It is unknown whether the longer duration of vibration training (VT) has a beneficial effect on Parkinson's disease (PD). And also, the mechanisms underlying the reported sensorimotor-improvement in PD induced by short-duration of VT has not been determined. Here, we investigated the effects of longer duration (4 weeks) of low amplitude vibration (LAV) training on the numbers of dopaminergic neurons in the substantia nigra by immunostaining and the levels of dopamine (DA) and brain-derived neurotrophic factor (BDNF) in the striatum by HPLC and ELISA in the chronic MPTP lesion mouse. We demonstrated for the first time that the longer duration of VT could significantly increase the numbers of nigrostriatal DA neurons and the contents of striatal DA and BDNF in the MPTP mice. Our findings implied that longer duration of VT could protect dopaminergic neurons from the MPTP-induced damage probably by upregulating BDNF and also provided evidence for the beneficial effect of longer duration of VT on PD at the cellular and molecular level.
Abstract This study aims to explore the role of FoxO1 and its acetylation in the alleviation of hypoxia‐induced muscle atrophy by resistance training. Forty male Sprague–Dawley rats were randomly divided into four groups: normoxic control group (C), normoxic resistance training group (R), hypoxic control group (H) and hypoxic resistance training group (HR). Rats in R and HR groups were trained on an incremental weight‐bearing ladder every other day, while those in H and HR groups were kept in an environment containing 12.4% O 2 . After 4 weeks, muscles were collected for analysis. Differentiated L6 myoblasts were analysed in vitro after hypoxia exposure and plasmids transfection (alteration in FoxO1 acetylation). The lean body mass loss, wet weight and fibre cross‐sectional area of extensor digitorum longus of rats were decreased after 4 weeks hypoxia, and the adverse reactions above was reversed by resistance training. At the same time, the increase in hypoxia‐induced autophagy was suppressed, which was accompanied by a decrease in the expression of nuclear FoxO1 and cytoplasmic Ac‐FoxO1 by resistance training. The L6 myotube diameter increased and the expression of autophagic proteins were inhibited under hypoxia via intervening by FoxO1 deacetylation. Overall, resistance training alleviates hypoxia‐induced muscle atrophy by inhibiting nuclear FoxO1 and cytoplasmic Ac‐FoxO1‐mediated autophagy.
PURPOSE: To research the effects of resistance training on skeletal muscle at hypoxia and Akt-FoxO1 pathway regulatory role during this process. METHODS: 40 male Sprague-dawley rats were divided into four groups randomly and were raised at normoxia and hypoxia (12.4% O2) respectively. Two groups were trained to climb ladder (height 1.2m, inclined at 85°) with load every other day lasting 4-week. Other two groups were quiet control group. Body composition was tested by using DEXA. Isolated extensor digitorum longus (EDL), becips and soleus were made HE stained paraffin section to analyze muscle fibre cross section area (CSA). Total protein and RNA were abstracted to detect Akt, FoxO1, FoxO1 (S256) and downstream E3 ligase (MuRF1 and Atrogin-1) transcription and expression level. RESULTS: Rats lean body mass and CSA of EDL and soleus were decreased significantly(P<0.05 and P<0.05) after 4-week hypoxic exposure. Akt and FoxO1 (S256) expression were decreased, while the expression of FoxO1, MuRF1 and Atrogin-1 were increased (P<0.05). Relatively, resistance training could effectively reduce this atrophy and stimulate rat biceps and EDL hypertrophy (P<0.05 and P<0.05). Meanwhile, Akt and FoxO1(S256) expression were higher than hypoxia training group (P<0.05 ). CONCLUSIONS: Akt-FoxO1 pathway plays an important role in regulating muscle protein during resistance training in hypoxia. Akt activation lead to the nuclear exclusion of phosphorylated FoxO1, which is an important mechanism of resistance training alleviate muscle atrophy.
Purple sweet potatoes were studied in this paper.The extraction process of purple sweet potato anthocyanin was studied by ethanol extraction.The extraction process was optimized by response surface method.The optimum extraction process parameters of purple sweet potato anthocyanin obtained by univariate and response surface experimental design were as follows.The extraction temperature was 70 ℃,concentration of ethanol extract was 80 %,extraction pH was 1.0 and the ratio of solid-liquid was 1∶15(g/mL).
Trimethylamine N-oxide (TMAO) has attracted interest because of its association with cardiovascular disease and diabetes, and evidence for the beneficial effects of TMAO is accumulating. This study investigates the role of TMAO in improving exercise performance and elucidates the underlying molecular mechanisms. Using C2C12 cells, we established an oxidative stress model and administered TMAO treatment. Our results indicate that TMAO significantly protects myoblasts from oxidative stress-induced damage by increasing the expression of Nrf2, heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase (NQO1), and catalase (CAT). In particular, suppression of Nrf2 resulted in a loss of the protective effects of TMAO and a significant decrease in the expression levels of Nrf2, HO-1, and NQO1. In addition, we evaluated the effects of TMAO in an exhaustive swimming test in mice. TMAO treatment significantly prolonged swimming endurance, increased glutathione and taurine levels, enhanced glutathione peroxidase activity, and increased the expression of Nrf2 and its downstream antioxidant genes, including HO-1, NQO1, and CAT, in skeletal muscle. These findings underscore the potential of TMAO to counteract exercise-induced oxidative stress. This research provides new insights into the ability of TMAO to alleviate exercise-induced oxidative stress via the Nrf2 signaling pathway, providing a valuable framework for the development of sports nutrition supplements aimed at mitigating oxidative stress.
Objective Brown adipose tissues (BAT) activation is important for losing weight as its high energy expenditure in Mammalian. Recent studies showed that exercise may also be essential for BAT activation. Uncoupling protein 1 (UCP1), specifically expressed in BAT's mitochondria, uncouples oxidative phosphorylation and dissipates energy from Free Fatty Acids into heat. Activating the Adrenergic Receptor β3 (Adrβ3) provides fuel for mitochondrial heat production and up-regulates Cyclooxygenase 2 (COX2), which is a key factor of UCP1 synthesis. Sympathetic nerve excitement stimulated by exercise can release norepinephrine as a neurotransmitter, which can affect Adrβ3. Brown adipocyte (BAC) is a kind of adipocyte in vitro as a model to study heat production. Isoprenaline Hydrochloride (ISO) is a widely used as an Adrβ agonist. In this research, we tried to figure out the response of BAC to Adrβ3 activations with different time points and whether ISO can be used as a BAC activator.
Methods C3H10T1/2 cells were maintained in a humidified, 37°C, 5% CO2 incubator in DMEM/F12 medium with 10% fetal bovine serum (FBS). For brown adipogenesis, cells were first split into differentiation medium (DMEM/F12 containing 10% FBS, 20nM insulin, 1nM 3,3’5-Triiodo-L-thyronine(T3)) for 4 days, the medium was changed every other day. Confluent cells were treated for 2 days with brown adipose adipogenesis cocktails (differentiation medium containing 2µg/mL dexamethasone, 0.5mM isobutylmethylxanthine (IBMX), 0.125mM indomethacin and 1µM rosiglitazone) on day 4. Then the medium was replaced by differentiation medium and changed every other day. At day 10, the full differentiation adipocytes were treated with 10µM ISO for 0 (as control), 1, 3, 6, 12 and 24 hours. For the lipid droplets staining, the cells were fixed by 4% paraformaldehyde solution then stained with Oil Red O. The cells were harvested and the total cell lysates were extracted for protein analysis after each time point. The UCP1, COX2, and Adrβ3 expression levels were detected by western blot, using Actin as the internal protein. The results were expressed as the mean ± standard error of the mean (SEM). Group comparisons were performed using two-way ANOVA and LSD’s post-hoc tests.
Results After differentiation, the cell shapes converted from fibroblastic to a spherical shape. Dispersed small lipid droplets were observed in the cells. After ISO treatment, the red color after Oil Red Staining became lighter and the size of the lipid droplets turned to smaller. The Adrβ3 protein expressions were 1.00±0.00, 1.34±0.32, 1.07±0.50, 4.65±1.84*, 2.44±0.73, and 3.43±1.09 at 0h, 1h, 3h, 6h, 12h, and 24h after ISO treatment, respectively. After introduced to ISO, the UCP1 expression levels were 1.00±0.00, 1.95±0.39, 2.72±0.57, 5.68±1.82*, 3.49±0.92, and 2.79±1.05 at 0h, 1h, 3h, 6h, 12h, and 24h, respectively. And for COX2, the protein expressions were 1.00±0.00, 2.13±0.67, 1.82±0.33, 4.67±1.82*, 2.88±0.44, and 2.65±0.54, respectively. The * means p ˂ 0.05, compared with oh controls. The proteins expressions were reached to peak after 6 hours ISO treatment from the above results.
Conclusions UCP1 and COX2 protein expressions were increased in BAC according to Adrβ3's expression in different time points, indicating that Adrβ3 may induce adipolysis in BAC and help to burn fat and produce heat.
Nonalcoholic fatty liver disease (NAFLD) is a pathological syndrome characterized by excessive fat deposition in hepatocytes. A sedentary lifestyle is a major risk factor for NAFLD, and regular exercise is considered a cornerstone of NAFLD treatment independent of weight loss. Even low-intensity activity could have beneficial effects on NAFLD. Fibroblast growth factor 21 (FGF21), a cytokine mainly secreted by the liver, improves glucolipid metabolism, reduces inflammation and oxidative stress, increases insulin sensitivity, and acts on multiple organs through autocrine, paracrine, and endocrine actions. Both clinical trials and animal experiments have shown a high correlation between liver fat content and circulating blood FGF21 levels, and abnormal FGF21 signaling appears to be an important mechanism for the development of NAFLD. FGF21 is an exerkine that responds to exercise; therefore, it may be a key target in exercise to improve NAFLD. This review provides an overview of NAFLD and its pathogenesis, and summarizes the effects of exercise intervention on NAFLD, as well as the role of FGF21 in NAFLD. Emphasis is placed on possible mechanisms for improving NAFLD by targeting FGF21 during exercise.
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