Earticle

We wanted to find the intensity of exercise that could increase brainderived neurotrophic factor (BDNF) expression and improve spatial learning and memory without dietary control. C57BL/6 mice were fed a 60% high-fat diet (HFD) for 6 weeks to induce obesity. Obesity-induced mice were exercised on a treadmill for 8 weeks at various exercise intensities: HFD-control (n= 7), HFD-low-intensity exercise (HFD-LIE, n= 7, 12 m/min for 75 min), HFD-middle intensity exercise (HFD-MIE, n= 7, 15 m/min for 60 min) and HFD-high-intensity exercise (HFD-HIE, n= 7, 18 m/min for 50 min). One week before sacrificing mice, the Morris water maze test was performed, and the hippocampus was immediately removed after sacrifice. The expression levels of BDNF (encoded by the gene Bdnf) and tropomyosin receptor kinase B (TrkB) in the hippocampus were analyzed by quantitative real-time reverse transcriptionpolymerase chain reaction and western blot. In the last probe test of the Morris water maze test, occupancy in the target quadrant was significantly higher in the HFD-HIE group (P< 0.05) than in the other groups. In addition, mRNA expression from the Bdnf promoter region was found to be significantly higher in the HFD-HIE group than in the other groups (P< 0.001). Although there were some differences in the levels of significance, the expression levels of both BDNF and TrkB were significantly higher in the HFD-HIE group than in the other groups. Therefore, relatively high-intensity aerobic exercise can resist the adverse effects of a high-fat diet on the brain without dietary control.

The purpose of this study was to determine whether combined inter-vention of treadmill exercise and bone marrow stromal cell (BMSC) transplantation would affect the expression of neurotrophic factors in the sciatic nerve injury (SNI) and neuropathic pain-related cascades in ipsilateral lumbar 4-5 dorsal root ganglion (DRG) during the early or late stage of sciatic nerve regeneration. The rats were randomly divided into the normal control group (CONT, n=6), sedentary group (SS, n=24), exercise group (SE, n=24), BMSC transplantation group (SB, n=24), BMSC transplantation+exercise group (SBE, n=24) 1, 2, 3, and 5 weeks after SNI. Single dose of 5×106 harvested BMSC was injected into the injury area sing by a 30 gauge needle. Treadmill exercise was performed at a speed of 8 m/min for 30 min once a day. Tropomyosin-receptor ki-nase B, brain-derived neurotrophic factor and ciliary neurotrophic fac-tor were significantly upregulated in the SE and SBE groups at 1- and 2-week postinjury than those in the CONT and SS groups, and SB and SBE groups continuously kept up proinflammatory cytokines until the late stage of regeneration. Nuclear factor kappa-light-chain-enhancer of activated B cells, interleukin and tumor necrosis factor alpha in ipsi-lateral DRG were progressively decreased by exercise alone application and/or BMSC transplantation at early and late stage of regeneration. Present results provide reliable information that combined intervention of treadmill exercise and BMSC transplantation might be one of the ef-fective treatment strategies for recovering sciatic nerve injury-induced neuropathic pain over time.

For humans, maternal old age means the age of 35 or older at the time of childbirth. Maternal metabolism not only affects the cognitive func-tion of the offspring, but also affects their physical and neurological de-velopment. This study aims to elucidate the effects of exercise training on spatial learning memory, neurogenesis, and apoptosis in the off-spring of old mice. Using mice, the offspring of old mothers showed im-paired spatial learning memory, decreased brain-derived neurotrophic factor and postsynaptic density protein 95 levels, suppressed neuro-genesis, and increased hippocampal apoptotic cell death. In contrast, the offspring of the old mothers had improved spatial learning memory, increased brain-derived neurotrophic factor and postsynaptic density protein 95 levels, increased neurogenesis, and decreased hippocampal apoptotic cell death when they received exercise training. The present results indicate that there is apparent spatial learning memory impair-ment among the offspring of old mothers, but by contrast, exercise can ameliorate spatial learning memory impairment. Exercise can be an ef-fective countermeasure against memory decline in the offspring of old mothers.

The effect of combined approach of exercise training and bone marrow stromal cell (BMSC) engraftment on activation of brain-derived neuro-trophic factor (BDNF)-extracellular signal-regulated kinase 1 and 2 (ERK1/2)-cyclic adenosine monophosphate response element-binding protein (CREB) signaling pathway after sciatic nerve injury (SNI) was investigated. Sixty male Sprague-Dawley rats divided into the normal control, nonexercise (NEX), exercise training (EX), BMSC transplanta-tion (TP), and exercise training+BMSC transplantation (EX+TP) groups 4 weeks after SCI. Exercise training was carried out on the treadmill de-vice at 5–10 m/min for 20 min for 4 weeks. Single dose of 5×106 harvest-ed BMSC was injected into the injury area of the injured sciatic nerve. In order to evaluate induction levels of BDNF-ERK1/2-CREB signaling molecules in the whole cell and nuclear cell lysates of the injured sciat-ic nerve, we applied Western blot analysis. BDNF was significantly in-creased only in EX+TP compared to NEX, EX, and TP groups. Phospho-inositide-dependent kinase-1 was more increased in EX, TP, and EX+TP groups than NEX group, but EX+TP group showed the most upregula-tion of phosphorylated protein kinase B compared to other groups. In addition, in the whole cell lysate, phosphorylated ERK1/2, but not acti-vating transcription factor-3 (ATF-3) and phosphorylated CREB, was sig-nificantly increased in TP and EX+TP groups. In the nuclear cell lysate, ATF-3 and phosphorylated CREB were strongly activated in EX+TP group compared to EX group. Regular exercise training combined with BMSC engraftment would seem to be more effective in controlling activation of regeneration-related signaling pathway after SNI.

Neuronal cell death in the hippocampus by cerebral ischemia causes disability of memory function. Cerebral ischemia also alters the expres-sions of brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate-responsive element binding protein (CREB), extracel-lular signal-regulated protein kinase (ERK), and phosphatidylinositol 3-kinase/protein kinase B (Akt). In the present study, we investigated the effect of treadmill exercise on cerebral ischemia in relation with ERK-Akt-CREB-BDNF signaling pathway in the hippocampus using ger-bils. Induction of cerebral ischemia deteriorated short-term memory with suppression of phosphorylation of ERK-Akt-CREB-BDNF pathway in the hippocampus of gerbils. Enhancement of apoptosis in the hippo-campus was accompanied in the ischemia gerbils. Treadmill exercise improved short-term memory through enhancing phosphorylation of ERK-Akt-CREB-BDNF pathway with suppressing apoptosis in the hip-pocampus of the ischemia gerbils. The present results suggest that im-provement of memory function after cerebral ischemia by treadmill ex-ercise may be involved in the ERK-Akt-CREB-BDNF signaling pathway, resulting in inhibition of apoptosis in the hippocampus.

Sciatic crushed nerve injury (SCI) causes pain-related gait and swelling in the affected limb. Electroacupuncture (EA) is a modified acupuncture technique, and analgesic effect of EA on different types of pain has been documented. Scientific functional index (SFI) is a mathematical formula to represent parameters of normal and experimental footprints. We investigated the effect of low-frequency EA on functional recovery following SCI in rats. For this study, immunohistochemistry for c-Fos in the ventral lateral periaqueductal gray (vlPAG) and paraventricular nu-cleus (PVN) and western blot for neurofilament (NF) and brain-derived neurotrophic factor (BDNF) in the sciatic nerve were conducted. To in-duce crush injury on the sciatic nerve, sciatic nerve was crushed for 30 sec using a surgical clip. The rats in the acupuncture groups received acupuncture bilaterally at respective site, once a day for 14 days. The rats in the EA group received 100-Hz electrical stimulation for 10 min once a day during 14 days. SCI decreased SFI value, in contrast, EA in-creased SFI value. c-Fos expression in the vlPAG and PVN was in-creased following SCI, in contrast, EA suppressed c-Fos expression. NF expression in the sciatic nerve was decreased by SCI, in contrast, EA increased NF expression. BDNF expression in the sciatic nerve was in-creased by SCI, in contrast, EA suppressed BDNF expression. In the present study, EA showed effectiveness on functional recovery from SCI.

Traumatic brain injury (TBI) causes deficit in spatial learning and mem-ory function. Physical activity ameliorates neurological dysfunction af-ter TBI. We investigated the effect of late starting treadmill exercise on spatial learning ability in relation with cAMP-response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway using TBI rats. For this study, radial 8-arm maze test, TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end label-ing) staining, caspase-3 immunohistochemistry, and western blot for Bax, Bcl-2, BDNF, tyrosine kinase B (TrkB), CREB, and phosphorylated CREP (p-CREB) were performed. TBI was induced by an electromag-netic-controlled cortical impact. The rats in the exercise groups were scheduled to run on a treadmill for 30 min once a day for 8 weeks start-ing 3 weeks after TBI. TBI impaired spatial learning ability and in-creased caspase-3 expression in the hippocampal dentate gyrus. TBI enhanced Bax expression and suppressed Bcl-2 expression in the hip-pocampus. TBI increased BDNF and TrkB expressions, resulted in the enhancement of p-CREB/CREB ratio in the hippocampus. However, treadmill exercise improved spatial learning ability, decreased caspase-3 expression, suppressed Bax expression, and increased Bcl-2 expression. Treadmill exercise alleviated TBI-induced over-expres-sion of BDNF and TrkB, which suppressed phosphorylation of CREB in the hippocampus. In the present study, late starting treadmill exercise improved spatial learning ability through suppressing TBI-induced acti-vation of CREB/BDNF/TrkB signaling pathway after TBI.

Transplantation of bone marrow stromal cells (BMSCs) has been known as one of the effective therapeutic methods for functional recov-ery of spinal cord injury (SCI). Treadmill exercise also facilitates the functional recovery of SCI. Previously, we reported that combination of BMSCs transplantation with treadmill exercise potentiated the locomo-tor function in SCI rats. In the present study, we investigated whether recovery effect of BMSCs transplantation or treadmill exercise appears through the brain-derived neurotrophic factor (BDNF)-extracellular sig-nal–regulated kinases 1/2 (ERK1/2) pathway. The spinal cord contusion injury was performed at the T9-T10 level using the impactor. Cultured BMSCs were transplanted directly into the lesion 1 week after SCI. Treadmill exercise was performed 6 days per a week for 6 weeks. Western blot for Bax, Bcl-2, BDNF, tyrosine kinase B (TrkB), and phos-phorylated ERK1/2 (p-ERK1/2), phosphorylated JNK was performed. In the present results, combination of BMSCs transplantation with tread-mill exercise potently decreased Bax expression, potently increased Bcl-2 expression, and potently enhanced BDNF and TrkB expressions in the injured spinal cord. Combination of BMSCs transplantation with treadmill exercise further facilitated p-ERK1/2 and p-c-Jun expression levels. The present findings demonstrated the synergistic effect of treadmill exercise on neuroregenerative effect of BMSCs transplanta-tion appeared through the activation of BDNF-ERK1/2 pathway in SCI.

Transplantation of bone marrow stromal cells (BMSCs) is regarded as a promising candidate for the spinal cord injury (SCI). In the present study, we investigated whether treadmill exercise potentiate the effect of BM-SCs transplantation on the functional recovery in the SCI rats. The spi-nal cord contusion injury applied at the T9–T10 level using the impactor. Cultured BMSCs were transplanted into the lesion at 1 week after SCI induction. Treadmill exercise was conducted for 6 weeks. Basso-Beat-tie-Bresnahan (BBB) scale for locomotor function was determined. Sprouting axons in the lesion cavity were detected by immunofluores-cence staining for neurofilament-200. Brain-derived neurotrophic factor (BDNF) and synapsin-I expressions were analyzed using western blot-ting. BMSCs transplantation improved BBB score and increased ex-pressions of neurofilament-200, BDNF, and synapsin-I in the SCI rats. Treadmill exercise potentiated the improving effect of BMSCs trans-plantation on BBB score in the SCI rats. This potentiating effect of treadmill exercise could be ascribed to the enhancement of BDNF ex-pression in the SCI rats.

Maternal infection is an important factor causing neonatal brain injury and later developmental disability. In the present study, we investigated the effects of treadmill exercise intensity on short-term memory, hippo-campal neurogenesis, and expression of brain-derived neurotrophic factor (BDNF), and tyrosine kinase receptor B (TrkB) in the rats born of lipopolysaccharide (LPS)-exposed maternal rats. The rats were divided into six groups: control group, mild-intensity exercise group, moder-ate-intensity exercise group, maternal LPS-exposed group, maternal LPS-exposed and mild-intensity exercise group, maternal LPS-exposed and moderate-intensity exercise group. The rats in the exercise groups were forced to run on a treadmill for 30 min 5 times a week for 4 weeks. The exercise load consisted of running at the speed of 8 m/min for the mild-intensity exercise groups and 14 m/min for moderate-intensity ex-ercise groups. The latency in the step-down avoidance task was deter-mined for the short-term memory. Immunohistochemistry for 5-bro-mo-2’-deoxyuridine was performed to determine hippocampal cell pro-liferation and neurogenesis. Western blot analysis was performed for the detection of BDNF and TrkB expression. In the present study, tread-mill exercise improved short-term memory deteriorated by maternal LPS exposure. Treadmill exercise increased cell proliferation and neu-rogenesis in the hippocampal dentate gyrus of the rats born of the LPS-exposed maternal rats. Treadmill exercise increased BDNF and TrkB expression in the hippocampus of the rats born of the LPS-ex-posed maternal rats. These effects of treadmill exercise were similarly appeared at both mild-intensity and moderate-intensity.

Brain-derived neurotrophic factor (BDNF) and its receptors tyrosine ki-nase B (trkB), and cyclic adenosine monophosphate response element binding protein (CREB) have been suggested as the neurobiological risk factors causing depressive disorder. Serotonin (5-hydroxytryptamine, 5-HT) plays an important role in the pathogenesis of depression. We in-vestigated the effect of treadmill exercise on social interaction in rela-tion with BDNF and 5-HT expressions following stress in rats. Stress was induced by applying inescapable 0.2 mA electric foot shock to the rats for 7 days. The rats in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 4 weeks. Social interaction test and western blot for BDNF, TrkB, pCREB, and 5-HT1A in the hippo-campus were performed. The results indicate that the spend time with unfamiliar partner was decreased by stress, in contrast, treadmill exer-cise increased the spending time in the stress-induced rats. Expres-sions of BDNF, TrkB, and pCREB were decreased by stress, in contrast, treadmill exercise enhanced expressions of BDNF, TrkB, and pCREB in the stress-induced rats. In addition, 5-HT1A receptor expression was de-creased by stress, in contrast, treadmill exercise enhanced 5-HT1A ex-pression in the stress-induced rats. In the present study, treadmill exer-cise alleviated stress-induced social interaction impairment through enhancing hippocampal plasticity and serotonergic function in the hip-pocampus. These effects of treadmill exercise are achieved through 5-HT1A receptor activation.

The purpose of this study was to investigate the effects of regular treadmill exericse after social isolation on brain-derived neurotrophic factor(BDNF), nerve growth factor(NGF) and 5-bromo-2'- deoxyuridine- 5'-mono-phosphate(BrdU) -positive cell in the hippocampus, and serotonin-, TPH-positive cells in the raphe nuclei, and depression behaviors in the adult rats. Forty male Sprague-Dawley rats (31 weeks) were divided into four groups: (1) group housing and control group (GCG, n = 10); (2) group housing and exercise group (GEG, n = 10); (3) isolated housing and control group (ICG, n = 10); and (4) isolated housing and exercise group (IEG, n = 10). After 2 week of housing under the normal condition of 3 animals per cage, rats were socially isolated via transfer to individual cages for 8 weeks. Rats were then subjected to treadmill exercise for 5 days per week for 8 weeks, during which time the speed of the treadmill was gradually increased. The blood corticosterone level in the ICG was intend to increase, whereas in the IEG was intend to decrease compared to the ICG. Compared to the GCG, levels of BDNF and NGF were significantly decreased in the ICG, and significantly increased in the IEG (p < .001 respectively). There were significantly more BrdU-positive cells in the IEG compared to the GCG and ICG(p < .001). Serotonin-, TPH-positive cells in the GEG and IEG were significantly increased compared to the GCG and ICG(p < .01, p < .001). In the forced swim test, immobility time was significantly increased in the ICG, and significantly decreased in the IEG compared to the ICG(p < .001). These results show that regular treadmill exercise after social isolation not only increases the levels of BDNF and NGF to induce survival of cells in the hippocampus, but also improves depression-like behavior by increasing the number of serotonin, TPH cells expression in the raphe nuclei.

Epilepsy is a common neurological disorder characterized by seizure and loss of neuronal cells by abnormal rhythmic firing of neurons in the brain. In the present study, we investigated the effect of treadmill exer-cise on gamma-aminobutyric acid (GABA)ergic neuronal loss in relation with neuronal activation using pilocarpine-induced epileptic rats. The rats were divided into four groups: control group, control and treadmill exercise group, pilocarpine-induced epilepsy group, and pilocarpine-in-duced epilepsy and treadmill exercise group. Epilepsy was induced by intraperitoneal injection of 320 mg/kg pilocarpine hydrochloride. The rats in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 2 weeks. In the present results, neuronal loss in the hippocampal CA1 region was increased after pilocarpine-in-duced seizure. Treadmill exercise inhibited hippocampal neuronal loss in the epileptic rats. Glutamic acid decarboxylase (GAD67) expression in the hippocampal CA1 region was reduced by pilocarpine-induced seizure. Treadmill exercise increased GAD67 expression in the epileptic rats. c-Fos expression in the hippocampal CA1 region was increased in response to epileptic seizure. Treadmill exercise inhibited c-Fos expres-sion in the epileptic rats. Epileptic seizure increased brain-derived neu-rotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) expres-sions in the hippocampus. Treadmill exercise suppressed BDNF and TrkB expressions in the epileptic rats. In the present study, treadmill ex-ercise prevented GABAergic neuronal loss and inhibited neuronal acti-vation in the hippocampal CA1 region through the down-regulation of BDNF-TrkB signaling pathway.

Alzheimer’s disease is the most common neurodegenerative disease and this disease induces progressive loss of memory function Scopol-amine is a non-selective muscarinic cholinergic receptor antagonist and it induces impairment of learning ability. Exercise is known to ame-liorate memory deficits induced by various brain diseases. In the pres-ent study, we investigated the effect of treadmill exercise on spatial learning ability in relation with cell proliferation in the hippocampus us-ing the scopolamine- induced amnesia mice. For the induction of amne-sia, 1 mg/kg scopolamine hydrobromide was administered intraperito-neally once a day for 14 days. Morris water maze test for spatial learning ability was conducted. Immonofluorescence for 5-bromo -2-deoxyuri-dine (BrdU) and western blot for brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) were performed. In the present results, scopolamine-induced amnesia mice showed deteriora-tion of spatial learning ability. Inhibition of cell proliferation and suppres-sion of BDNF and TrkB expressions were observed in the scopol-amine-induced amnesia mice. Treadmill exercise improved spatial learning ability and increased cell proliferation through activating of BD-NF-TrkB pathway in the amnesia mice. These findings offer a possibility that treadmill exercise may provide preventive or therapeutic value for the memory loss induced by variable neurodegenerative diseases in-cluding Alzheimer’s disease.

Schizophrenia is a serious psychiatric disorder with several symptoms including cognitive dysfunction. Although the causes of schizophrenia are still unclear, there is a strong suspicion that the abnormality in N- methyl-D-aspartate (NMDA) receptor may contribute to schizophrenia symptoms. In the present study, the effect of treadmill exercise on the NMDA receptor expression was evaluated using MK-801-induced schizophrenia mice. Immunohistochemistry for expressions of NMDA receptor tyrosine hydroxylase (TH) was conducted. Western blot for brain-derived neurotrophic factor (BDNF) was also performed. In the present results, the mice in the MK-801-treated group displayed re-duced NMDA receptor expression. Enhanced TH expression and sup-pressed BDNF expression were also observed in the MK-801-treated mice. Treadmill exercise improved NMDA receptor expression in the MK-801-induced schizophrenia mice. Treadmill exercise also suppressed TH expression and enhanced BDNF expression in the MK-801-in-duced schizophrenia mice. The present study showed that down-regu-lation of NMDA receptor demonstrated schizophrenia-like parameters, meanwhile treadmill running improved schizophrenia-related parame-ters through enhancing NMDA receptor expression.

In the present study, we investigated the effect of swimming training and sudden detraining on learning ability and spatial memory capability and on neurogenesis and brain-derived neurotrophic factor (BDNF) expression in the hippocampus of mice. Male ICR mice were randomly assigned into three groups (n= 15 in each group): the control group, the swimming training group, and the detraining group. The mice in the swimming training group were made to swim (6 days/week, 60 min/day) for 8 weeks. The mice in the detraining group were accomplished the same swimming program for 4 weeks and then discontinued exercise for 4 weeks. In the present results, enhanced short-term and spatial learning memories and increased hippocampal neurogenesis and BDNF expression were observed in the mice of the swimming training group. In contrast, decreased short-term and spatial learning memories were observed in the mice of the swimming detraining group compared to the control level. Hippocampal neurogenesis and BDNF expression were also decreased in the mice of the detraining group near to the control level. Here in this study, we suggest that sudden cessation of exercise training might bring decline of the brain functions.

Brain-derived neurotrophic factor (BDNF) and its receptor neurotrophic tyrosine receptor kinase-2 (NTRK2) have known important roles in the central nervous system for neurite growth, survival, and differentiation. Nevertheless, the significance of BDNF in spermatogenesis remains unclear in stallions. Therefore, the present study was designed 1) to investigate the expression of BDNF and its receptor NTRK2 and 2) the seasonal variation in the expression patterns of BDNF and NTRK2 in stallions’ testes. We used testes from eight postpubertal Thoroughbred stallions collected after a field castration during two different seasons of the year (breeding season [BS] and nonbreeding season [NBS]). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting (WB), and immunofluorescence were performed. RT-qPCR results showed upregulation of mRNA levels of BDNF and NTRK2 in the testes collected during the NBS. The quantification of the protein bands obtained after WB displayed significantly higher relative intensity in NBS. The immunofluorescence assay identified the localization of BDNF in the cytoplasm of Sertoli and Leydig cells in BS. The cytoplasm of germs cells and Leydig cells were stained with BDNF in NBS. NTRK2 was observed in the cytoplasm of Leydig cells of BS and NBS. Moreover, different stages of germ cells including undifferentiated spermatogonia and spermatocytes were immune labeled with NTRK2 in the NBS. These findings provided the first evidence of the localization of BDNF and NTRK2 in the testicular cells of stallions, suggesting the potential role of BDNF signaling in testes development and spermatogenesis. Further investigation is necessary to explore the functional implications of BDNF signaling on spermatogenesis, focusing on the regulatory mechanisms that govern the seasonal expression patterns observed. This will help confirm the paracrine/autocrine importance of this neurotrophin in the stallions testes.

Objective To investigate the effect of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism on the recovery after subcortical stroke, using the modified Rankin Scale (mRS).Methods Subcortical stroke patients with copies of BDNF Val66Met polymorphism (n=7) were compared to their controls (n=7) without a copy of BDNF Val66Met polymorphism after matching for initial severity, location and type of stroke. The mRS scores at 1 and 3 months after discharge from the neurorehabilitation unit were compared between the groups.Results A repeated measures ANOVA for mRS revealed significant interaction between time and group (F(2, 24) =37.2, p<0.001) and a significant effect of time (F(2, 24)=10.8, p<0.001), thereby reflecting significant differences between the Met allele (+) group and the Met allele (-) group. There was a significant difference in mRS scores at 3 months post-discharge between the two groups (p=0.01) although no difference was evident in mRS scores at 1 month post-discharge between the two groups. There were significant improvements between mRS scores on admission and mRS scores at 1 month post-discharge (p=0.02), and between mRS scores at 1 month post-discharge and mRS scores at 3 months post-discharge (p=0.004) in the Met allele (-) group.Conclusion BDNF Val66Met polymorphism may be associated with worse functional outcome in Korean patients with subcortical stroke. Therefore, BDNF Val66Met polymorphism should be considered as an important prognostic factor for recovery and responses to rehabilitation therapies after stroke in Korean patients. There is a need for developing different rehabilitation strategies for the population with BDNF Val66Met polymorphism. Further studies assessing different outcomes for various functional domains of stroke recovery are needed to clarify the role of BDNF Val66Met polymorphism.

본 연구의 목적은 20대 비만 여성을 대상으로 8주간 유산소 운동이 BDNF 및 혈중지질에 미치는 영향 을 규명하고 연구를 통해 20대 비만 여성의 인지기능 향상과 비만 개선을 위한 기초 과학적 정보를 제 공하고자 하였다. 연구의 목적을 달성하기 위해 20대 비만 여성 17명을 대상으로 유산소운동그룹(AEG) 9명과 통제그룹(CG) 8명으로 나누어 트레이닝을 실시하였다. 자료처리 방법은 SPSS/PC+Ver. 21.0K 프로 그램을 사용하여 모든 종속변인들의 기술통계량(Mean ± Standard Error)을 산출하였다. 동집단 내 트레 이닝 전과 후의 평균 비교를 위해 대응표본 t-검정(paired t-test)을 실시하였으며, 집단 간 트레이닝 전 과 후의 변화량 차이를 비교하기 위해 독립표본 t-검정을 실시하였다. 이에 다음과 같은 결론을 얻었다. 8주간 유산소 운동을 실시한 후 AEG에서 BDNF가 유의하게 증가하였으며 체중, 체지방률, TG, TC, LDL-C의 유의한 감소가 나타났다. 이러한 결과로 유산소 운동이 젊은 비만 여성들에게 인지기능의 긍정 적인 영향을 끼치며, 비만 개선에 효과가 나타났다고 볼 수 있다.

Objectives This study aimed to elucidate the effects of an 8-week aerobic exercise on Brain-Derived Neurotrophic Factor (BDNF) and blood lipids among young obese women in their 20s to provide foundational scientific information for the enhancement of cognitive function and obesity improvement. Methods Participants were young obese women aged 19–25 years old, with a body fat percentage of 29%. They were divided into two groups: an Aerobic Exercise Group (AEG) with nine members and a Control Group (CG) with eight members. The exercise regimen employed a 50–60% Target Heart Rate (THR) intensity and was conducted for eight weeks. The training sessions took place four times a week and comprised a 10-minute warm-up, 50 minutes of aerobic exercise, and a 10-minute cooldown, which totaled 70 minutes per session. Results Increased BDNF and significantly reduced weight, body fat percentage, triglycerides, total cholesterol, and low-density lipoprotein-cholesterol were observed in the aerobic exercise group. There were significant differences in weight, body fat, body fat percentage, and waist circumference before & after training combined excise group and combined excise protein intake group. Conclusions Therefore, aerobic exercise had a positive impact on cognitive functions and was effective in improving obesity in young obese women. Additionally, compound exercise or a combination of compound exercise and protein intake effectively improved body composition.

Background: Brain-derived neurotrophic factor (BDNF) and its receptor, neurotrophic tyrosine receptor kinase-2 (NTRK2), are well known for their roles in the central nervous and animal reproductive systems. Several studies have observed the extensive expression of BDNF and NTRK2 in non-neuronal tissues, especially reproductive organs. However, most of these studies focused on ovarian development and regulation; thus, scientific research on BDNF and NTRK2 in males is required to determine their roles in the male reproductive system. Therefore, this study aimed to investigate BDNF and NTRK2 expression in bovine testes. Methods: Testes were collected from six Hanwoo bulls (6-8 months old). Reverse transcription-polymerase chain reaction (RT-PCR) analysis was performed to investigate the mRNA expression of BDNF and NTRK2 in the testes. Western blot analysis was performed to verify the cross-reactivity of BDNF and NTRK2 antibodies with bovine testicular tissues. Immunohistochemistry was conducted to determine BDNF and NTRK2 protein expression in the testes. Results: RT-PCR analysis revealed BDNF and NTRK2 mRNA expression in bovine testes. In Western blotting, BDNF and NTRK2 protein bands were observed at 32 and 45 kDa, respectively. Immunofluorescence demonstrated BDNF expression in the nuclei of spermatogonia and Sertoli cells as well as in the cytoplasm of Leydig cells. NTRK2 was exclusively expressed in Sertoli cells. These results suggest that BDNF plays a potential role in spermatogenesis via BDNF and NTRK2 signaling in bovine testes, a finding supported by previous results in different animal species. Conclusions: The expression patterns of BDNF and NTRK2 indicate their functional importance in the bovine reproductive system.