الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
 |  | from | 231 |  |  |
| | | from | 231 | | |
Abstract
Muscle atrophy is a physiological consequence of aging (age-related sarcopenia), defined as the presence of both low muscle mass and low muscle function (strength or performance), reduced cross-sectional area of myofibers with subsequent impaired strength is the main characteristic of muscle atrophy accompanied with a consistent depletion of contractile proteins. Unfortunately there are no specific medications to date.
The present study was undertaken to explore the mechanisms by which Tfg and/or BM-MSCs either locally or intravenous could activate the antioxidant system, repress inflammation, apoptosis, molecular and genetic expression and consequently, ameliorate muscle atrophy disease in the experimental rat model.
A total number of 70 of adult male albino rats (" ~ "3 months old) Weighing 150-170 gm. After acclimation period of one week animals were divided into two groups negative control (n=10) and Muscle atrophy (MA) group (n=60) treated with Simvastatin (80 mg/Kg b.wt./ day) for 46 days then (MA) group is divided into 6 subgroups for to test various treatments each group contains 10 rats.
(1) : Muscular atrophy group (MA) and served as positive control group and immediately sacrificed by the end of the 46 days.
(2) : (MA+Tfg) which was treated with Tfg only (500mg/day.).
(3):(MA + L.BM-MSCS) this group was treated with BM-MSCS only where each rat received a single dose of 0.5 ml phosphate-buffered saline as a vehicle of stem cells injected locally (1x 106 cell in PBS) in the gastrocnemius muscles. (4): (MA + IV.BM-MSCS) this group was treated with BM-MSCS (1x 106 cell in PBS) only where each rat received a single dose of 0.5 ml phosphate- buffered saline as a vehicle of stem cells injected intravenously in the caudal vein.
Summary and Conclusion
(5) : Received co-treatment of Tfg and BM-MSCs (1x 106 cell in PBS)injected locally (MA+L.BM-MSCS+Tfg).
(6) : (MA+IV.BM-MSCS+Tfg) animals were administrated a double treatment of Tfg and BM-MSCs (1x 106 cell in PBS) served intravenously within the caudal vein.
After 30 days, orbital blood samples were obtained from the retro-orbital venous plexus using microcapillaries. The blood samples were collected in a clean dry centrifuge tubes and allowed to clot for obtaining the sera. Serum samples were separated by centrifugation at 10000 rpm for 15 minutes at 4°C, frozen and stored at -20°C for further analysis.
Following blood collection all the experimental animals were sacrificed by cervical dislocation and the gastrocnemius muscles were dissected and used for molecular biology analysis, as well as, Histopathological techniques.
In order to figure out muscle atrophy and the treatment efficacy serum biomarkers CK and Troponine, oxidative stress, apoptosis and inflammatory markers were determined also, molecular investigations of atrogin-1, FoxO-3, m-TOR, C-miR-486 and PAX3 were carried out accompanied to histopathological analysis using hematoxylin and eosin (H & E) stain.
The present results showed that:
Tfg and/or BM-MSCs showed gradual improvement in most of the parameters which was confirmed by the histopathological determinations, all together confirmed the present scientific team assumption that Tfg and BM- MSCs have promising therapeutic role in the treatment of muscular atrophy which needs more studies and investigations.
133
Conclusion:
The present results could conclude that Trigonella foenum-graecum and Bone marrow mesenchymal stem cells have a promising therapeutic role against Muscle atrophy induced in male rats by Simvastatin as indicated the observed improvement in biochemical and molecular genetic markers which were confirmed by histological examination. This role was achieved through powerful antioxidants activity, anti-inflammatory properties and anti-apoptotic effects of the active constituents of Tfg and BM-MSCS.