Key findings
Brain-derived neurotrophic factor (BDNF), identified as one of the critical growth factors promotes the neuronal survival and regulate the different neuronal functions such as differentiation, migration and synaptic function in the central nervous system (CNS). Glial cell line-derived neurotrophic factor (GDNF) also has been shown to have neuroprotective effects. A 3 weeks pretreatment with flaxseed oil was used, and after 24 h of ischemia-reperfusion, its effects on neurotrophic factors were evaluated following transient middle cerebral artery occlusion (tMCAo) model of ischemia. The finding of the present study demonstrated that the pattern of the neurotrophic factors (BDNF and GDNF) expression was disrupted in motor cortex area after tMCAo. Further, pretreatment with FSO could upregulate the expression of neurotrophic factors (BDFN and GDNF) in the cerebral motor cortex area following brain I/R. pretreatment with FSO can protect the neurons of motor cortex area against the IR injury by increasing the BDNF and GDNF levels. Based on the findings, the percentage of dark neurons in the motor cortex area increased in the tMCAo group. Pretreatment with FSO effectively enhanced the functional motor recovery following the ischemia. Moreover, the percentage of dark neurons in motor cortex area reduced in this group compared to the tMCAo group. It was concluded that pretreatment with FSO exhibits neuroprotective effects on neurons of motor cortex area and enhances the functional motor recovery following the cerebral I/R injury by increasing the BDNF and GDNF levels.
ABSTRACT
Cerebral ischemic stroke is a common leading cause of disability. Flaxseed is a richest plant-based source of antioxidants. In this study, the effects of flaxseed oil (FSO) pretreatment on functional motor recovery and gene expression and protein content of neurotrophic factors in motor cortex area in rat model of brain ischemia/reperfusion (I/R) were assessed. Transient middle cerebral artery occlusion (tMCAo) in rats was used as model brain I/R. Rats (6 in each group) were randomly divided into four groups of Control (Co+normal saline [NS]), Sham (Sh+NS), tMCAo+NS and tMCAo+FSO. After three weeks of pretreatment with vehicle or FSO (0.2 ml~800 mg/kg body weight), the rats were operated in sham and ischemic groups. Ischemia was induced for 1 h and then reperfused. After 24 h of reperfusion, neurological examination was performed, and animals were sacrificed, and their brains were used for molecular and histopathological studies. FSO significantly improved the functional motor recovery compared with tMCAo+NS group (P<0.05). A significant reduction in brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF) mRNAs and protein levels were observed in the tMCAo+NS group compared with Co+NS and Sh+NS group (P<0.05). A significant increase of BDNF and GDNF mRNAs and proteins was recorded in the tMCAo+FSO group compared with Co+NS, Sh+NS and tMCAO+NS groups (P<0.05). The results of the current study demonstrated that pretreatment with FSO had neuroprotective effects on motor cortex area following cerebral ischemic stroke by increasing the neurotrophic factors (BDNF, GDNF).
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