Neuroprotective effects of ginseng pectin through the activation of ERK/MAPK and Akt survival signaling pathways

Abstract

Abstract. In this study, we investigated the neuroprotective activities of ginseng pectin (GP) against hydrogen peroxide (H 2 O 2 )-induced neuronal toxicity in different neuronal cells. GP selectively attenuated H 2 O 2 -induced damage up to 26% in primary cortical neuron cells and human glioblastoma U87 cells. Following H 2 O 2 exposure, DAPI staining and neuron-specific β-tubulin antibody probing indicated that GP maintained cell integrity and decreased nuclei condensation. Data from western blot analysis revealed that pre-treatment with GP increased the phosphorylation of both the extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Akt in cortical neuron cells. However, the phosphorylation of ERK1/2 was increased, but that of Akt was decreased in U87 cells. These results suggest that the protective effects of GP against H 2 O 2 -induced apoptosis may be due to the activation of the phosphorylation of ERK1/2 and Akt; however, the mechanisms involved differ depending on the cell line. This neuroprotective property indicates that GP could serve as a potential therapeutic agent for neurodegenerative diseases.

Inositol pyrophosphates mediate the effects of aging on bone marrow mesenchymal stem cells by inhibiting Akt signaling

“…Similarly, Satyanarayana et al [32,33] have revealed that aging-induced muscle atrophy is associated with differences in the regulation of Akt and mTOR. Furthermore, it has been reported that reduced activation of extracellular signal-regulated kinase (ERK) and Akt kinase contributes to lower survival of aged hepatocytes which are more sensitive to H 2 O 2 -induced apoptosis [34,35]. In the present study, we observed impaired activation of Akt in the MSCs.…”

Beneficial effects of Panax ginseng for the treatment and prevention of neurodegenerative diseases: past findings and future directions

“…By contrast, ginseng polysaccharides are mainly composed of neutral polysaccharides (starch-like glucans) and acidic substances (ginseng pectin) [39] . Ginseng pectins have been reported to show a wider range of pharmacological activities compared with neutral polysaccharides [40] , [41] , and they are known to be composed of galacturonic acid, galactose, glucose, arabinose, rhamnose, glucuronic acid, and mannose [41] ; however, their exact structure is also unknown.…”

Emerging signals modulating potential of ginseng and its active compounds focusing on neurodegenerative diseases

“…Various studies have shown that ginsenosides Rg1 and Rg5 show beneficial effects through this pathway. Ginsenoside Rg1 enhances neurite outgrowth and protects against Aβ 25–35 -induced damage, and its mechanism may involve the activation of Akt signaling [71]. In LPS-stimulated BV-2 microglial cells and rat primary microglia, Rg5 produced an antiinflammatory activity.…”

“…Ginseng pectin pretreatment enhanced the phosphorylation of both the extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cortical neuron cells and in U87 cells, it also increased the ERK1/2 phosphorylation. Owing to the activation of the phosphorylation of ERK1/2, ginseng pectin produced this neuroprotective activity against H 2 O 2 -induced apoptosis [71]. In LPS-induced RAW 264.7 cells, synthesized gold nanoparticles (AuNPs) using Panax ginseng exert antiinflammatory effects through p38 MAPK [72].…”

“…In addition, due to the NF-κB–mediated transcription, an increase of cAMP responsive element-binding protein might have been identified.[90]ReLPS-induced BV-2 microgliaProduces the neuroprotective events through the phospho-p38, iNOS and COX-2 signaling pathways.[89]RMOLPS-induced RAW 264.7 macrophagesReduces the p38 MAPK and its upstream kinases including MAPK kinases 3/6 (MKK3/6) phosphorylation.[70]LPS-induced RAW 264.7 macrophagesReduces the iNOS and COX-2 at both mRNA and protein levels, blockade of nuclear translocation of the p65 subunit. Henceforth, due to the inhibition of NF-κB transcriptional activity, it might have produced this anti-inflammatory effect.[70]Ginseng PectinH 2 O 2 -induced apoptosis in cortical neuron cells and U87 cellsPretreatment enhances the phosphorylation of both the extracellular signal-regulated kinases 1 and 2 (ERK1/2).[71]AuNPsLPS-induced RAW 264.7 cellsExerts anti-inflammatory effects through the suppression of NF-κB signaling pathway activation through p38 MAPK.[72]LPS-induced RAW 264.7 cellsDecreases inflammatory mediators such as NO, prostaglandin E2, interleukin-6 and tumor necrosis factor-α, expression.[72]GintoninLPS-induced RAW 264.7 cellsProduces anti-inflammatory activity via the signal transduction through MAPK, and potently suppresses the nitric oxide production and also efficiently suppressed the proinflammatory cytokines levels.[73]LPS-induced RAW 264.7Effectively suppresses the NO production without any cytotoxicity and also proficiently suppresses the proinflammatory cytokines levels. Furthermore, facilitates signal transduction through NF- κ B pathways and recovers the mir-34a and mir-93 levels.[73]NGR1H 2 O 2 -induced PC12 cellsProduces neuroprotective activity the effect by inducing an estrogen receptor-dependent ERK1/2 pathway.[83]Compound KPhorbol myristate acetate–mediated human astroglioma cellsSignificantly suppresses the p38 MAPK, ERK, and JNK activation, which are upstream modulators of activator protein-1.[84]GinsengAdvanced glycation end product– induced AD in ratShows neuroprotective effects through the significant decreasing the expression of receptor for advanced glycation end-products and NF-κB.[86]AD, Alzheimer's disease; APP, amyloid β-protein precursor; AuNPs, synthesized gold nanoparticles; CaMKIIα, calcium/calmodulin-dependent protein kinase type II alpha chain; JNK, c-Jun N-terminal kinase; LPS, lypopolysaccharide; MAPK, mitogen-a...…”