Parthenolide attenuates cerebral ischemia/reperfusion injury via Akt/GSK-3β pathway in PC12 cells

Zhang, Junfeng; Zhang, Li; Shi, Lili; Zhao, Zhaohua; Xu, Hao; Liang, Fei; Li, Hongbo; Zhao, Yan; Xu, Xi; Yang, Ke; Tian, Yingfang

doi:10.1016/j.biopha.2017.03.009

Cited by 33 publications

(40 citation statements)

References 29 publications

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“…Winherb Medical Science Co., Ltd. (Shanghai, China), and the purity of NOB higher than 98% was detected by high-performance liquid chromatography (HPLC) analysis as previous demonstrations (11,13). PC12 cells were obtained from the American Type Cell Culture Collection (ATCC; Manassas, VA) (16). Dulbecco's modified Eagle's medium (DMEM), fetal bovine serum (FBS), 0.25% trypsin, and PBS were obtained from Gibco; Thermo Fisher Scientific, Inc. (Waltham, MA, USA).…”

Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

“…Cell culture. The PC12 cells were routinely cultured in DMEM/F12 medium supplemented with 10% FBS, 100 U/ml of penicillin, and 100 mg/ml of streptomycin in a humidified atmosphere of 5% CO 2 and 95% O 2 at 37˚C (16)(17)(18). The cells were fed every 2-3 days and sub-cultured once they reached 70-80% confluent.…”

Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

“…OGD/R injury and experimental designation. To mimic the I/R conditions in vitro, the PC12 cells were subjected to OGD/R treatment according to a prior demonstrations with minor modifications (16)(17)(18). In detail, the cells were washed two times with glucose-free Earle's balanced salt solution, and were maintained in glucose-free DMEM without FBS.…”

Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

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Nobiletin protects PC12 cells from ERS‑induced apoptosis in OGD/R injury via activation of the PI3K/AKT pathway

Yang

Zhang

et al. 2018

Exp Ther Med

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Nobiletin (NOB) possesses multiple pharmacological effects, but its anti-apoptotic property has acquired a great deal of attention. Endoplasmic reticulum (ER) stress (ERS)-induced apoptosis acts as the pivotal aetiology in neuronal oxygen-glucose deprivation and reoxygenation (OGD/R) injury. The aim of this study focused on whether NOB exerts neuro-protective effects on OGD/R injury by repressing ERS-induced apoptosis. The PC12 neuronal cell line was subjected to 4 h OGD and 24 h reoxygenation following NOB treatment. A PI3K/AKT inhibitor (LY294002) was added during the mechanistic experiments. Cell viability, lactate dehydrogenase (LDH) release and apoptosis were determined. Western blotting was used to measure protein expression levels. The results showed that OGD/R caused neuronal damageas exhibited by the increase in LDH release and the reduction of cellular viability. Moreover, ERS-induced apoptosis was markedly stimulated by OGD/R in PC12 cells, as evidenced by the elevation in the apoptotic rate and protein levels of C/EBP homologous protein/glucose-regulated protein-78. However, NOB administration significantly reversed neuronal damage and the ERS-induced apoptosis in response to OGD/R injury. Mechanistic detections showed that the neuron-favorable and ERS-repressing contributions of NOB were, in part, a result of the activation of the PI3K/AKT pathway, which was validated by a specific PI3K/AKT inhibitor (LY294002). Therefore, NOB protects PC12 cells from ERS-induced apoptosis in OGD/R injury mainly through enhancement of the PI3K/AKT pathway, which may provide a novel therapeutic avenue for the prevention of cerebral ischemia/reperfusion injury.

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Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

Section: Chemicals and Reagents Nob Was Purchased From Shanghaimentioning

confidence: 99%

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Nobiletin protects PC12 cells from ERS‑induced apoptosis in OGD/R injury via activation of the PI3K/AKT pathway

Yang

Zhang

et al. 2018

Exp Ther Med

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“…23 In addition, other studies have also argued that PTL ameliorated oxygen-glucose deprivation-induced apoptosis and oxidative stress in PC12 cells. 24 Although evidence has proved that it could effectively alleviate cancer cachexia and improve skeletal muscle characteristics in vivo, 25 little is known regarding the effects of PTL on the pathophysiological processes of oxidative stress-associated skeletal muscle diseases. In the present study, hydrogen peroxide (H 2 O 2 ), a strong oxidant, was sufficient for inducing oxidative stress in vitro.…”

Section: Introductionmentioning

confidence: 99%

Parthenolide regulates oxidative stress‐induced mitophagy and suppresses apoptosis through p53 signaling pathway in C2C12 myoblasts

Ren

et al. 2019

J of Cellular Biochemistry

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Muscle redox disturbances and oxidative stress have emerged as a common pathogenetic mechanism and potential therapeutic intervention in some muscle diseases. Parthenolide (PTL), a sesquiterpene lactone found in large amounts in the leaves of feverfew, possesses anti‐inflammatory, anti‐migraine, and anticancer properties. Although PTL was reported to alleviate cancer cachexia and improve skeletal muscle characteristics in a cancer cachexia model, its actions on oxidative stress‐induced damage in C2C12 myoblasts have not been reported and the regulatory mechanisms have not yet been defined. In our study, PTL attenuated H2O2‐induced growth inhibition and morphological changes. Furthermore, PTL exhibited scavenging activity against reactive oxygen species and protected C2C12 cells from apoptosis in response to H2O2. Meanwhile, PTL suppressed collapse of the mitochondrial membrane potential, thereby contributing to normalizing H2O2‐induced autophagy flux and mitophagy, correlating with inhibiting degradation of mitochondrial marker protein TIM23, the increase in LC3‐II expression and the reduction of mitochondria DNA. Besides its protective effect on mitochondria, PTL also prevented H2O2‐induced lysosomes damage in C2C12 cells. In addition, the phosphorylation of p53, cathepsin B, and Bax/Bcl‐2 protein levels, and the translocation of Bax from the cytosol to mitochondria induced by H2O2 in C2C12 cells was significantly reduced by PTL. In conclusion, PTL modulates oxidative stress‐induced mitophagy and protects C2C12 myoblasts against apoptosis, suggesting a potential protective effect against oxidative stress‐associated skeletal muscle diseases.

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“…PC12 cells possess the phenotypic and physiological properties of sympathetic neurons . Moreover, as reported, OGD is widely used as an in vitro model for CCH‐related diseases because cessation of blood flow deprives the brain of essential components (oxygen and glucose), while restoration of oxygen and glucose represents a return of blood flow to the hypoperfusion injured brain . Hence, differentiated PC12 cells exposed to OGD have been commonly used for studying the mechanism of hypoxia‐induced neurological disease.…”

Section: Introductionmentioning

confidence: 99%

Ligustrazine suppresses neuron apoptosis via the Bax/Bcl‐2 and caspase‐3 pathway in PC12 cells and in rats with vascular dementia

et al. 2017

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The aim of this study was to examine the comprehensive neuroprotective mechanism of ligustrazine, which is extracted from Ligusticum Chuanxiong Hort., against vascular dementia (VD) in rats and apoptosis in oxygen and glucose deprivation (OGD) PC12 cells. Rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery and administered ligustrazine intragastrically for 6 weeks. At the end of the experiments, the hippocampal biomarkers brain-derived neurotrophic factor (BDNF), monocyte chemotactic protein 1 (MCP-1), and homocysteine (Hcy) were examined. In experiments in vitro, OGD PC12 cells were treated with ligustrazine for 0.5, 1, 3, 6, 12, or 24 h. The cell-released biomarkers BDNF, MCP-1, and Hcy were examined. Microscopy, acridine orange-ethidium bromide (AO/ EB) staining, and flow cytometry assays were performed to investigate apoptosis. Cleaved caspase-3, Bcl-2 associated X protein (Bax), and B cell lymphoma 2 (Bcl-2) expression was examined using Western blot assays. The results showed that biomarkers, including MCP-1 and Hcy, were significantly increased in both the in vivo and in vitro models, while the BDNF level was significantly decreased compared with the sham or vehicle models. Microscopy, AO/EB staining, and flow cytometry analysis showed that severe cell damage occurred in OGD PC12 cells, and apoptosis played a major role in this environment. Further Western blot studies showed that the apoptosis-related Bax/Bcl-2 protein ratio and cleaved caspase-3 were significantly increased in the experiment. However, ligustrazine profoundly suppressed the imbalance of these biomarkers, reduced cell damage, decreased the Bax/Bcl-2, and downregulated cleaved caspase-3. Pro-and anti-apoptotic biomarkers of multiple pathways including BDNF, MCP-1, and Hcy played a joint role in triggering the activation of the mitochondria-related Bax/Bcl-2 and caspase-3 apoptosis pathway in VD. Ligustrazine attenuated VD by comprehensively regulating BDNF, MCP-1, and Hcy and inactivating the Bax/Bcl-2 and caspase-3 apoptosis pathway. Our data provide novel insight into ligustrazine, which is a promising neuroprotective agent for VD disease treatment strategies.

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Parthenolide attenuates cerebral ischemia/reperfusion injury via Akt/GSK-3β pathway in PC12 cells

Cited by 33 publications

References 29 publications

Nobiletin protects PC12 cells from ERS‑induced apoptosis in OGD/R injury via activation of the PI3K/AKT pathway

Nobiletin protects PC12 cells from ERS‑induced apoptosis in OGD/R injury via activation of the PI3K/AKT pathway

Parthenolide regulates oxidative stress‐induced mitophagy and suppresses apoptosis through p53 signaling pathway in C2C12 myoblasts

Ligustrazine suppresses neuron apoptosis via the Bax/Bcl‐2 and caspase‐3 pathway in PC12 cells and in rats with vascular dementia

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