Electroacupuncture Increases the Expression of Gas7 and NGF in the Prefrontal Cortex of Male Rats with Focal Cerebral Ischemia

Abstract

Objective: To investigate the potential mechanisms underlying the migration of endogenous neural stem cells (eNSCs) to the frontal cortex to differentiate into neurons, and to monitor the effect of electroacupuncture (EA) regulation of focal cerebral ischemia (FCI) in rats on the expression of growth arrest-specific protein 7 (Gas7) and nerve growth factor (NGF) in the prefrontal cortex (PFC). Methods: Randomly, forty-eight male Sprague-Dawley rats were divided into four groups: Normal, Sham operation, Model, and EA. The right middle cerebral artery was embolized utilizing the thread-embolism technique. In the EA group, "Baihui" and "Zusanli" points were treated with electroacupuncture for 30 minutes, once a day, for 21 days. Nissl staining revealed the neuronal morphology of the PFC. Using immunohistochemistry and Western blot, the expression of Gas7 and NGF in the right PFC was observed. Results: Nissl staining showed clear PFC neurons with centered nuclei and distinct nucleoli in the Normal and Sham groups. In the Model group, the PFC nuclei were distinctively smaller. The neuronal morphology in the EA group resembled that of the Normal group. Results from Western blot and immunohistochemistry were comparable. The expression of Gas7 and NGF in the Sham surgery group did not differ significantly from the Normal group. However, the expression of Gas7 and NGF in the Model group was significantly lower than in the Normal group. The expression of Gas7 and NGF was significantly higher in the EA group than in the Model group. Conclusions: EA can increase the expressions of Gas7 and NGF in the ischemic prefrontal cortex, which may be one of the mechanisms by which EA promotes the differentiation of eNSCs into neurons in the injured area.

Gastrodin combined with electroacupuncture prevents the development of cerebral ischemia via rebalance of brain-derived neurotrophic factor and interleukin-6 in stroke model rats

“…Recent research indicates that EA applied to the ST36 and GV20 acupoints can augment the expression of growth arrest-specific 7 and nerve growth factor. This augmentation fosters the differentiation of endogenous neural stem cells into neurons within the injured area, subsequently facilitating cortical neuron regeneration after cerebral ischemia [ 15 ]. Additionally, EA targeting the Quchi (LI11) and ST36 points demonstrates the ability to stimulate the synthesis and secretion of BDNF in the ischemic side’s cortex in cerebral ischemia-afflicted rats [ 16 ].…”

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

“…SERPINA1 [521], LRRK2 [649], TF (transferrin) [650], REN (renin) [651], TLR2 [652], MOBP (myelin associated oligodendrocyte basic protein) [653], SYK (spleen associated tyrosine kinase) [654], MBP (myelin basic protein) [625], SHH (sonic hedgehog signaling molecule) [655], RBP4 [590], SNCB (synuclein beta) [543], MMP3 [656], VWF (von Willebrand factor) [657], EGFR (epidermal growth factor receptor) [658], ABCA1 [659] and GPR39 [618] are associated with the clinical stages of dementia. Altered expression of LRRK2 [660], GPR17 [661], TF (transferrin) [662], NEUROD1 [663], RELN (reelin) [664], LCP1 [665], TFAP2B [666], HOXA5 [667], MSR1 [668], REN (renin) [669], OLIG2 [670], TLR2 [671], WT1 [672], SLC22A3 [673], CADM2 [674], PRKCH (protein kinase C eta) [675], MBP (myelin basic protein) [676], XAF1 [677], GPR37 [678], SHH (sonic hedgehog signaling molecule) [679], VTN (vitronectin) [680], SIRT2 [681], RBP4 [682], BMP2 [683], CDH13 [684], NR3C2 [685], TRPC6 [686], MMP3 [687], FGF19 [688], HLA-DRB1 [689], CD74 [690], VWF (von Willebrand factor) [691], ANGPT2 [692], CHRDL1 [693], AKR1C3 [694], NEDD4L [695], CASP1 [696], PDE2A [697], GAS7 [698], TET1 [699], EFNB2 [700], EGFR (epidermal growth factor receptor) [701], ABCA1 [702], PDPN (podoplanin) [703], SLCO1B1 [704], COMT (catechol-O-methyltransferase) [705] and GPR39 [706] have been reported to be associated with stroke. CHRNA4 [707], RELN (reelin) [708], VEGFC (vascular endothelial growth factor C) [709], FRMPD4 [710], SCN4B [711], SLCO5...…”

“…[688], HLA-DRB1 [689], CD74 [690], VWF (von Willebrand factor) [691], ANGPT2 [692], CHRDL1 [693], AKR1C3 [694], NEDD4L [695], CASP1 [696], PDE2A [697], GAS7 [698], TET1 [699], EFNB2 [700], EGFR (epidermal growth factor receptor) [701], ABCA1 [702], PDPN (podoplanin) [703], SLCO1B1 [704], COMT (catechol-O-methyltransferase) [705] and GPR39 [706] have been reported to be associated with stroke. CHRNA4 [707], RELN (reelin) [708], VEGFC (vascular endothelial growth factor C) [709], FRMPD4 [710], SCN4B [711], SLCO5A1 [712] and GPR39 [713] are involved in the development of epilepsy.…”