively attenuated LPS-induced injury in Min6 cells by suppressing cell apoptosis and promoting insulin secretion. Further investigation revealed that TMP exerted protective effect through down-regulating miR-101, and MKP-1 was demonstrated as a target of miR-101. Moreover, TMP attenuated LPS-triggered inflammation by inactivating the JNK1/2 and NF-jB through the down-regulation of miR-101. In conclusion, our present study revealed that TMP alleviated LPS-induced injury in pancreatic b-cell Min6 injury via regulation of miR-101/MKP-1 with the bluntness of JNK1/2 and NF-jB pathways.

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Tetramethylpyrazine attenuates lipopolysaccharide-induced cardiomyocyte injury via improving mitochondrial function mediated by 14-3-3γ

Cited by 29 publications

References 48 publications

Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3η in Anoxic or Anoxic/Reoxygenated Cardiomyocytes

Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3η in Anoxic or Anoxic/Reoxygenated Cardiomyocytes

6-Gingerol protects cardiocytes H9c2 against hypoxia-induced injury by suppressing BNIP3 expression

RETRACTED ARTICLE: Tetramethylpyrazine relieves LPS-induced pancreatic β-cell Min6 injury via regulation of miR-101/MKP-1

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