title: Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations.
abstract: Protectants and executioners have been demonstrated to be used by gap junctions in focal cerebral ischemia. Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration. In order to examine this hypothesis directly, the effects of octanol, a frequently used drug, were examined to investigate the role of gap junctions, in rats following middle cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, respectively. Octanol significantly reduced the infarct volume following 2 h of occlusion concomitant with lower neurological deficits, whereas it enlarged the infarct volume following 30 min of occlusion. Consistently, octanol attenuated the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the hippocampal CA1 region following 2 h of occlusion, while opposite effects were observed for 30 min of occlusion. Further immunohistochemical studies demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) was downregulated following 2 h of occlusion in the octanol group compared with the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 protein concomitant with increased Bax protein following 30 min of occlusion. These results indicated that the gap junction blocker octanol can protect against ischemic injury following long-term occlusion, however, can aggravate ischemic injury following short-term occlusion.
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Wenting
authors.initials: W
authors.lastname: Ding
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Lequan
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Li
authors.initials: L
authors.lastname: Guan
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Haimei
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Fuman
authors.initials: F
authors.lastname: Yan
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Jinwen
authors.initials: J
authors.lastname: Xu
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Weiyong
authors.initials: W
authors.lastname: Zeng
authors.affiliation: Department of Physiology, College of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
authors.forename: Min
authors.initials: M
authors.lastname: Qiu
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017629:Gap Junctions / Q000187:drug effects*; D015870:Gene Expression; D008297:Male; D000442:Octanols / Q000008:administration & dosage / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D017966:Pyramidal Cells / Q000378:metabolism; D051381:Rats; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D000442:Octanols; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein