AIM: We want to demonstrate that the antioxidant properties of Swietenia macrophylla ethanol extract nanoparticles can prevent kidney cell damage brought on by streptozotocin (STZ) in the current investigation.
METHODS: This study employs high-energy ball milling to produce nanoparticles from S. macrophylla extract. Additionally, dynamic light scattering (DLS) is utilized to characterize the nanoparticle sizes of the S. macrophylla ethanol extract. Five groups, each consisting of 8 rats, were formed from 40 rats. Control rats received distilled water, the diabetic rats were administered STZ injections, while S. macrophylla rats were given S. macrophylla extract nanoparticles orally and STZ injection. After the trial, blood from a rat was drawn intracardially to check the levels of blood urea nitrogen (BUN) and creatinine. The levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA) were then assessed in kidney tissue samples. Histological alterations were evaluated in kidney section samples.
RESULTS: A DLS analysis estimated the size of the S. macrophylla ethanol extract nanoparticles to be about 91.50 ± 23.06 nm. BUN and creatinine levels were significantly raised after STZ treatment. STZ significantly decreased SOD and GPx levels in kidney tissue while raising MDA levels (p < 0.05). Swietenia macrophylla ethanol extract nanoparticle caused the decreased levels of BUN and creatinine in blood to normal levels (p < 0.05), indicating that S. macrophylla ethanol extract prevented the STZ-induced kidney cell damage. Additionally, S. macrophylla nanoparticles significantly raise GPx and SOD levels in kidney tissue while lowering MDA levels (p < 0.05). These actions are thought to have prevented kidney histological alterations (degeneration and necrosis) in diabetic rats.
CONCLUSION: According to these results, the anti-oxidative stress properties of S. macrophylla nanoparticles make them potentially effective nephroprotective therapies for STZ-induced kidney cell damage.
MATERIAL AND METHODS: Transmission and field emission scanning electron microscopy (TEM and FESEM) were used for the characterisation of CaCO3 nanocrystals. Cytotoxicity and genotoxic effect of calcium carbonate nanocrystals in cultured mouse embryonic fibroblast NIH 3T3 cell line using various bioassays including MTT, and Neutral red/Trypan blue double-staining assays. LDH, BrdU and reactive oxygen species were used for toxicity analysis. Cellular morphology was examined by scanning electron microscopy (SEM) and confocal fluorescence microscope.
RESULTS: The outcome of the analyses revealed a clear rod-shaped aragonite polymorph of calcium carbonate nanocrystal. The analysed cytotoxic and genotoxicity of CaCO3 nanocrystal on NIH 3T3 cells using different bioassays revealed no significance differences as compared to control. A slight decrease in cell viability was noticed when the cells were exposed to higher concentrations of 200 to 400 µg/ml, while increase in ROS generation and LDH released at 200 and 400 µg/ml was observed.
CONCLUSIONS: The study has shown that CaCO3 nanocrystal is biocompatible and non toxic to NIH 3T3 fibroblast cells. The analysed results offer a promising potential of CaCO3 nanocrystal for the development of intracellular drugs, genes and other macromolecule delivery systems.
METHODS: Participants (N.=27) with the mean age of 16.95±0.8 years, height of 165.6±6.1 cm and weight of 54.19±8.1 kg were matched into either modified exponential taper (N.=7), normal exponential taper (N.=7), or control (N.=7) groups using their initial VO2max values. Both experimental groups followed a 12-week progressive endurance training program and subsequently, a 2-week tapering phase. A simulated 20-km time trial performance along with VO2max, power output, heart rate and rating of perceived exertion were measured at baseline, pre and post-taper. One way ANOVA was used to analyze the difference between groups before the start of the intervention while mixed factorial ANOVA was used to analyze the difference between groups across measurement sessions. When homogeneity assumption was violated, the Greenhouse-Geisser Value was used for the corrected values of the degrees of freedom for the within subject factor the analysis.
RESULTS: Significant interactions between experimental groups and testing sessions were found in VO2max (F=6.67, df=4, P<0.05), power output (F=5.02, df=4, P<0.05), heart rate (F=10.87, df=2.51, P<0.05) rating of perceived exertion (F=13.04, df=4, P<0.05) and 20KM time trial (F=4.64, df=2.63, P<0.05). Post-hoc analysis revealed that both types of taper exhibited positive effects compared to the non-taper condition in the measured performance markers at post-taper while no different were found between the two taper groups.
CONCLUSIONS: It was concluded that both taper protocols successfully inducing physiological adaptations among the junior cyclists by reducing the volume and maintaining the intensity of training.
METHODS: Ten male collegiate rowers and physically active untrained subjects were recruited. Muscle synergies were extracted from 16 rowing-specific muscles using Principal Component Analysis with varimax rotation. Incremental rowing VO2 max Test was performed on slides ergometer (SE). Rowing performance and physiological variables were analyzed.
RESULTS: Rowers exerted greater power output, more energy expenditure and better rowing economy compared to untrained subjects. Rowers preferred to row slower with longer strokes compared to the untrained subjects. Three muscle synergies with high indices of similarity of waveform patterns were extracted in both groups. Significant association was found between muscle synergies and rowing economy.
CONCLUSIONS: The findings of this study showed that muscle synergies were robust during aerobic-dominant activity for collegiate rowers and untrained subjects. Rowers and coaches could utilize the findings by emphasizing on muscle coordination training, which may enhance the rowing economy.
PURPOSE: This study aimed to compare the kinetics of power output using FI and FR of an anaerobic performance (Wingate test) under 2, 3 and 4% state of hypohydrations.
METHOD: Thirty two collegiate cyclists (age = 22 ± 2 years; body weight = 71.45 ± 3.43 kg; height = 173.23 ± 0.04 cm) were matched using their baseline anaerobic peak power (APP) then randomly divided into 4 groups of EU (euhydrated), 2H, 3H and 4H respectively.
RESULTS: As expected the, FI, APP, anaerobic lower power (ALP) and rating of perceived exertion (RPE) did not show significant differences between and within the groups. However, the FR in 3H (0.018 ± 0.005 s(-1)) and 4H (0.019 ± 0.010 s(-1)) were significantly lower than EU (0.033 ± 0.012 s(-1)). Post-test FR also showed significant reduction in 3H and 4H compared to their pre-test values (p<0.05).
CONCLUSION: Despite the lack of changes in APP and RPE, subjects in 3H and 4H showed evidence of lower reduction of power output over time. The findings support earlier reports which showed no change in anaerobic performance under mild hypohydrations. The relatively lower FR suggests higher drive in maintaining power output under hypohydrations of 3 and 4% body weight.
MATERIALS AND METHODS: The STIM1 effect was assessed via dicersubstrate siRNA-mediated STIM1 knockdown. The effect of STIM1 knockdown on the expression of AKT and MAPK pathway-related genes and reactive oxygen species (ROS) generation-related genes was tested using real-time polymerase chain reaction. Cellular functions, including ROS generation, cell proliferation, and colony formation, were also evaluated following STIM1 knockdown.
RESULTS: The findings revealed that STIM1 knockdown reduced intracellular ROS levels via downregulation of NOX2 and PKC. These findings were associated with the downregulation of AKT, KRAS, MAPK, and CMYC. BCL2 was also downregulated, while BAX was upregulated following STIM1 knockdown. Furthermore, STIM1 knockdown reduced THP-1 cell proliferation and colony formation.
CONCLUSION: This study has demonstrated the role of STIM1 in promoting AML cell proliferation and survival through enhanced ROS generation and regulation of AKT/MAPK-related pathways. These findings may help establish STIM1 as a potential therapeutic target for AML treatment.