Effect of basic fibroblast growth factor on rat brain intracellular free calcium following focal ischemia-reperfusion injury

Hongying BAI; Gongling WEN; Jiyu LOU

ABSTRACT

BACKGROUND:

Basic fibroblast growth factor (bFGF) possesses multiple functions such as promoting neuronal survival and growth of cell processes in vitro and antagonizing the toxicity of excitatory amino acids,thereby playing import roles in functional recovery of the central nervous system (CNS). But whether bFGF offers neuroprotection on ischemic brain tissues by modulating intracellular free calcium content remains unknown.

OBJECTIVE:

To explore the effect of bFGF on intracellular free Ca2+ in the neural cells in the event of focal cerebral ischemia-reperfusion (IR)injury.

DESIGN:

Randomized controlled study.

SETTING:

Department of Neurology of Second Hospital Affiliated to Zhengzhou University.MATERIALS This study was conducted in the Laboratory of the Department of Neurology, Second Hospital Affiliated to Zhengzhou University between August and December 2003. Totally 24 SD were randomized into sham operation group, ischemic group, IR group and bFGF exposure group with 8 rats in each group.

METHODS:

Middle cerebral artery occlusion (MCAO) model was established in rats in IR group and bFGF exposure group by inducing arterial thrombosis with thread, which was not preformed in rats in the sham operation group. Rats in bFGF exposure group received intraperitoneal injection of 10 μg/kg bFGF immediately after ischemia,which was replaced by the same volume of physical saline in the other two groups. Free Ca2+ in brain cells was detected at 24 hours of IR.MAIN OUTCOME

MEASURES:

Free Ca2+ in the brain cells at 24hours of IR.

RESULTS:

All the 24 rats survived the experiment. Free Ca2+ in IR group was significantly higher than that of the sham operation group [(673.46±18.44) vs (224.71±10.58) nmol/L, F=1 329.06, P ＜ 0.01], and also significantly higher in bFGF exposure group [(378.37±21.08) nmol/L,F=1 329.06, P ＜ 0.01].

CONCLUSION:

Intracellular free calcium can be obviously depressed by bFGF following IR injury, which benefits cell membrane stability and help prevent intracellular Ca2+ overload.