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J Ethnopharmacol. 2015 Aug 22;172:232-7. doi: 10.1016/j.jep.2015.05.060. Epub 2015 Jun 20.

Trichilia catigua ethyl-acetate fraction protects against cognitive impairments and hippocampal cell death induced by bilateral common carotid occlusion in mice.

Author information

  • 1Laboratory of Neuropsychopharmacology, Department of Pharmacology and Therapeutics, Maringá 87020-900, Paraná, Brazil.
  • 2Laboratory of Pharmaceutical Biology, Palafito, Maringá, Brazil.
  • 3Laboratory of Microbiology, Universidade Estadual de Maringá, Av. Colombo, 5790, Maringá 87020-900, Paraná, Brazil.
  • 4Laboratory of Neuropsychopharmacology, Department of Pharmacology and Therapeutics, Maringá 87020-900, Paraná, Brazil. Electronic address: rmmwoliveira@uem.br.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE:

Trichilia catigua preparations have antinociceptive, antiinflammatory, and neuroprotective activity. Recently, a neuroprotective role for T. catigua was proposed using an in vitro model of ischemia-reperfusion in rat hippocampal slices. The aim of the present study was to evaluate the effects of an ethyl-acetate fraction (EAF) of T. catigua, which has potent antioxidant activity, in mice subjected to an in vivo model of cerebral ischemia.

MATERIAL AND METHODS:

Male Swiss mice were subject to the bilateral common carotid occlusion (BCCAO) model of cerebral ischemia. The animals were orally administered the T. catigua EAF (200, 400, or 800 mg/kg) 30 min before and once per day for 7 days after BCCAO. Histological and behavioral outcomes were assessed using Nissl staining and the Morris water maze test of cognition, respectively.

RESULTS:

Mice that were subjected to BCCAO exhibited cognitive impairments in the Morris water maze. The spatial cognitive deficits were counteracted by T. catigua EAF administration (200-800 mg/kg). The T. catigua EAF significantly increased the number of intact-appearing Nissl-stained cells in the hippocampus in BCCAO mice.

CONCLUSIONS:

These results show that the T. catigua EAF promoted functional recovery, decreased the delayed hippocampal cell loss, and mitigated the ongoing neurodegenerative processes induced by BCCAO in mice.

KEYWORDS:

ANOVA=analysis of variance; BCCAO=bilateral common carotid occlusion; Bilateral common carotid occlusion; CE=crude extract; Cognition; DPPH=2,2-diphenyl-1-picryl-hydrazyl; EAF=Trichilia catigua ethyl-acetate fraction; EPC=epicatechin; HPLC=high performance liquid chromatography; Morris water maze; Neurodegeneration; OGD=oxygen and glucose deprivation; PB2=procyanidin B2; ROS=reactive oxygen species; SOD=superoxide dismutase; TFA=trifluoroacetic acid; TGCI=transient global cerebral ischemia; Trichilia catigua ethyl-acetate fraction

PMID:
26099636
DOI:
10.1016/j.jep.2015.05.060
[PubMed - indexed for MEDLINE]
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