Comparison of neuroprotective effects of extract and fractions fromAgarum clathratumagainst experimentally induced transient cerebral ischemic damage

Abstract

Objective: We investigated the neuroprotective effects of crude-extract, ethyl acetate (EA)-, n-butanol (BU)-, dichloromethane (DCM)-and n-hexane (Hx)-fractions from A. clathratum on ischemic damage in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. Materials and methods: Agarum clathratum was collected in Kangwon province (South Korea) and treated with 95% ethanol. The ethanol extract was suspended in distilled water and subjected to a series of partitions with EA, BU, DCM and Hx. Each of extract and fraction was orally administered with 50 mg/kg once a day for one week before ischemia-reperfusion (I-R).Result: In the crude-extract-, EA-and BU-fraction-treated ischemia groups, we found strong neuroprotection in the CA1 -about 80-89% of CA1 pyramidal neurons survived. However, in the DCM-and Hx-fraction-treated ischemia groups, we did not find any significant neuroprotection. In addition, we observed changes in astrocytes and microglia in the ischemic CA1. In the crude-extract, EA-and BU-fraction-treated ischemia groups, the distribution pattern and activity of the glial cells were similar to that found in the sham group. Discussion: Repeated supplements of crude-extract, EA-and BU-fractions of A. clathratum could protect neurons from I-R injury in the hippocampal CA1 induced by transient cerebral ischemia via decrease of glial activation.

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

“…We found a significant loss of pyramidal neurons in stratum pyramidale of the ischemic CA1 region in the ischemia-groups 5 days after ischemia-reperfusion using NeuN immunohistochemistry and F-J B histofluorescence staining. This outcome is consistent with our previous studies using the same animal model [21,29,30].…”

“…To examine neuronal damage in the hippocampal CA1 region after transient cerebral ischemia in each group, using NeuN immunohistochemistry according to our previous method [21], the sections were sequentially treated with 0.3 % hydrogen peroxide (H 2 O 2 ) in PBS for 30 min and 10 % normal goat serum in 0.05 M PBS for 30 min. The sections were next incubated with diluted mouse antiNeuN (a neuron-specific soluble nuclear antigen) (diluted 1:1000, Chemicon International, Temecula, CA) overnight at 4°C.…”

Pre-treatment with Chrysanthemum indicum Linné extract protects pyramidal neurons from transient cerebral ischemia via increasing antioxidants in the gerbil hippocampal CA1 region

“…This result corresponds to findings of previous studies (23,32,33). In addition, it was identified that the oral pre-treatment of 200 mg/kg CIL to the gerbils protected CA1 pyramidal cells (~67% of the sham-operated gerbils) from 5 min of transient cerebral ischemia; this finding was identical to a previous study of the authors (22).…”

Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils

“…For example, extract from Dictyopteris divaricate, belonging to the Dictyotaceae family, displays protective effect via regulating expressions of apoptosis-related proteins in an oxygen and glucose deprivation/reperfusion cell culture model using human neuroblastoma cells [16]. Additionally, extract and fractions from Agarum clathratum, a family of Agaraceae, show neuroprotective effects by reducing reactive astrogliosis and microgliosis following TFI in gerbils [17]. In particular, Kang et al (2012) reported that fucoidan, a sulfated polysaccharide derived from brown seaweeds, displayed neuroprotective effects in a rat model of lipopolysaccharide-accelerated ischemic injury following middle cerebral artery occlusion through inhibition of cytokine expression and neutrophil infiltration [18].…”