Premium
Combustion smoke‐induced inflammation in the cerebellum and hippocampus of adult rats
Author(s) -
Zou YY.,
Kan E. M.,
Cao Q.,
Lu J.,
Ling EA.
Publication year - 2013
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12001
Subject(s) - cerebellum , enos , hippocampus , endocrinology , medicine , proinflammatory cytokine , pathology , inflammation , nitric oxide synthase , nitric oxide
Aims The effect of combustion smoke inhalation on the respiratory system is widely reported but its effects on the central nervous system remain unclear. Here, we aimed to determine the effects of smoke inhalation on the cerebellum and hippocampus which are areas vulnerable to hypoxia injury. Methods Adult male S prague– D awley rats were subjected to combustion smoke inhalation and sacrificed at 0.5, 3, 24 and 72 h after exposure. The cerebellum and hippocampus were subjected to Western analysis for VEGF , iNOS , eNOS , nNOS and AQP4 expression; ELISA analysis for cytokine and chemokine levels; and immunohistochemistry for GFAP / AQP4 , RECA ‐1/ RITC and TUNEL . Aminoguanidine ( AG ) was administered to determine the effects of iNOS after smoke inhalation. Results Both the cerebellum and hippocampus showed a significant increase in VEGF , iNOS , eNOS , nNOS and AQP4 expression with corresponding increases in inflammatory cytokines and chemokines and increased AQP4 expression and RITC permeability after smoke exposure. AG was able to decrease the expression of iNOS , followed by VEGF , eNOS , nNOS , RITC and AQP4 after smoke exposure. There was also a significant increase in TUNEL + cells in the cerebellum and hippocampus which were not significantly reduced by AG . Beam walk test revealed immediate deficits after smoke inhalation which was attenuated with AG . Conclusion The findings suggest that iNOS plays a major role in the central nervous system inflammatory pathophysiology after smoke inhalation exposure with concomitant increase in proinflammatory molecules, vascular permeability and oedema, for which the cerebellum appears to be more vulnerable to smoke exposure than the hippocampus.