Regulation of BK channel on intracellular Ca2 + level and neuronal cells apoptosis after focal cerebral ischemia-reperfusion in rats

Abstract

Objective To investigate the regulation of BK channel on intracelullar free calcium concentration[Ca2 +]i and apoptosis in neuronal cells in the rat brain following focalcerebral ischemia injury. Methods 108 SD rats were randomly assigned to sham group (n =36) , ischemic reperfusion group ( n =36), IBTX group ( n =36), compared neurological function defect and infarct size of different groups at the same reperfusing time. Laser scanning confocal microscope imaging of the calcium fluorescent indicator dye Fluo-2/AM was used to determine the changes of[Ca2+]i in neurons, the expression of BK tunnel was investigated by immunohistochemistry and neuronal cells apoptosis were measured by TUNEL. Results At 24 h after ischemic reperfusion, the neurological deficit scores in IBTX group were (2. 17 ± 0. 44),which obviously higher than ischemic reperfusion group ( 1.83 ± 0. 42, P ＜ 0.05 ) ;The brain infarct volume in IBTX group was (27. 97 ± 5.84 ) ％, which larger than ischemic reperfusion group ( 22. 83 ± 4. 74 ) ％( P ＜ 0. 05 ). The[Ca2 +]i and the cell apoptosis rate of IBTX group had significant difference at 24 h after ischemic reperfusion compared with ischemic reperfusion group: (914. 50 ± 86. 57 ) nmol/L VS (732. 09 ±51.30) nmol/L (P＜0. 01); (15.20±6. 11)％ vs (10.49±1.91)％ (P＜0.05).The results of immunohistochemistry indicate that the expression of BK channel in ischemic reperfusion group decreased, but the defference of three groups was not different significantly (P ＞ 0. 05). Conclusion BK channels could play a role in protecting the neuronal cells in mice following cerebral ischemia-reperfusion by inhibited the ascension of[Ca2+]i and decrease neurons apotosis. Key words: BK channel ; Cerebral ischemia-reperfusion; Calcium overload; Neurons apoptosis