Abstract: Objective To explore the effect of lavender essential oil on the expression of brain-derived neurotrophic factor (BDNF)/pro-brain-derived neurotrophic factor (proBDNF) and the recovery of depression in the ischemic hippocampus of rats after stroke. 
Methods A total of 45 male SD rats were randomly divided into a control group, a model group, and an intervention group, with 15 rats in each group. Rats in the control group raised under conventional conditions were subjected to intraperitoneal injection of physiological saline as a control experiment. In the model group, middle cerebral artery occlusion/reperfusion (MCAO/r) model was established and rats were given intraperitoneal injection of physiological saline. In the intervention group, rats were given lavender essential oil and exercise intervention after MCAO/r. The anxiety and depression behaviors of rats were tested through outdoor venues, forced swimming, and sucrose preference. The levels of oxidative stress biomarkers in rats were detected using commercial kits, and the expression of BDNF/proBDNF signaling pathway was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). The ratio of BDNF/proBDNF in CA1 region, CA3 region and dentategyrus (DG) regions of ischemic hippocampal tissue was analyzed by Western blotting (WB). The correlation analysis was performed between the BDNF/proBDNF ratio and behavioral tests for depression. Neurobehavioral (sensory and motor) testing was used to detect neural defects in rats. 
〖MM(〗〖HT6SS〗〖CM10-8〗河北医科大学学报第44卷第11期〖MM)〗
Results The stationary time of the model group was longer than that of the control group, and the sucrose preference, climbing frequency, and exercise distance were lower than those of the control group. The static time of the intervention group was longer than that of the control group and shorter than that of the model group, while the sucrose preference, climbing frequency, and exercise distance were lower than those of the control group and higher than those of the model group (P＜0.05). The levels of superoxide dismutase (SOD), glutathione，r-glutamyl cysteingl + glycine (GSH) and fluoride resistant acid phosphatase (FRAP) in the model group were lower than those in the control group, and the levels of malondialdehyde (MDA) were higher than those in the control group. The levels of SOD, GSH and FRAP in the intervention group were higher than those in the model group, while the level of MDA was lower than that in the control group and the model group (P＜0.05). The mRNA expressions of BDNF, neurotrophic receptor (TrkB) and microtubule-associated protein (DCX) in the model group were lower than those in the control group, while the mRNA expressions of proBDNF and neurotrophic receptor P75 (p75NTR) were higher than those in the control group. The mRNA expressions of BDNF, TrkB, and DCX in the intervention group were lower than those in the control group and higher than those in the model group, while the mRNA expressions of proBDNF and p75NTR were higher than those in the control group but lower than those in the model group (P＜0.05). The BDNF/proBDNF ratio in the CA1, CA3, and DG regions of the model group was lower than that of the control group, which was higher in the intervention group than in the model group (P＜0.05). The BDNF/proBDNF ratio was negatively correlated with resting time during forced swimming (r=-0.74, P＜0.01), while the BDNF/proBDNF ratio was positively correlated with sucrose preference (r=0.63, P＜0.01). The neurological deficit score in the model group was higher than that in the control group, which was higher in the intervention group than in the control group and lower than that in the model group (P＜0.05). The expression of Bcl-2 related X protein (Bax)/B-cell lymphoma-2 gene (Bcl-2) in the model group was higher than that in the control group, while the expression of Bcl-2 was lower than that in the control group. The expression of Bax and Bax/Bcl-2 in the intervention group was lower than that in the model group, while the expression of Bcl-2 was higher than that in the model group (P＜0.05). 
Conclusion Lavender essential oil may improve neurological function, enhance endogenous antioxidant defense, inhibit oxidative stress pathway and nerve apoptosis by regulating the relative level of BDNF and proBDNF, and then improve the depressive behavior of PSD rats.

Key words: stroke, depression, lavender essential oil