摘要目的:探讨银杏叶提取物(ginkgo biloba extract，EGb)是否可以通过提高血清脑源性神经营养因子(brain-derived neurotrophic factor，BDNF)活性来改善迟发性运动障碍(tardive dyskinesia，TD)症状，进而探讨BDNF基因型Val66Met对TD疗效的影响。方法:共纳入78例男性精神分裂症伴TD的住院患者，完成EGb(治疗剂量240 mg/d)治疗12周者为77例。在基线期和治疗12周后测量异常不自主活动量表(abnormal involuntary movement scale，AIMS)、阳性和阴性症状量表(positive and negative syndrome scale，PANSS)、采用酶联免疫吸附测定法(enzyme linked immunosorbent assay，Elisa)测定血清BDNF水平。另外采用限制性片段长度多态性方法检测所有患者BDNF Val66Met多态性。结果:与治疗前比较，治疗后TD患者AIMS总分[(7.0±2.9)分，(4.9±2.2)分]、PANSS总分[(55.8±14.0)分，(51.1±9.7)分]，P量表分[(9.6±3.3)分，(8.6±2.2)分]，N量表分[(23.2±8.3)分，(21.4±6.3)分]，G量表分[(23.0±4.9)分，(21.1±2.7)分]均显著下降，差异有统计学意义(均 P<0.01)。治疗后TD患者BDNF水平[(10.8±2.9)μg/L]高于治疗前[(9.6±3.3)μg/L] ( P<0.01)，且BDNF增高与AIMS降低显著正相关( r＝0.28， P＝0.014)；但BDNF增高与PANSS总分和三个分量表的改善均无显著性相关(均 P>0.05)。治疗后，Val/Val型患者的AIMS的下降幅度明显大于Val/Met或Met/Met基因型患者(均 P<0.05)。进一步分析表明，只有携带Val/Met杂合子的患者BDNF水平治疗后才显著性增加( P<0.05)。 结论:EGb可能通过神经保护和调节作用来改善TD症状，BDNF基因型参与调控EGb治疗TD的疗效，可能与其调节BDNF血清水平有关。

abstractsObjective:To investigate whether ginkgo biloba extract(EGb) can improve the symptoms of tardive dyskinesia(TD) by increasing the levels of serum brain-derived neurotrophic factor (BDNF), and to explore whether the BDNF Val66Met genotype can influence the efficacy of TD by EGb.Methods:A total of 78 male schizophrenia inpatients with TD were enrolled, and 77 patients completed 12 weeks of treatment with EGb(240 mg/d). The abnormal involuntary movement scale (AIMS), positive and negative syndrome scale (PANSS) and serum BDNF levels were measured at before and after 12 weeks of treatment.Serum BDNF levels were measured by enzyme linked immunosorbent assay (Elisa). In addition, the BDNF Val66Met polymorphism was genotyped by the method of PCR-restriction fragment length polymorphism (PCR-RFLP) in all patients.Results:Compared with before treatment, the scores of total AIMS((7.0±2.9) vs (4.9±2.2)), total PANSS ((55.8±14.0) vs(51.1±9.7)), subscale P((9.6±3.3) vs (8.6±2.2)), subscale N((23.2±8.3) vs (21.4±6.3)) and subscale G((23.0±4.9) vs (21.1±2.7)) were significantly decreased( P<0.01), while the levels of BDNF were significantly increased((10.8±2.9)μg/L vs (9.6±3.3)μg/L, P<0.05) in TD patients after treatment.The increased level of BDNF was positively correlated with the decrease of AIMS( r=0.28, P=0.014), but no significantly correlated with the improvement of PANSS total scores and the three subscales were found(all P>0.05). After treatment, the decrease of AIMS in patients with Val/Val genotype was significantly greater than that in patients with Val allele (Met/Val plus Met/Met genotype) (both P<0.05). Further analysis showed that only patients with Val/Met heterozygotes had a significant increase in BDNF levels after treatment ( P<0.05). Conclusions:EGb may improve TD symptoms through neuroprotective and regulatory effects.The BDNF genotype is involved in regulating the efficacy of EGb in the treatment of TD, which may be related to its regulation of BDNF serum levels.