Effect of exercise on Mesencephalic astrocyte derived neurotrophic factor levelsin the striatum of rats suffering from Parkinsons

Background and aims: The aim of this study, regarding the results of the previous researches and the effects of voluntary exercise on neurotrophic factors in treating PD, was to evaluate changes MANF level of rats` stratum exposed to neurotoxin injected by the stereotaxic surgery following the four weeks of treadmill running. Methods: Twenty four rats were divided into four groups: Sham, Parkinson control, Parkinson exercise, and healthy control. Exercise group exercised for 4 weeks, 5 days per week and 2 15-minute sessions having at least 1 h interval. The purpose of injecting 6-OHDA into the brain striatum was to create an experimental model of PD. Three weeks after the injection of 6-hydroxydopamine (6-OHDA), Apo morphine rotational test was carried out in order to verify the rats with Parkinson latest. MANF levels in the striatum were measured by ELISA. Data was analyzed by one-way analysis of variance (ANOVA) and Tukey post-hoc test. Results: The findings showed that there is a significant difference in the striatum MANF level of Parkinson control group (26.91±9 pg/mg) compared to the healthy control group (45.22±2 pg/mg) (P≤0.05). Furthermore, the striatum MANF level in Parkinson exercise group (29.35±2 pg/mg) had an increase in comparison with the Parkinson control group (26.91±9 pg/mg), but the difference was not significant (P=0.997). Conclusion: This research has shown that performing treadmill running program cannot increase the MANF level of striatum. Therefore, we cannot decisively consider a neural protective role for this training protocol and it necessitates further studies

Resistance training-induced muscle hypertrophy is mediated by TGF-β1-Smad signaling pathway in male Wistar rats

The TGF-β1-Smad pathway is a well-known negative regulator of muscle growth; however, its potential role in resistance training-induced muscle hypertrophy is not clear. The present study proposed to determine whether and how this pathway may be involved in resistance training-induced muscle hypertrophy. Skeletal muscle samples were collected from the control, trained (RT), control + SB431542 (CITGF), and trained + SB431542 (RTITGF) animals following 3, 5, and 8 weeks of resistance training. Inhibition of the TGF-β1-Smad pathway by SB431542 augmented muscle satellite cells activation, upregulated Akt/mTOR/S6K1 pathway, and attenuated FOXO1 and FOXO3a expression in the CITGF group (all p <.01), thereby causing significant muscle hypertrophy in animals from the CITGF. Resistance training significantly decreased muscle TGF-β1 expression and Smad3 (P-Smad3S423/425) phosphorylation at COOH-terminal residues, augmented Smad2 (P-Smad2-LS245/250/255) and Smad3 (P-Smad3-LSer208) phosphorylation levels at linker sites (all p <.01), and led to a muscle hypertrophy which was unaffected by SB431542, suggesting that the TGF-β1-Smad signaling pathway is involved in resistance training-induced muscle hypertrophy. The effects of inhibiting the TGF-β1-Smad signaling pathway were not additive to the resistance training effects on FOXO1 and FOXO3a expression, muscle satellite cells activation, and the Akt/mTOR/S6K1 pathway. Resistance training effect of satellite cell differentiation was independent of the TGF-β1-Smad signaling pathway. These results suggested that the effect of the TGF-β1-Smad signaling pathway on resistance training-induced muscle hypertrophy can be attributed mainly to its diminished inhibitory effects on satellite cell activation and protein synthesis. Suppressed P-Smad3S423/425 and enhanced P-Smad2-LS245/250/255 and P-Smad3-LSer208 are the molecular mechanisms that link the TGF-β1-Smad signaling pathway to resistance training-induced muscle hypertrophy. © 2020 Wiley Periodicals, Inc