Polygalasaponin F against rotenone-induced apoptosis in PC12 cells via mitochondria protection pathway

Wu, Miaomiao; Yuan, Yu‐He; Chen, Jiao; Li, Chuang‐Jun; Zhang, Dongming; Chen, Nai‐Hong

doi:10.1080/10286020.2013.864283

Cited by 8 publications

(3 citation statements)

References 25 publications

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“…Recent pharmacological studies have shown that P. tenuifolia could improve memory impairment caused by scopolamine, stress, glutamate, and Aβ, and promote neuronal proliferation in normal brains (Chung et al, 2002;Lin et al, 2012;Li et al, 2014). Polygalasaponins, such as polygalasaponin B, F, G, and XXXII, are the main components responsible for the action of P. tenuifolia and have been shown to improve cognitive impairment in AD effectively (Ikeya et al, 2004;Xu et al, 2009;Wu et al, 2014). However, reports have shown that polygalasaponins could be toxic to animals, leading to nose bleeding, gastrointestinal tract abnormality, and even death (Xue et al, 2009;Lin et al, 2012), which seriously limits their application and development.…”

Section: Introductionmentioning

confidence: 99%

Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Wang

et al. 2016

J. Zhejiang Univ. Sci. B

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Abstract:Objectives: The aim of the study is to evaluate the cognitive-enhancing effects of hydrolysate of polygalasaponin (HPS) on senescence accelerate mouse P8 (SAMP8) mice, an effective Alzheimer's disease (AD) model, and to research the relevant mechanisms. Methods: The cognitive-enhancing effects of HPS on SAMP8 mice were assessed using Morris water maze (MWM) and step-through passive avoidance tests. Then N-methyl-D-aspartate (NMDA) receptor subunit expression for both the cortex and hippocampus of mice was observed using Western blotting. Results: HPS (25 and 50 mg/kg) improved the escape rate and decreased the escape latency and time spent in the target quadrant for the SAMP8 mice in the MWM after oral administration of HPS for 10 d. Moreover, it decreased error times in the passive avoidance tests. Western blotting showed that HPS was able to reverse the levels of NMDAR1 and NMDAR2B expression in the cortex or hippocampus of model mice. Conclusions: The present study suggested that HPS can improve cognitive deficits in SAMP8 mice, and this mechanism might be associated with NMDA receptor (NMDAR)-related pathways.

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Section: Introductionmentioning

confidence: 99%

Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Wang

et al. 2016

J. Zhejiang Univ. Sci. B

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“…Apoptosis is a form of cell death, and it is also the main cause of rotenone damage to PC12 cells (19) . PARP is an important DNA repair enzyme, which can specifically recognize and bind to the broken ends of DNA.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Tetrahydroxystilbene Glucoside against Rotenone-Induced Toxicity in PC12 Cells

Xing

Wang

et al. 2022

Biological & Pharmaceutical Bulletin

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To investigate the mechanism of the protective effect of tetrahydroxystilbene glucoside (TSG) on nerve cells, an injury model induced by rotenone in PC12 cells was constructed. Cell viability was detected by using CCK8 assay. Apoptosis was detected by using flow cytometry. The mitochondrial membrane potential (MMP) was detected by using the fluorescent probe JC-1. Generation of reactive oxygen species (ROS) in PC12 cells was determined using the CM-H 2 DCFDA probe. Protein expression in PC12 cells was detected using western blotting. The results showed that TSG (20-100 μM) attenuated the cytotoxic effects of rotenone on PC12 cells. TSG pretreatment attenuated the apoptosis rate, the degradation of PARP and the activation of cleaved caspase 3, which was induced by rotenone. TSG can significantly reduce the effect of rotenone on the reduction of MMP and the expression of cytoC in the cytosolic fraction. TSG attenuated rotenone-induced de-phosphorylation and mitochondrial translocation of cofilin, as well as rotenone-induced accumulation of ROS. The western blot results showed that ROT could decrease the expression level of p-GSK-3β and p-AKT, and TSG could weaken these effects of rotenone. In addition, TSG increased the expression level of Nrf2 in the nuclear fraction. These results suggest that TSG could protect PC12 cells against rotenone through multiple pathways. Thus, TSG has the potential to become a novel neuroprotective agent.

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“…Polygalasaponin F (PS-F), the structure of which is shown in Figure 1, is an oleanane-type triterpenoid saponin extracted from P. japonica. Previous research has demonstrated that PS-F is a neuroprotective compound [1,2] that can attenuate the expression of tumor necrosis factor a (TNFa) in BV2 microglial cells stimulated by lipopolysaccharides (LPS), demonstrating its anti-inflammation function. However, its molecular mechanism requires further research.…”

Section: Introductionmentioning

confidence: 99%

The molecular mechanism of polygalasaponin F-mediated decreases in TNFα: emphasizing the role of the TLR4-PI3K/AKT-NF-κB pathway

Yan

Shao

Zhang

et al. 2015

Journal of Asian Natural Products Research

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Polygalasaponin F (PS-F), an oleanane-type triterpenoid saponin extracted from Polygala japonica, decreases the release of the inflammatory cytokine tumor necrosis factor α (TNFα), but the precise molecular mechanisms by which this event occurs are not fully understood. To study the anti-neuroinflammatory mechanisms of PS-F, enzyme-linked immunosorbent assay was used to detect the secretion of TNFα from BV-2 microglial cells. Nuclear proteins extracted from BV-2 microglial cells stimulated by lipopolysaccharide (LPS) and pretreated with/without inhibitors were measured by Western blotting, and cell viability was evaluated by MTT analysis. The results indicated that inhibition of toll-like receptor (TLR) 4 (CLI-095 1 μg/ml), phosphatidylinositol 3-kinase (PI3K) (Ly294002 10 μM) or IκBα phosphorylation (Bay11-7082 10 μM) completely prevents the release of TNFα induced by LPS without affecting cell viability and attenuated the nuclear translocation of p65 stimulated by LPS. In addition, PS-F exhibited a similar trend regarding TNFα release, AKT phosphorylation and NF-κB translocation. These results suggest that PS-F reduces neuroinflammatory cytokine secretion through the regulation of the TLR4-PI3K/AKT-NF-κB signaling pathway.

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Polygalasaponin F against rotenone-induced apoptosis in PC12 cells via mitochondria protection pathway

Cited by 8 publications

References 25 publications

Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Cognitive-enhancing effects of hydrolysate of polygalasaponin in SAMP8 mice

Neuroprotective Effects of Tetrahydroxystilbene Glucoside against Rotenone-Induced Toxicity in PC12 Cells

The molecular mechanism of polygalasaponin F-mediated decreases in TNFα: emphasizing the role of the TLR4-PI3K/AKT-NF-κB pathway

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