scholarly journals Combination of Aerobic Exercise and Continuous Environmental Enrichment Improves Adult Male Rats’ Spatial Memory: Study on Hippocampal Insulin Like Growth Factor 1 (IGF-1) and Fibroblast Growth Factor 2 (FGF-2) Expression

2019 ◽  
Vol 11 (2) ◽  
pp. 210-6
Author(s):  
Sophie Yolanda ◽  
Sri Redjeki ◽  
Trinovita Andraini ◽  
Dewi Irawati Soeria Santoso ◽  
Nurhadi Ibrahim ◽  
...  

BACKGROUND: Memory declines with the progression of age through the neurodegeneration process. Aerobic exercise and environmental enrichment can delay neurodegeneration by improving neuroplasticity via expression of insulin like growth factor 1 (IGF-1), fibroblast growth factor 2 (FGF-2) and other proteins. Combination treatment of aerobic exercise and continuous environmental enrichment and their effect on the expression of IGF-1 and FGF-2 which were expected to improve memory function has not been studied previously. Thus, this study aimed to observe it.METHODS: This is an experimental research using 24 male Wistar rats (Rattus norvegicus, 300-400 g, age 7-8 months) divided randomly into 4 groups: control (C), aerobic exercise (A), continuous (EE), and combination of aerobic exercise and continuous environmental enrichment (A-EE). At the end of an 8-week treatment, rats were sacrificed, and an enzyme-linked immunosorbent assay (ELISA) examination was performed to assess hippocampal IGF-1 and FGF-2 levels.RESULTS: In the 8th week, A-EE group showed the best improvement in rats’ spatial memory (47.84±10.6 %) followed by EE group (45.03±4.1 %), A group (38.61±3.8 %), and C group (22.76±7.12 %). However, A-EE group’s hippocampal IGF-1 (16.21±7.56 ng/mg protein) and FGF-2 (1.29±0.57 ng/mg protein) expression were not higher than other groups.CONCLUSION: Improvement in memory function in the combination group is a result of induction of various growth factors’ expression in the hippocampus, including IGF-1 and FGF-2, but the primary pathway of memory function improvement may be from other growth factors.KEYWORDS: spatial memory, aerobic exercise, environmental enrichment, hippocampus, IGF-1, FGF-2

2019 ◽  
Author(s):  
Jian Wang ◽  
Weishan Zhuge ◽  
Xiaoai Lu ◽  
Ruimin You ◽  
Leping Liu ◽  
...  

AbstractBackgroundMinimal hepatic encephalopathy (MHE) is implicated in the impairment of memory function. Fibroblast growth factor-2 (FGF2) is involved in modulating synaptic and neuronal formation.MethodsThe aim of this study is to examined the impacts of FGF2 on MHE pathology. Our study addressed whether FGF2 could trigger neuregulin-1 (NRG1) release to ameliorate synaptic impairment in MHE rats and in primary cultured neurons.ResultsThe results showed the decreased FGF2 expression in MHE brains. After treatment with FGF2, secreted neuregulin-1 (NRG1) and ErbB4 were increased, and the interaction of the 2 proteins was enhanced. Additionally, treatment with FGF2 or NRG1 induced synaptic formation, with increase in the activity of synapse and the density of dendritic spine, through Sirt1. NRG1 signaling was prevented by administration of FGF2, which acts through the FGFR1 in MHE rats. Finally, intracerebroventricular injection with FGF2 or NRG1 mitigated the impairment of synaptogenesis.ConclusionThe data suggest that FGF2 may be a promising latent therapeutic reagent for MHE pathogenesis.


2020 ◽  
Author(s):  
Saidan Ding ◽  
Jian Wang ◽  
Weishan Zhuge ◽  
Yiru Ye ◽  
Xiaoai Lu ◽  
...  

Abstract Minimal hepatic encephalopathy (MHE) is implicated in the impairment of memory function. Fibroblast growth factor-2 (FGF2) is involved in modulating synaptic and neuronal formation. The aim of this study is to examined the impacts of FGF2 on MHE pathology. Our study addressed whether FGF2 could trigger neuregulin1 (NRG1) release to ameliorate synaptic impairment in MHE rats and in primary cultured neurons. The results showed the decreased FGF2 expression in MHE brains. After treatment with FGF2, secreted neuregulin1 (NRG1) and ErbB4 were increased, and the interaction of the 2 proteins was enhanced. Additionally, treatment with FGF2 or NRG1 induced synaptic formation, with increase in the activity of synapse and the density of dendritic spine, through Sirt1.NRG1 signaling was prevented by administration of FGF2, which acts through the FGFR1 in MHE rats. Intracerebroventricular injection with FGF2 or NRG1 mitigated the impairment of synaptogenesis. The data suggest that FGF2 may be a promising latent therapeutic reagent for MHE pathogenesis.


2000 ◽  
Vol 279 (2) ◽  
pp. R548-R553 ◽  
Author(s):  
Alon Eliakim ◽  
Youngman Oh ◽  
Dan Michael Cooper

Anabolic effects of exercise are mediated, in part, by fibroblast growth factor-2 (FGF-2), insulin-like growth factor-I (IGF-I), and growth hormone (GH). To identify local vs. systemic modification of these mediators, 10 male subjects performed 10 min of unilateral wrist-flexion exercise. Blood was sampled from catheters placed in basilic veins of both arms. Lactate was significantly increased only in the exercising arm. FGF-2 decreased dramatically ( P < 0.01) in both the resting (from 1.49 ± 0.32 to nadir at 0.11 ± 0.11 pg/ml) and exercising arm (1.80 ± 0.60 to 0.29 ± 0.14 pg/ml). Small but significant increases were found in both the resting and exercising arm for IGF-I and IGF binding protein-3 (IGFBP-3). GH was elevated in blood sampled from both the resting (from 1.04 ± 0.68 to a peak of 2.57 ± 0.53 ng/ml) and exercising arm (1.04 ± 0.66 to 2.43 ± 0.42 ng/ml, P < 0.05). Unilateral wrist exercise was not sufficiently intense to increase circulating lactate or heart rate, but it led to systemic changes in GH, IGF-I, IGFBP-3, and FGF-2. Low-intensity exercise involving small muscle groups can influence the circulating levels of growth factors.


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