Effect of brain-derived neurotrophic factor on apoptotic early events in hippocampal cells after status convulsivus

Abstract

Objective To explore the effect of brain-derived neurotrophic factor(BDNF)on brain damage and its mechanism by investigating the influence of exogenous BDNF on mitochondrial membrane potential(△ Ψm)and cytochrome C(cytC)release in the hippocampus after status convulsivus(SC). Methods Sixty-four healthy adult Wistar rats were randomly divided into normal group(n=32)and SC group(n=32)which were injected with lithium-pilocarpine intraperitoneally for SC continuing 30 min. The rats in these two groups were intraventricularly injected(IV)with normal sodium(NS)2 μL, BDNF 4 μL(0.1 μg/μL), or BDNF antibody 2 μL(200 μg/mL)in left lateral ventricle(or no injection), and sacrificed 6 h later. The levels of △Ψm and cytC of hippocampal cells were determined by flow cytometry. Results (1)As compared with subgroups of normal group, the levels of △Ψm significantly decreased and cytC significantly increased in the SC subgroups, respectively(P<0.05).(2)In normal group, the levels of △Ψm significantly decreased and cytC significantly increased in the lateral hippocampus of normal-anti-BDNF subgroup as compared with those in normal-non-IV subgroup(P< 0.05), and the levels of △Ψm was significantly higher and cytC significantly lower in the lateral of normal-BDNF subgroup than those in the lateral of normal-anti-BDNF subgroup(P<0.05).(3)In SC group, as compared with those in the lateral of SC-NS subgroup and SC-non-IV subgroup, the level of △Ψm significantly decreased and cytC level significantly increased in the lateral of SC-anti-BDNF subgroup(P<0.05), however they were reversed in the lateral of SC-BDNF subgroup(P<0.05). Conclusions SC could induce △Ψm decrease and cytC release of hippocampal cells. The exogenous BDNF could partly inhibit the decrease of △Ψm and the release of cytC in the lateral hippocampus after SC, which indicates that BDNF might protect the brain after SC through inhibiting the early event of apoptosis. Key words: Status convulsivus; Mitochondrial membrane potential; Cytochrome C; Brainderived neurotrophic factor