Key findings
Cerebral ischemic stroke is a major leading cause of death around the world. As flaxseed (FS) is one of the richest dietary sources of PUFAs and antioxidants, 3 weeks pretreatment with FSO 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 evaluations in rats. 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. According to the results, pretreatment with FSO protected the neurons of motor cortex area against the IR injury by increasing the BDNF and GDNF levels. In the current study, 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 exhibit neuroprotective effects on neurons of motor cortex area and enhance 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).
Link to Full Text