Protective effects of icariin extracted from epimedii herba on fetal rat hippocampal neurons

Trimethyltin (TMT) is an organotin compound with potent neurotoxic action characterized by neuronal degeneration in the hippocampus. This study evaluated the protective effects of a Scolopendra water extract (SWE) against TMT intoxication in hippocampal neurons, using both in vitro and in vivo model systems. Specifically, we examined the actions of SWE on TMT- (5 mM) induced cytotoxicity in primary cultures of mouse hippocampal neurons (7 days in vitro) and the effects of SWE on hippocampal degeneration in adult TMT- (2.6 mg/kg, intraperitoneal) treated C57BL/6 mice. We found that SWE pretreatment (0–100 μg/mL) significantly reduced TMT-induced cytotoxicity in cultured hippocampal neurons in a dose-dependent manner, as determined by lactate dehydrogenase and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assays. Additionally, this study showed that perioral administration of SWE (5 mg/kg), from −6 to 0 days before TMT injection, significantly attenuated hippocampal cell degeneration and seizures in adult mice. Furthermore, quantitative analysis of Iba-1 (Allograft inflammatory factor 1)- and GFAP (Glial fibrillary acidic protein)-immunostained cells revealed a significant reduction in the levels of Iba-1- and GFAP-positive cell bodies in the dentate gyrus (DG) of mice treated with SWE prior to TMT injection. These data indicated that SWE pretreatment significantly protected the hippocampus against the massive activation of microglia and astrocytes elicited by TMT. In addition, our data showed that the SWE-induced reduction of immune cell activation was linked to a significant reduction in cell death and a significant improvement in TMT-induced seizure behavior. Thus, we conclude that SWE ameliorated the detrimental effects of TMT toxicity on hippocampal neurons, both in vivo and in vitro. Altogether, our findings hint at a promising pharmacotherapeutic use of SWE in hippocampal degeneration and dysfunction.

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Protective effects of T-588, a novel cognition enhancer, on β-amyloid protein, serum deprivation and glutamate induced neurotoxicity in primary rat hippocampal neurons and cerebellar granule cells

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)45621-7 ◽

1997 ◽

Vol 73 ◽

pp. 280

Author(s):

Noboru Iwakami ◽

Hidetoshi Yamaguchi ◽

Satoshi Ono ◽

Hirokazu Narita

Keyword(s):

Hippocampal Neurons ◽

Granule Cells ◽

Cerebellar Granule Cells ◽

Serum Deprivation ◽

Protective Effects ◽

Amyloid Protein ◽

Cerebellar Granule ◽

Β Amyloid ◽

Protein Serum

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11beta-hydroxylase and aldosterone synthase expression in fetal rat hippocampal neurons

Journal of Molecular Endocrinology ◽

10.1677/jme.0.0290319 ◽

2002 ◽

Vol 29 (3) ◽

pp. 319-325 ◽

Cited By ~ 13

Author(s):

SM MacKenzie ◽

M Lai ◽

CJ Clark ◽

R Fraser ◽

CE Gomez-Sanchez ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Hippocampal Neurons ◽

Primary Cultures ◽

Local System ◽

Model System ◽

Biochemical Reactions ◽

Aldosterone Synthase ◽

Fetal Rat ◽

The Central Nervous System

The central nervous system produces many of the enzymes responsible for corticosteroid synthesis. A model system to study the regulation of this local system would be valuable. Previously, we have shown that primary cultures of hippocampal neurons isolated from the fetal rat can perform the biochemical reactions associated with the enzymes 11beta-hydroxylase and aldosterone synthase. Here, we demonstrate directly that these enzymes are present within primary cultures of fetal rat hippocampal neurons.

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Protective effects of phytoestrogen α-zearalanol on beta amyloid25–35 induced oxidative damage in cultured rat hippocampal neurons

Endocrine ◽

10.1007/s12020-007-9032-z ◽

2007 ◽

Vol 32 (2) ◽

pp. 206-211 ◽

Cited By ~ 6

Author(s):

Yi-Long Dong ◽

Ping-Ping Zuo ◽

Qing Li ◽

Feng-Hua Liu ◽

Shun-Ling Dai ◽

...

Keyword(s):

Oxidative Damage ◽

Hippocampal Neurons ◽

Protective Effects

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Adiponectin Protects against Glutamate-Induced Excitotoxicity via Activating SIRT1-Dependent PGC-1αExpression in HT22 Hippocampal Neurons

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/2957354 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 19

Author(s):

Liang Yue ◽

Lei Zhao ◽

Haixiao Liu ◽

Xia Li ◽

Bodong Wang ◽

...

Keyword(s):

Western Blot ◽

Cell Viability ◽

Cell Apoptosis ◽

Hippocampal Neurons ◽

Caspase 3 ◽

Critical Role ◽

Tunel Staining ◽

Peroxisome Proliferator ◽

Protective Effects ◽

Expression Levels

Glutamate- (Glu-) induced excitotoxicity plays a critical role in stroke. This study aimed to investigate the effects of APN on Glu-induced injury in HT22 neurons. HT22 neurons were treated with Glu in the absence or the presence of an APN peptide. Cell viability was assessed using the MTT assay, while cell apoptosis was evaluated using TUNEL staining. Levels of LDH, MDA, SOD, and GSH-Px were detected using the respective kits, and ROS levels were detected using dichlorofluorescein diacetate. Western blot was used to detect the expression levels of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), cleaved caspase-3, Bax, and Bcl-2. In addition to the western blot, immunofluorescence was used to investigate the expression levels of SIRT1 and PGC-1α. Our results suggest that APN peptide increased cell viability, SOD, and GSH-Px levels and decreased LDH release, ROS and MDA levels, and cell apoptosis. APN peptide upregulated the expression of SIRT1, PGC-1α, and Bcl-2 and downregulated the expression of cleaved caspase-3 and Bax. Furthermore, the protective effects of the APN peptide were abolished by SIRT1 siRNA. Our findings suggest that APN peptide protects HT22 neurons against Glu-induced injury by inhibiting neuronal apoptosis and activating SIRT1-dependent PGC-1αsignaling.

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