Inhibition of β-amyloid1-40 Peptide Aggregation and Neurotoxicity by Citrate

Park, Yong Hoon; Kim, Young‐Jin; Son, Ilhong; Yang, Hyun Duk

doi:10.4196/kjpp.2009.13.4.273

Cited by 7 publications

(6 citation statements)

References 53 publications

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“…Cells were stained with Hoechst 33342 to distinguish apoptotic cells as previously described method with slight modifications [23]. Cells were treated with PAM with or without OLA for 2 days, washed with PBS, fixed with 4% paraformalin for 15 min, and then stained with 1 µM Hoechst 33342 for 60 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms

Ahn

Kim

Kwon

et al. 2013

Korean J Physiol Pharmacol

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Palmitic acid (PAM), one of the most common saturated fatty acid (SFA) in animals and plants, has been shown to induce apoptosis in exocrine pancreatic AR42J cells. In this study, we investigated cellular mechanisms underlying protective effects of oleic acid (OLA) against the lipotoxic actions of PAM in AR42J cells. Exposure of cells to long-chain SFA induced apoptotic cell death determined by MTT cell viability assay and Hoechst staining. Co-treatment of OLA with PAM markedly protected cells against PAM-induced apoptosis. OLA significantly attenuated the PAM-induced increase in the levels of pro-apoptotic Bak protein, cleaved forms of apoptotic proteins (caspase-3, PARP). On the contrary, OLA restored the decreased levels of anti-apoptotic Bcl-2 family proteins (Bcl-2, Bcl-xL, and Mcl-1) in PAM-treated cells. OLA also induced up-regulation of the mRNA expression of Dgat2 and Cpt1 genes which are involved in triacylglycerol (TAG) synthesis and mitochondrial β-oxidation, respectively. Intracellular TAG accumulation was increased by OLA supplementation in accordance with enhanced expression of Dgat2 gene. These results indicate that restoration of anti-apoptotic/pro-apoptotic protein balance from apoptosis toward cell survival is involved in the cytoprotective effects of OLA against PAM-induced apoptosis in pancreatic AR42J cells. In addition, OLA-induced increase in TAG accumulation and up-regulation of Dgat2 and Cpt1 gene expressions may be possibly associated in part with the ability of OLA to protect cells from deleterious actions of PAM.

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Section: Methodsmentioning

confidence: 99%

Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms

Ahn

Kim

Kwon

et al. 2013

Korean J Physiol Pharmacol

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“…Recently, the time-and concentration-dependent aggregation of Aβ was mathematically quantified [3]. Alternatively, the fibrous cross-β sheet form of tau-protein fibrils in the cerebrospinal fluid (CSF) was also found to be cerebrum toxic [5][6][7][8]. Antrodia cinnamomea (AC) (Fomitopsidaceae), once named Antrodia camphorata by Wu et al (1997), is the unique medicinal fungus merely grown in Taiwan [9].…”

mentioning

confidence: 99%

Antrodia cinnamomea Exhibits a Potent Neuroprotective Effect in the PC12 Cell-Aβ25–35 Model – Pharmacologically through Adenosine Receptors and Mitochondrial Pathway

et al. 2012

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Antrodia cinnamomea has a diversity of therapeutic effects including anticancer properties. Its neuroprotective effect is rarely cited. We hypothesized that due to its high phenol, triterpenoid, and adenosine contents, it might exhibit a potent neuroprotective effect. The PC12 cell model was used to investigate its pharmaceutical effects. Congo red staining was used to identify the activation of Aβ25-35. Chemical analysis indicated that the ethanolic extract of Antrodia cinnamomea contained a huge amount (mg/g ethanolic extract of Antrodia cinnamomea) of polyphenolics (133 ± 7), flavonoids (114 ± 6), triterpenoids (175 ± 26), and adenosine (370 ± 17). When tested with Aβ25-35 (15 µM), the cell viability was suppressed in a dose-dependent fashion with an IC50 value of 10 µM. The biochemical parameters upregulated by Aβ25-35 (15 µM) involved TNF-α, ROS, MDA, NO, and the intracellular calcium ions. These adverse effects were effectively ameliorated by the ethanolic extract of Antrodia cinnamomea (1 µg/mL). The Western blot analysis revealed that Aβ25-35 downregulated BcL-2/Bax and upregulated cleaved caspases-9 and - 3 without affecting cleaved caspase-8. The G2/M arrest elicited by Aβ25-35 was ameliorated by the ethanolic extract of Antrodia cinnamomea. TUNEL assay confirmed the apoptosis, and the ethanolic extract of Antrodia cinnamomea downregulated adenosine A1 and adenosine A2A receptors. Taken together, Aβ25-35 tends to induce neurotoxicity on PC12 cells. The ethanolic extract of Antrodia cinnamomea is capable of suppressing its neurotoxicity by rescuing the mitochondrial apoptosis pathway and simultaneously by downregulating adenosine A1 and adenosine A2A receptors to retard neurodegeneration and memory dysfunction.

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“…After pretreatment with ω-3 fatty acids, Aβ1-40 in serum-free medium was added to the H19-7 cells. Based on previous studies, 30 μM of Aβ1-40 peptide was chosen to induce neurotoxicity including oxidative stress, inflammation and apoptosis [ 30 ]. For Aβ-induced neuroinflammation, 100 ng/mL LPS (Sigma, St. Louis, MO, USA) was added together with Aβ1-40.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective Effect of Stearidonic Acid on Amyloid β-Induced Neurotoxicity in Rat Hippocampal Cells

Lai

Zheng

et al. 2022

Antioxidants

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Dietary intake of omega-3 fatty acids found in fish has been reported to reduce the risk of Alzheimer’s Disease (AD). Stearidonic acid (SDA), a plant-based omega-3 fatty acid, has been targeted as a potential surrogate for fish-based fatty acids. However, its role in neuronal degeneration is unknown. This study was designed to evaluate effects of SDA on Amyloid-β(A-β)-induced neurotoxicity in rat hippocampal cells. Results showed that SDA effectively converted to eicosapentaenoic acid (EPA) in hippocampal cells. Aβ-induced apoptosis in H19-7 cells was protected by SDA pretreatment as evidenced by its regulation on the expression of relevant pro- and anti-apoptotic genes, as well as the inhibition on caspase activation. SDA also protected H19-7 cells from Aβ-induced oxidative stress by regulating the expression of relevant pro- and anti-oxidative genes, as well as the improvement in activity of catalase. As for Aβ/LPS-induced neuronal inflammation, SDA pretreatment reduced the release of IL-1β and TNFα. Further, we found that the anti-Aβ effect of SDA involves its inhibition on the expression of amyloid precursor protein and the regulation on MAPK signaling. These results demonstrated that SDAs have neuroprotective effect in Aβ-induced H19-7 hippocampal cells. This beneficial effect of SDA was attributed to its antiapoptotic, antioxidant, and anti-inflammatory properties.

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Inhibition of β-amyloid1-40 Peptide Aggregation and Neurotoxicity by Citrate

Cited by 7 publications

References 53 publications

Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms

Protective Effects of Oleic Acid Against Palmitic Acid-Induced Apoptosis in Pancreatic AR42J Cells and Its Mechanisms

Antrodia cinnamomea Exhibits a Potent Neuroprotective Effect in the PC12 Cell-Aβ25–35 Model – Pharmacologically through Adenosine Receptors and Mitochondrial Pathway

Neuroprotective Effect of Stearidonic Acid on Amyloid β-Induced Neurotoxicity in Rat Hippocampal Cells

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