Neuroprotective effect of polysaccharide separated from Perilla frutescens Britton var. acuta Kudo against H2O2-induced oxidative stress in HT22 hippocampus cells. Issue 8 (3rd August 2018)

• Record Type: Journal Article
• Authors: Byun, Eui-Baek; Cho, Eun-Ji; Kim, Yi-Eun; Kim, Woo Sik; Byun, Eui-Hong
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 82:Issue 8(2018)
• Page Start: 1344
• Page End: 1358
• Publication Date: 2018-08-03
• Subjects: Perilla frutescens Britton var. acuta Kudo -- polysaccharide -- neurotoxicity -- oxidative stress -- neuroprotection; ABTS2: 2′-azino-bis-(3-ethylbenzothiazoline-6-sulfonicacid) -- AD: Alzheimer's disease -- ARE: antioxidant response element -- DPPH: 1, 1-diphenyl-picrylhydrazyl -- DCFH-DA: 2′, 7′-dichlorofluorescin diacetate -- ECL: electrochemiluminescence -- ERK: extracellular regulated kinase -- FBS: Fetal bovine serum -- FITC: fluorescein isothiocyanate -- FRAP: ferric reducing antioxidant power -- HO-1: Heme oxygenase-1 -- JNK: c-jun N-terminal kinase -- MAPKs: mitogen-activated protein kinases -- MDA: malondialdehyde -- MMP: mitochondrial membrane potential -- MTT: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide -- NQO1: NAD(P)H quinine oxidoreductase 1 -- Nrf2: nuclear factor-E2-related factor 2 -- PD: parkinson's disease -- PEPF: polysaccharide extracts isolated from Perilla frutescens -- PI3K: phosphatidylinositol-3kinase -- PVDF: polyvinylidene difluoride -- ROS: reactive oxygen species -- SOD: Superoxidedismutase -- TPTZ: tripydyltriazine; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2018.1460572
• Languages: English
• ISSNs: 0916-8451

Abstract

ABSTRACT: This study was carried out to evaluate the neuroprotective activity of polysaccharide extracts isolated from Perilla frutescens (PEPF) in H2 O2 -treated HT22 hippocampus cells. The PEPF treatment was found to increase the anti-oxidant activities of HT22 hippocampus cells. PEPF treatment resulted in a significant protection of HT22 hippocampus cells against H2 O2 -induced neurotoxicity, this protection ultimately occurred through an inhibition of ROS-mediated intracellular Ca 2+ levels leading to MAPKs and NF-κB, as well as the accumulation of PI3K/AKT and Nrf2-mediated HO-1/NQO1 pathways. Furthermore, PEPF not only decreased the expression of Bax, cytochrome c, and cleaved caspases-3, -8, and -9, but also increased the expression of PARP and Bcl-2 in the H2 O2 -treated HT22 hippocampus cells, which overall contributed to the neuroprotective action. PEPF retains its mitochondrial membrane potential and reduces the elevated levels of sub-G1 phase and apoptotic morphological features induced by H2 O2 . It also reduces the malondialdehyde levels and enhances the intracellular SOD activity. Abstract : : Neuroprotective effect of PEPF against H2 O2 -induced oxidative stress in HT22 hippocampus cells.