We investigated the effect of moderate- and high-intensity resistance training on hippocampal neurotrophic factors and peripheral CCL11 levels in high-fat diet (HFD)-induced obese mice. C57/black male mice received a 4 weeks diet of normal (control, CON; n = 9) or a high-fat diet (HF; n = 27) to induce obesity. Thereafter, the HF group was subdivided equally into the HF, HF + moderate-intensity exercise (HFME), and HF + high-intensity exercise (HFHE) groups (n = 9, respectively), and mice were subjected to ladder-climbing exercise for 8 weeks. The hippocampal brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels were significantly lower in the HF group than in the CON group (p < 0.05). In addition, in the HFME and HFHE groups were significantly higher than in the HF group (p < 0.05). The peripheral CCL11 levels were significantly higher in the HF group than in the CON group (p < 0.05). In addition, in the HFME and HFHE groups were significantly lower than in the HF group (p < 0.05). However, there was no significant difference according to the exercise intensity among the groups. Collectively, these results suggest that obesity can induce down-regulation of neurotrophic factors and inhibition of neurogenesis. In contrast, regardless of exercise intensity, resistance training may have a positive effect on improving brain function by inducing increased expression of neurotrophic factors.

Acute ischemic stroke results from sudden decrease or loss of blood supply to an area of the brain, resulting in a coinciding loss of neurological function. The antioxidant action of melatonin is an important mechanism among its known effects to protective activity during ischemic/reperfusion injury. The focus of this research, therapeutic efficacy of melatonin on recovery of neurological function following long term treatment in ischemic brain injured rats. Male Sprague-Dawley rats (n=40; 8 weeks old) were divided into the control group, and MCAo groups (Vehicle, MT7 : MCAo+ melatonin injection at 7:00, MT19 : MCAo+melatonin injection at 19:00, and MT7,19 : MCAo+melatonin injection at 7:00 and 19:00). Rat body weight and neurological function were measured every week for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of zoletil (40 mg/kg) and xylazine (10 mg/kg) and sacrificed for further analysis. Tissues were then collected for RNA isolation from brain tissue. Also, brain tissues were analyzed by histological procedures. We elucidated that melatonin was not toxic in vital organs. MT7,19 was the most rapidly got back to mild symptom on test of neurological parameter. Also, exogenous melatonin induces both the down-regulation of detrimental genes, such as NOSs and the up-regulation of beneficial gene, including BDNF during long term administration after focal cerebral ischemia. Melatonin treatment reduced the loss of primary motor cortex. Therefore, we suggest that melatonin could be act as prophylactic as well as therapeutic agent for neurorehabilitative intervention.

Melatonin is induced by light information through the retina and leads to growth factor activation. Thus, we investigated the effects of melatonin by controlling the photoperiod of growing young rats. Male Sprague‐gDawley rats (n=6; 4 weeks old) were divided into two experimental groups: the L/D group (normal photoperiod; light/dark: 12/12 h; lights on at 9:00 a.m.) and the L/L group (light/light: 24 h). Rat body weight and food consumption were measured daily for 8 weeks. After 8 weeks, the rats were anesthetized with a mixture of ketamine (50 mg/kg) and xylazine (10 mg/kg) and sacrificed. Tissue was then collected for RNA isolation (from brain, heart, liver, kidney, adrenal gland, testis, tibia, hind limb muscles). Also, serum was isolated from blood using a centrifugal separation. The L/L group had significantly lower body weight than the L/D group from 4 to 6 weeks (p<0.05). The L/D group had increased tissue mass, compared with the L/L group, but the difference was not statistically significant. The L/D group had a significantly higher melatonin concentration than the L/L group between the hours of midnight and 2:00 a.m (p<0.01). These results indicate that photoperiod length may affect the secretion of melatonin from the pineal gland. Also, the reduction of nocturnal melatonin secretion may retard the development of growing young rats. In future studies, we plan to compare exogenous melatonin administration with endogenous melatonin concentration induced by photoperiod control. Moreover, we will confirm whether the effects seen in pathological animal models can be reversed by controlling the photoperiod.