Inhibition of Autophagy via Activation of PI3K/Akt Pathway Contributes to the Protection of Ginsenoside Rb1 against Neuronal Death Caused by Ischemic Insults

Luo, Tianfei; Liu, Guiying; Ma, Haiying; Lü, Bin; Xu, Haidong; Wang, Yujing; Wu, Jiang; Ge, Pengfei; Liang, Jing

doi:10.3390/ijms150915426

Cited by 89 publications

(67 citation statements)

References 43 publications

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“…Similar result was found in human SH-SY5Y cells OGD model. In this model, activation of autophagy also relies on the PI3K/Akt/mTOR signaling pathway (Luo et al, 2014). Taken together, these studies strongly suggested that in neonatal hypoxia/ischaemia (HI) and primary cortical neurons OGC, rapamycin (mTOR) target axis could be a critical part of those integrated signalings which participate in the activation of autophagy.…”

Section: Autophagy Hypoxia and Mtormentioning

confidence: 80%

Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells

Fang

Tan

Zhang

2015

Cell Biology International

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Section: Autophagy Hypoxia and Mtormentioning

confidence: 80%

Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells

Fang

Tan

Zhang

2015

Cell Biology International

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“…Thus it is likely that miR-145 exerted its cardioprotective effects through an increase in autophagy and activation of the Akt signaling axis. On the other hand, some previous studies revealed that Akt inhibited autophagy (5,15). However, this variation may have been due to differences in the cells, tissues, organs, and species studied.…”

Section: Signal Transductionmentioning

confidence: 77%

MicroRNA-145 repairs infarcted myocardium by accelerating cardiomyocyte autophagy

Higashi

Yamada

Minatoguchi

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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We investigated whether microRNA-145 (miR-145) has a cardioprotective effect in a rabbit model of myocardial infarction (MI) and in H9c2 rat cardiomyoblasts. Rabbits underwent 30 min of coronary occlusion, followed by 2 days or 2 wk of reperfusion. Control microRNA (control group; 2.5 nmol/kg, n = 10) or miR-145 (miR-145 group, 2.5 nmol/kg, n = 10) encapsulated in liposomes was intravenously administered immediately after the start of reperfusion. H9c2 rat cardiomyoblasts were transfected with miR-145. The MI size was significantly smaller in the miR-145 group than in the control group at 2 days and 2 wk post-MI. miR-145 had improved the cardiac function and remodeling at 2 wk post-MI. These effects were reversed by chloroquine. Western blot analysis showed that miR-145 accelerated the transition of LC3B I to II and downregulated p62/SQSTM1 at 2 days or 2 wk after MI, but not at 4 wk, and activated Akt in the ischemic area at 2 days after MI. miR-145 inhibited the growth of H9c2 cells, accelerated the transition of LC3B I to II, and increased phosphorylated Akt in the H9c2 cells at 2 days after miR-145 transfection. Antagomir-145 significantly abolished the morphological change, the transition of LC3B I to II, and the increased phosphorylated Akt induced by miR-145 in H9c2 cells. We determined fibroblast growth factor receptor substrate 2 mRNA to be a target of miR-145, both in an in vivo model and in H9c2 cells. In conclusion, post-MI treatment with miR-145 protected the heart through the induction of cardiomyocyte autophagy by targeting fibroblast growth factor receptor substrate 2.

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“…However in another study, Rg1 was demonstrated to reduce aldosterone-induced autophagy via the AMPK/mTOR pathway in NRK-52E cells [38]. Similarly, Rb1 was reported to have positive [39] and negative [40] effects on neuronal autophagy, respectively, in two different papers. Although the difference in cell types and observation indexes may contribute to these inconsistent results, further work is needed to identify the specific effects of gisenosides on autophagy and the underlying mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb2 Alleviates Hepatic Lipid Accumulation by Restoring Autophagy via Induction of Sirt1 and Activation of AMPK

Huang

Wang

Yang

et al. 2017

IJMS

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Although Panax ginseng is a famous traditional Chinese medicine and has been widely used to treat a variety of metabolic diseases including hyperglycemia, hyperlipidemia, and hepatosteatosis, the effective mediators and molecular mechanisms remain largely unknown. In this study we found that ginsenoside Rb2, one of the major ginsenosides in Panax ginseng, was able to prevent hepatic lipid accumulation through autophagy induction both in vivo and in vitro. Treatment of male db/db mice with Rb2 significantly improved glucose tolerance, decreased hepatic lipid accumulation, and restored hepatic autophagy. In vitro, Rb2 (50 µmol/L) obviously increased autophagic flux in HepG2 cells and primary mouse hepatocytes, and consequently reduced the lipid accumulation induced by oleic acid in combination with high glucose. Western blotting analysis showed that Rb2 partly reversed the high fatty acid in combination with high glucose (OA)-induced repression of autophagic pathways including AMP-activated protein kinase (AMPK) and silent information regulator 1 (sirt1). Furthermore, pharmacological inhibition of the sirt1 or AMPK pathways attenuated these beneficial effects of Rb2 on hepatic autophagy and lipid accumulation. Taken together, these results suggested that Rb2 alleviated hepatic lipid accumulation by restoring autophagy via the induction of sirt1 and activation of AMPK, and resulted in improved nonalcoholic fatty liver disease (NAFLD) and glucose tolerance.

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Inhibition of Autophagy via Activation of PI3K/Akt Pathway Contributes to the Protection of Ginsenoside Rb1 against Neuronal Death Caused by Ischemic Insults

Cited by 89 publications

References 43 publications

Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells

Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells

MicroRNA-145 repairs infarcted myocardium by accelerating cardiomyocyte autophagy

Ginsenoside Rb2 Alleviates Hepatic Lipid Accumulation by Restoring Autophagy via Induction of Sirt1 and Activation of AMPK

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