β-Asarone protects PC12 cells against OGD/R-induced injury via attenuating Beclin-1-dependent autophagy

Mo, Zhentao; Fang, Yongqi; He, Yue; Zhang, Sheng

doi:10.1038/aps.2012.35

Cited by 66 publications

(46 citation statements)

References 22 publications

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“…In addition, we found that up‐expression of Beclin‐1‐dependent autophagy protected against β‐amyloid‐induced cell injury in PC12 cells . Also, β‐asarone protects PC12 cells against oxygen‐glucose deprivation and reperfusion‐induced injury by attenuating Beclin‐1‐dependent autophagy . A previous report from our group showed that β‐asarone attenuated ischemia‐reperfusion‐induced autophagy in rat brains by modulating c‐Jun N‐terminal kinase (JNK), phosphorylation of JNK, B‐cell lymphoma 2, and Beclin‐1 .…”

Section: Introductionmentioning

confidence: 70%

“…To further clarify the effect of β‐asarone and l ‐dopa co‐administration on autophagy, we employed trasmission electron microscopy, the standard method to detect autophagy . Coronal sections (50–150 μ m) were cut with a vibratome (UC7; Leica EM, Solms, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…and reperfusion-induced injury by attenuating Beclin-1-dependent autophagy. 16 A previous report from our group showed that b-asarone attenuated ischemia-reperfusion-induced autophagy in rat brains by modulating c-Jun N-terminal kinase (JNK), phosphorylation of JNK, B-cell lymphoma 2, and Beclin-1. 17 That is, b-asarone can regulate autophagy by Beclin-1.…”

Section: Introductionmentioning

confidence: 99%

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β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

Huang

Deng

et al. 2015

Clin Exp Pharma Physio

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In this study, we investigated Beclin-1, light chain (LC)3B, and p62 expression in 6-hydroxydopamine (6-OHDA)-induced parkinsonian rats after β-asarone and levodopa (l-dopa) co-administration. Unilateral 6-OHDA injection into the medial forebrain bundle was used to create the models, except in sham-operated rats. Rats were divided into eight groups: sham-operated group; 6-OHDA model group; madopar group (75 mg/kg, per os (p.o.)); l-dopa group (60 mg/kg, p.o.); β-asarone group (15 mg/kg, p.o.); β-asarone + l-dopa co-administered group (15 mg/kg + 60 mg/kg, p.o.); 3-methyladenine group (500 nmol, intraperitoneal injection); and rapamycin group (1 mg/kg, intraperitoneal injection). Then, Beclin-1, LC3B, and p62 expression in the mesencephalon were detected. The mesencephalon was also observed by transmission electron microscope. The results showed that Beclin-1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l-dopa, β-asarone, and co-administered groups when compared with the 6-OHDA model. Beclin-1 and LC3B expression in the β-asarone and co-administered groups were less than in the madopar or l-dopa groups, whereas p62 expression in the β-asarone and co-administered groups was higher than in the madopar or l-dopa groups. In addition, a significant decrease in autophagosome was exhibited in the β-asarone and co-administered groups when compared with the 6-OHDA group. Our findings indicate that Beclin-1 and LC3B expression decreased, whereas p62 expression increased after co-administration treatment. In sum, all data suggest that the co-administration of β-asarone and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity.

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Section: Introductionmentioning

confidence: 70%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

Huang

Deng

et al. 2015

Clin Exp Pharma Physio

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“…Cells were treated with OGD/R exposure as previously described [14]. Briefly, balanced salt solution was adopted to wash cells twice, which were then subjected to OGD medium without glucose (in mM: NaCl 116, CaCl 2 0.9, MgSO 4 0.8, KCl 5.4, NaH 2 PO 4 1, phenol red 110, pH 7.4).…”

Section: Oxygen Glucose Deprivation/reoxygenation (Ogd/r)mentioning

confidence: 99%

MALAT1 Activates the P53 Signaling Pathway by Regulating MDM2 to Promote Ischemic Stroke

Zhang

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study focused on evaluating the effect of MALAT1 and MDM2 on ischemic stroke through regulation of the p53 signaling pathway. Materials: Bioinformatics analysis was performed to identify abnormally expressed lncRNAs, mRNAs and their associated pathways. Oxygen-glucose deprivation/reoxygenation (OGD/R) in cells and middle cerebral artery occlusion/reperfusion (MCAO/R) in mice were performed to simulate an ischemic stroke environment. Western blot and qRT-PCR were used to examine lncRNA expression and mRNA levels. Fluorescence in situ hybridization (FISH) LncRNA was used to locate mRNA. MTT and flow cytometry were performed to examine cell proliferation and apoptosis. Finally, immunohistochemistry was used to observe the expression of genes in vivo. Results: MALAT1 and MDM2, which exhibit strong expression in stroke tissues, were subjected to bioinformatics analysis, and the p53 pathway was chosen for further study. MALAT1, MDM2 and p53 signaling pathway-related proteins were all up regulated in OGD/R cells. Furthermore, Malat1, Mdm2 and p53 pathway related-proteins were also up regulated in MCAO/R mice. Both MALAT1 and MDM2 were localized in the nuclei. Down regulation of MALAT1 and MDM2 enhanced cell proliferation ability and reduced apoptosis, resulting in decreased infarct size in MCAO/R brains. Conclusion: These results indicate that MALAT1/MDM2/p53 signaling pathway axis may provide more effective clinical therapeutic strategy for patients with ischemic stroke.

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“… The characteristic ultrastructural morphology of autophagosome (Mo et al, 2012) ( A ) Normal morphology was observed in cytoplasm of the normal control group. Autophagosomes can be hardly observed in this group.…”

Section: Resultsmentioning

confidence: 99%

Change of Beclin‐1 dependent on ATP, [Ca²⁺]_i and MMP in PC12 cells following oxygen‐glucose deprivation‐reoxygenation injury

Fang

et al. 2012

Cell Biology International

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Autophagy is usually up-regulated to provide more ATP in response to starvation or OGD (oxygen-glucose deprivation), but the relationship between autophagy and ATP, [Ca2+]i (intracellular free Ca2+ concentration) or MMP (mitochondrial membrane potential) during reoxygenation is not yet fully clear. The role of autophagy is unknown in PC12 cells subjected to 2 h OGD with different time points of reoxygenation. In the present study, we showed that Beclin-1 was up-regulated beginning at 0 h reoxygenation peaking at 24 h and lasting for 48 h. Cell viability was decreased from 0 to 48 h reoxygenation, reaching its minimum at 10 h reoxygenation. ATP was decreased from 0 to 10 h reoxygenation, reaching its minimum at 4 h reoxygenation. A significant negative correlation was observed between ATP and Beclin-1 (r = -0.61, P<0.05) at 0 h reoxygenation, but ATP was not significant related (r = 0.24, P>0.05) to Beclin-1 at 24 h reoxygenation. Besides, Nimodipine, a calcium antagonist, significantly reduced [Ca2+]i and Beclin-1, but increased MMP in OGD/R-treated cells. At 24 h reoxygenation, Beclin-1 expression reached its maximum, cell viability continued to increase, and ATP was higher than that before OGD. These results suggest that energy metabolism dysfunction can induce autophagy during OGD in PC12 cells. Increased [Ca2+]i and decreased MMP may induce autophagy during reoxygenation in PC12 cells. Autophagy may be a protective effect on PC12 cells treated with different time points of reoxygenation after 2 h OGD.

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β-Asarone protects PC12 cells against OGD/R-induced injury via attenuating Beclin-1-dependent autophagy

Cited by 66 publications

References 22 publications

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

MALAT1 Activates the P53 Signaling Pathway by Regulating MDM2 to Promote Ischemic Stroke

Change of Beclin‐1 dependent on ATP, [Ca²⁺]_i and MMP in PC12 cells following oxygen‐glucose deprivation‐reoxygenation injury

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β-Asarone protects PC12 cells against OGD/R-induced injury via attenuating Beclin-1-dependent autophagy

Cited by 66 publications

References 22 publications

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

MALAT1 Activates the P53 Signaling Pathway by Regulating MDM2 to Promote Ischemic Stroke

Change of Beclin‐1 dependent on ATP, [Ca2+]i and MMP in PC12 cells following oxygen‐glucose deprivation‐reoxygenation injury

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Change of Beclin‐1 dependent on ATP, [Ca²⁺]_i and MMP in PC12 cells following oxygen‐glucose deprivation‐reoxygenation injury