Male Institute Of Cancer Research Research Articles

Investigation of Mild Traumatic Brain Injury Home Cage Behavior: The Home Cage Assay Advantages.

This study utilized the Noldus PhenoTyper Home Cage Monitoring system (HCM) to assess the behavioral and cognitive changes of experimental closed-head mild traumatic brain injury (mTBI). Seventy-nine adult male Institute of Cancer Research (ICR) mice were subjected to either a sham procedure or closed-head mTBI using the weight-drop model. Seven days post-injury, separate cohorts of mice underwent either a non-cognitive or a cognitive home cage assessment, a treadmill fatigue test, or the Open Field Test. mTBI significantly influenced habituation behavior and circadian wheel-running activity. Notably, mTBI mice exhibited an increased frequency of visits to the running wheel, but each visit was shorter than those of controls. No significant differences between the groups in discrimination or reversal learning performance were observed. However, during the reversal learning stage, mTBI mice performed similarly to their initial discrimination learning levels, suggesting an abnormally faster rate of reversal learning. Home cage monitoring is a valuable tool for studying the subtle effects of mTBI, complementing traditional assays. The automated evaluation of habituation to novel stimuli (e.g., novel environment) could serve as a potentially sensitive tool for assessing mTBI-associated behavioral deficits.

Cuproptosis mediates copper-induced testicular spermatogenic cell death.

Cuproptosis, a novel mechanism of programmed cell death, has not been fully explored in the context of spermatogenic cells. This study investigated the potential involvement of cuproptosis in spermatogenic cell death using a mouse model of copper overload. Sixty male Institute of Cancer Research (ICR) mice were randomly divided into four groups that received daily oral gavage with sodium chloride (control) or copper sulfate (CuSO4) at 50 mg kg-1, 100 mg kg-1, or 200 mg kg-1, for 42 consecutive days. Mice subjected to copper overload exhibited a disruption in copper homeostasis. Additionally, significant upregulated expression of key cuproptosis factors was accompanied by a significant rise in the rates of testicular tissue cell apoptosis. Immunohistochemical analysis revealed the presence of ferredoxin 1 (Fdx1) in Sertoli cells, Leydig cells, and spermatogenic cells at various stages of testicular development, and the Fdx1-positive staining area was significantly increased in copper-overloaded mice. Mitochondrial dysfunction and decreased adenosine triphosphate levels were also observed, further implicating mitochondrial damage under cuproptosis. Further analyses revealed pathological lesions and blood-testis barrier destruction in the testicular tissue, accompanied by decreased sperm concentration and motility, in copper-overloaded mice. In summary, our results indicate that copper-overloaded mice exhibit copper homeostasis disorder in the testicular tissue and that cuproptosis participates in spermatogenic cell death. These findings provide novel insights into the pathogenic mechanisms underlying spermatogenic cell death and provide initial experimental evidence for the occurrence of cuproptosis in the testis.

Enhanced anti-fatigue and exercise performances due to Huáng qí polysaccharide supplementation in mice

In modern society, people have busy and competitive lives, with different stresses causing fatigue and overwork, which may ultimately harm their health. We investigated the beneficial effects of Astragalus polysaccharide (rAPS) on fatigue and exercise performance. Forty male Institute of Cancer Research (ICR) mice were randomly divided into four groups according to body weight (BW): control group (distilled water), 1-fold dose group (0.70 g rAPS/kg BW/day), 2-fold dose group (1.40 g rAPS/kg BW/day) and a 5-fold dose group (3.50 g rAPS/kg BW/day). In terms of exercise performance, rAPS supplementation significantly improved grip strength performance and time to exhaust-loaded swim times when compared with controls (p < 0.05). Moreover, rAPS supplementation significantly reduced fatigue-related biochemical parameters, including blood lactate and BUN levels, while significantly improve muscle strength and swimming endurance times t(p < 0.05). Hence, we recommend that rAPS elicit antifatigue and performance-enhancing health benefits.

Toxicologic effect and transcriptome analysis for sub-chronic exposure to carbendazim, prochloraz, and their combination on the liver of mice.

Carbendazim (CBZ) and prochloraz (PCZ) are broad-spectrum fungicides used in agricultural peat control. Both fungicides leave large amounts of residues in fruits and are toxic to non-target organisms. However, the combined toxicity of the fungicides to non-target organisms is still unknown. Therefore, we characterized the toxic effects of dietary supplementation with CBZ, PCZ, and their combination for 90days in 6-week-old male Institute of Cancer Research (ICR) mice. CBZ-H (100mg/kg day), PCZ-H (10mg/kg day), and their combination treatments increased the relative liver weights and caused liver injury. The serum total cholesterol (TC), triglyceride (TG), glucose (Glu), pyruvate (PYR), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels were reduced, and synergistic toxicity was observed. Hepatic transcriptome revealed that 326 differentially expressed genes (DEGs) of liver were observed in the CBZ treatment group, 149 DEGs in the PCZ treatment group, and 272 DEGs in the combination treatment group. According to KEGG enrichment analysis, the fungicides and their combination affected lipid metabolism, amino acid metabolism, and ferroptosis. In addition, the relative mRNA levels of key genes involved in lipid metabolism were also examined. Compared with individual exposure, combined exposure to CBZ and PCZ caused a more obvious decrease in the expression of some genes related to glycolipid metabolism. Furthermore, the relative mRNA levels of some key genes in the combination treatment group were lower than those in the CBZ and PCZ treated groups. In summary, CBZ, PCZ, and their combination generally caused hepatotoxicity and glycolipid metabolism disorders, which could provide new insights for investigating the combined toxicity of multiple fungicides to animals.

Nasal Absorption Enhancement of Mometasone Furoate Nanocrystal Dispersions.

We designed a 0.05% mometasone furoate (MF) nanocrystal dispersion and investigated whether the application of MF nanocrystals in nasal formulations enhanced local absorption compared to traditional nasal MF formulations (CA-MF). MF nanocrystal dispersions (MF-NPs) were prepared by bead milling MF microcrystal dispersions (MF-MPs) consisting of MF, 2-hydroxypropyl-β-cyclodextrin, methylcellulose, and purified water. Pluronic F-127 combined with methylcellulose, Pluronic F-68, or carbopol was used as a base for in situ gelation (thickener). MF concentrations were measured using high-performance liquid chromatography, and nasal absorption of MF was evaluated in 6 week-old male Institute of Cancer Research (ICR) mice. The particle size range of MF prepared with the bead mill treatment was 80-200 nm, and the nanoparticles increased the local absorption of MF, which was higher than that of CA-MF and MF-MPs. In addition, unlike the results obtained in the small intestine and corneal tissue, the high absorption of nanocrystalline MF in the nasal mucosa was related to a pathway that was not derived from energy-dependent endocytosis. Moreover, the application of the in situ gelling system attenuated the local absorption of MF-NPs, owing to a decrease in drug diffusion in the dispersions. We found that nanoparticulation of MF enhances local intranasal absorption, and nasal bioavailability is higher than that of CA-MF. In addition, we demonstrate that viscosity regulation is an important factor in the design of nasal formulations based on MF nanocrystals. These findings provide insights for the design of novel nanomedicines with enhanced nasal bioavailability.

Arctiin alleviates functional constipation by enhancing intestinal motility in mice.

Functional constipation (FC), a common symptom that is primarily associated with intestinal motility dysfunction, is a common problem worldwide. Arctiin (Arc) is a lignan glycoside isolated from the Chinese herbal medicine Arctium lappa L., which is a health food in China. The present study aimed to evaluate the laxative effects of Arc against FC in mice. A model of FC induced by loperamide (5 mg/kg) was established in male Institute of Cancer Research (ICR) mice. Arc was administered at a dose of 100 mg/kg as a protective agent. The faecal status, intestinal motility and histological analyses were evaluated. Furthermore, the levels of gastrointestinal motility-associated neurotransmitters, such as motilin (MTL), nitric oxide (NO), and brain-derived neurotrophic factor (BDNF) and the protective effect of Arc on interstitial cells of Cajal (ICC) were assessed. Arc treatment reversed the loperamide-induced reduction in faecal number and water content and the intestinal transit ratio in ICR mice. Histological analysis confirmed that Arc administration mitigated colonic injury. Moreover, Arc treatment increased levels of motilin and brain-derived neurotrophic factor while decreasing nitric oxide levels and ICC injury in the colon of FC mice. Arc decreased inflammation induction and aquaporin expression levels. Owing to its pro-intestinal motility property, Arc was shown to have a protective effect against FC and may thus serve as a promising therapeutic strategy for the management of FC.

Effects of Salinomycin and Deferiprone on Lead-Induced Changes in the Mouse Brain.

Lead (Pb) is a highly toxic heavy metal that has deleterious effects on the central nervous system. This study aimed to investigate the effects of salinomycin (Sal) and deferiprone (DFP) on brain morphology and on the content of some essential elements in Pb-exposed mice. Adult male Institute of Cancer Research (ICR) mice were exposed to a daily dose of 80 mg/kg body weight ( b.w.) Pb(II) nitrate for 14 days and subsequently treated with Sal (16 mg/kg b.w.) or DFP (19 mg/kg b.w.) for another 14 days. At the end of the experimental protocol, the brains were processed for histological and inductively coupled plasma mass spectrometry (ICP-MS) analyses. Pb exposure resulted in a 50-fold increase in Pb concentration, compared with controls. Magnesium (Mg) and phosphorus (P) were also significantly increased by 22.22% and 17.92%, respectively. The histological analysis of Pb-exposed mice revealed brain pathological changes with features of neuronal necrosis. Brain Pb level remained significantly elevated in Sal- and DFP-administered groups (37-fold and 50-fold, respectively), compared with untreated controls. Treatment with Sal significantly reduced Mg and P concentrations by 22.56% and 18.38%, respectively, compared with the Pb-exposed group. Administration of Sal and DFP ameliorated brain injury in Pb-exposed mice and improved histological features. The results suggest the potential application of Sal and DFP for treatment of Pb-induced neurotoxicity.

Neuroprotective effects of betanin in mice with cerebral ischemia-reperfusion injury.

Cerebral ischemia reperfusion (IR) injury as found in stroke is a complex and heterogeneous disorder and closely related to disability and death. Today, nutraceuticals and protective therapy to increase neuronal integrity and prevent pathological complication are common. We investigated the neuroprotective effect of betanin against cerebral IR injury in mice. Forty male institute of cancer research (ICR) mice were divided into Sham-veh, IR-veh, IR-Bet50 and IR-Bet100 groups. After 2 weeks of oral administration of normal saline (vehicle; veh) or 50 mg/kg or 100 mg/kg of betanin (Bet), mice were subjected to IR induction using 30-min bilateral common carotid artery occlusion, followed by 24 h of reperfusion. Brain infarction, oxidative status, cortical and hippocampal neurons and white matter pathologies were evaluated. Results showed that IR significantly increases brain infarction, Cornus Ammonis 1 (CA1) hippocampal and corpus callosum (CC) and internal capsule (IC) white matter degeneration (P<0.05). Brain oxidative status revealed significant elevation of malondialdehyde (MDA) together with a significant decrease in catalase (CAT) activity, induced by IR (P<0.05). Pretreatment with betanin 100 mg/kg led to a significant reduction in brain infarction and MDA, CA1 hippocampus, CC and IC white matter degeneration. Betanin also led to a significant increase in CAT activity (P<0.05), with enhancing effect on reduced glutathione levels (GSH, P<0.05). The present study revealed the neuroprotective efficacy of betanin against IR injury in mice's brains, including its inhibition of lipid peroxidation, and boosting of GSH and CAT activity.

Branched-chain amino acid supplementation suppresses the detraining-induced reduction of mitochondrial content in mouse skeletal muscle.

Exercise training enhances oxidative capacity whereas detraining reduces mitochondrial content in skeletal muscle. The strategy to suppress the detraining-induced reduction of mitochondrial content has not been fully elucidated. As previous studies reported that branched-chain amino acid (BCAA) ingestion increased mitochondrial content in skeletal muscle, we evaluated whether BCAA supplementation could suppress the detraining-induced reduction of mitochondrial content. Six-week-old male Institute of Cancer Research (ICR) mice were randomly divided into four groups as follows: control (Con), endurance training (Tr), detraining (DeTr), and detraining with BCAA supplementation (DeTr + BCAA). Mice in Tr, DeTr, and DeTr + BCAA performed treadmill running exercises [20-30 m/min, 60 min, 5 times/week, 4 weeks]. Then, mice in DeTr and DeTr + BCAA were administered with water or BCAA [0.6mg/g of body weight, twice daily] for 2 weeks of detraining. In whole skeletal muscle, mitochondrial enzyme activities and protein content were decreased after 2 weeks of detraining, but the reduction was suppressed by BCAA supplementation. Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein content, a master regulator of mitochondrial biogenesis, was decreased by detraining irrespective of BCAA ingestion. Regarding mitochondrial degradation, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a mitophagy-related protein, was significantly higher in the Tr group than in the DeTr + BCAA group, but not different from in the DeTr group. With respect to mitochondrial quality, BCAA ingestion did not affect oxygen consumption rate (OCR) and reactive oxygen species (ROS) production in isolated mitochondria. Our findings suggest that BCAA ingestion suppresses the detraining-induced reduction of mitochondrial content partly through inhibiting mitophagy.

Benefits of p-coumaric acid in mice with rotenone-induced neurodegeneration.

The paper examines the use of natural antioxidant and anti-inflammation substances as therapeutic candidates for brain disease. Para-coumaric acid (pCA), a phenolic compound with a variety of medicinal properties, was used against deterioration caused by various diseases. Recently, pCA has gained attention for use against cardiovascular disease but less so for neurodegenerative disease (i.e., Parkinson's disease). Therefore, the present study intended to investigate the effect of pCA against rotenone-induced Parkinson's disease-like pathology in mice. Thirty male institute of cancer research (ICR) mice were randomly divided into three experimental groups: Sham-veh, Rot-veh, and Rot-pCA100. Rotenone (Rot) 2.5mg/kg was subcutaneously injected every 48h in the rotenone groups. Alternately, a 100mg/kg pCA dose was given every 48h via intragastric gavage to the Rot-pCA100 group for 6weeks. Motor ability was assessed at the second, fourth, and sixth week before brain collection for biochemical and histological analyses. Results indicated significant motor deficits appeared from the second to sixth week after rotenone injection. Brain analysis detected a significant effect of rotenone in the increase of malondialdehyde and tumor necrosis factor-alpha (TNF-α). This result was observed in accordance with a reduction of tyrosine hydroxylase (TH) and an increase of neuronal degeneration in the substantia nigra par compacta (SNc) and striatum. However, pCA was able to reverse all of the deterioration (i.e., reduced malondialdehyde and TNF-α) rotenone had caused, and it protected against TH and neuronal loss in the SNc and striatum. Therefore, the present study has depicted the neuroprotective effect of pCA against rotenone-induced Parkinson's disease-like pathology in mice. Benefits of pCA include anti-lipid peroxidation and anti-inflammatory effects, inhibition of neurodegeneration, and a nurturing effect on the TH level in the SNc and striatum, leading to mitigation of motor deficits.

Probiotic Lactiplantibacillus plantarum Tana Isolated from an International Weightlifter Enhances Exercise Performance and Promotes Antifatigue Effects in Mice.

Exercise causes changes in the gut microbiota, and in turn, the composition of the gut microbiota affects exercise performance. In addition, the supplementation of probiotics is one of the most direct ways to change the gut microbiota. In recent years, the development and application of human-origin probiotics has gradually attracted attention. Therefore, we obtained intestinal Lactiplantibacillus plantarum “Tana” from a gold-medal-winning weightlifter, who has taken part in various international competitions such as the World Championships and the Olympic Games, to investigate the benefits of Tana supplementation for improving exercise performance and promoting antifatigue effects in mice. A total of 40 male Institute of Cancer Research (ICR) mice were divided into four groups (10 mice/group): (1) vehicle (0 CFU/mice/day), (2) Tana-1× (6.15 × 107 CFU/mice/day), (3) Tana-2× (1.23 × 108 CFU /mice/day), and (4) Tana-5× (3.09 × 108 CFU/mice/day). After four weeks of Tana supplementation, we found that the grip strength, endurance exercise performance, and glycogen storage in the liver and muscle were significantly improved compared to those in the vehicle group (p < 0.05). In addition, supplementation with Tana had significant effects on fatigue-related biochemical markers; lactate, ammonia, and blood urea nitrogen (BUN) levels and creatine kinase (CK) activity were significantly lowered (p < 0.05). We also found that the improved exercise performance and antifatigue benefits were significantly dose-dependent on increasing doses of Tana supplementation (p < 0.05), which increased the abundance and ratio of beneficial bacteria in the gut. Taken together, Tana supplementation for four weeks was effective in improving the gut microbiota, thereby enhancing exercise performance, and had antifatigue effects. Furthermore, supplementation did not cause any physiological or histopathological damage.

Sea Bass Essence from Lates calcarifer Improves Exercise Performance and Anti-Fatigue in Mice.

Sea bass (Lates calcarifer) is rich in protein, amino acids, and long-chain omega 3 (omega-3), which have many health benefits. In East Asian food culture, soup is often eaten as a nutritional supplement. The purpose of this study was to investigate the benefits of Hi-Q sea bass essence (SBE) supplementation for improved exercise performance and anti-fatigue. Fifty male Institute of Cancer Research (ICR) mice were divided to five groups (10 mice/group) and administered different doses of SBE (EC): (1) vehicle (water); (2) isocaloric (0.94 g casein/kg/mice/day); (3) SBE-1X (1.04 g/kg/mice/day); (4) SBE-2X (2.08 g/kg/mice/day); and (5) SBE-4X (4.16 g/kg/mice/day). We found that SBE supplementation significantly improved more than 1.96-fold endurance exercise performance (p < 0.05) and more than 1.13-fold glycogen storage in the liver and muscles (p < 0.05), and had dose-dependent by SBE dose (p < 0.05). In addition, supplementation with SBE at different doses had significant effects on the fatigue-related biochemical markers, i.e., lactate, ammonia, and blood urea nitrogen (BUN) levels were reduced significantly (p < 0.05), and were also dose-dependent. In conclusion, supplementation with SBE for 4 weeks was able to effectively improve exercise performance and had an anti-fatigue effect. In addition, it did not cause any physiological or histopathological damage.

2,2',4,4'-Tetrabromodiphenyl ether disrupts spermatogenesis in mice by interfering with the ER-Nrf1-Tfam-mitochondria pathway.

2,2',4,4' -tetrabromodiphenyl ether (BDE47), a well-known endocrine disruptor of the estrogen receptor (ER) is toxic to the mitochondria and spermatogenesis. This study aimed to explore the mechanism of BDE47 on spermatogenesis in mammals. Adult male Institute of Cancer Research (ICR) mice were gavaged daily with BDE47 (0, 1, or 10mg/kg bw) for 8weeks. Testicular weight, sperm production and motility, morphology of spermatogenic cells, nuclear respiratory factor 1 (Nrf1) level, and its expression in testes were determined. In vitro, cell viability, and key molecules in the ER-Nrf1-mitochondrial transcription factor A (Tfam)-mitochondria pathway in the immortalized mouse spermatogonia line (GC1) were determined at 48h and 0-5h after exposure; RNA interference (RNAi) was also performed to verify that the decreased Nrf1 was associated with mitochondrial dysfunction and the impaired viability of germ cells. The results indicated that BDE47 impaired testis weight and spermatogenesis, impaired mitochondria and germ cells, and decreased Nrf1 in the testes of mice. In vitro, after 48h exposure, BDE47 reduced cell viability, Nrf1 protein, and mRNA of Nrf1, Tfam, ATP synthase subunit β (Atp5b), and cytochrome c oxidase subunit I (mt-CO1) in GC1 while also reducing mRNA of Nrf1 and Tfam promptly (from 1 to 5h) after exposure. Furthermore, Nrf1 RNA interference decreased viability and mitochondrial function in GC1. These results indicated that BDE47 disrupts spermatogenesis in mice, probably by interfering with the ER-Nrf1-Tfam-mitochondria pathway, and Nrf1 is a target molecule of BDE47 estrogen receptor.

Evaluation of genotoxicity of ethanolic extracts of Platostoma palustre by micronucleus assay

Platostoma palustre (Pp) jelly is a traditional food. Pp has been used as folk medicine and is effective against heat-shock, hypertension and diabetes. Therefore, the aim of this study was to evaluate the ethanolic extracts of Pp’ genotoxicity. The ethanolic extracts of Pp by using 40% ethanol for extraction. Evaluation of genotoxicity of ethanolic extracts of Pp by micronucleus assay was performed in vivo. During the in vivo genotoxicity-evaluated experiment, the experimental animal’s clinical behavior, body weight (BW), food consumption, and the percentage of RET/RBCs (reticulocytes/red blood cells) and MN-RET/RETs (micronucleated reticulocytes/reticulocytes) after the treatments of Pp ethanolic extracts were evaluated. Both sexes Institute of Cancer Research (ICR) mice were given three daily treatments by intraperitoneal injection of 2 mg/kg of mitomycin C (genotoxicity induction) or by oral route of 200 μL of PBS (normal control group). Until 48 h after the last treatment, K2-EDTA-anticoagulated peripheral blood specimens were collected. These blood samples were processed for the microscopy-based analysis using Giemsa stain and the percentage of reticulocytes and micronucleated reticulocytes was determined. The results were shown that the experimental animal’s clinical behaviors were normal in all groups. The BW and food consumption were no significant difference between all groups. RET/RBCs (‰) in male or female ICR mice in the negative control group, the normal control group, the high dose of Pp ethanolic extract group, the middle dose of Pp ethanolic extract group, and the low dose of Pp ethanolic extract group were respectively 7.8 ± 0.8 / 8.6 ± 0.8, 23.2 ± 1.5 / 22.1 ± 1.3, 22.8 ± 1.6 / 22.1 ± 1.7, 23.2 ± 1.5 / 22.6 ± 1.0 and 22.2 ± 1.9 / 23.9 ± 1.9; MN-RET/RETs (‰) in male or female ICR mice in the negative control group, the normal control group, the high dose of Pp ethanolic extract group, the middle dose of Pp ethanolic extract group, and the low dose of Pp ethanolic extract group were 2.0 ± 0.0 / 2.0 ± 0.0, 43.2 ± 10.6 / 39.6 ± 10.9, 1.8 ± 0.4 / 1.6 ± 0.5, 1.6 ± 0.5 / 1.4 ± 0.5, and 1.8 ± 0.4 / 1.6 ± 0.5, respectively. Both RET/RBCs (‰) and MN-RET/RETs (‰) in male or female ICR mice in the negative control group were significantly difference than the other groups (p &lt; 0.001). Taken all results together, Pp ethanolic extracts were without genotoxicity. Therefore, Pp ethanolic extracts were safety.

Anti-Fatigue and Exercise Performance Improvement Effect of Glossogyne tenuifolia Extract in Mice.

Glossogyne tenuifolia (GT) is a native perennial plant growing across the coastline areas in Taiwan. The current study aimed to examine the efficacy of GT extract in ameliorating physical fatigue during exercise and increasing exercise performance. Fifty male Institute of Cancer Research (ICR) mice were randomly segregated into five groups (n = 10) to GT extract orally for 4 weeks, at different concentrations (50, 100, 250, and 500 mg/kg BW/day): LGT 1X, MGT 2X, HGT 5X, and HGT 10X groups. Forelimb grip strength, endurance swimming time, serum biochemical marker levels, blood lipid profile and histological analysis of various organs were performed to assess the anti-fatigue effect and exercise performance of GT extract. The forelimb-grips strength and endurance-swimming time of GT-administered mice were increased significantly in a dose-dependent manner when compared to the control. Serum glucose, creatine kinase, and lactate levels were increased significantly in the HGT 10X group. Liver marker serum glutamic-oxaloacetic transaminase (GOT) was increased in the HGT 5X and HGT 10X groups, whereas Serum Glutamic Pyruvic Transaminase (GPT) was not altered. Renal markers, creatinine and uric acid levels, were not altered. Muscle and hepatic glycogen levels, which are essential for energy sources during exercise, were also significantly increased in a dose-dependent manner in all GT extract groups. No visible histological aberrations were observed in the vital organs after GT extract administration. The supplementation with GT extract could have beneficial effects on exercise performance and anti-fatigue function without toxicity at a higher dose.

Effects of Perch Essence Supplementation on Improving Exercise Performance and Anti-Fatigue in Mice.

Silver perch (Bidyanus bidyanus) has many nutrition and health benefits, being a rich source of macro and micronutrients, phospholipids, polyunsaturated fatty acids, and a variety of essential minerals while having a high protein content. In addition to direct consumption, it is often made into a soup as an important nutritional supplement for strengthening the body and delaying fatigue. By extracting the essence, its quality can be controlled, and it is convenient to supplement. This study aimed to evaluate the effect of supplementation with Santé premium silver perch essence (SPSPE) on improving exercise performance and anti-fatigue. Fifty male institute of cancer research (ICR) mice were divided into five groups (n = 10/group): (1) vehicle (vehicle control or water only), (2) isocaloric (0.93 g casein/kg/mice/day), (3) SPSPE-1X (0.99 g/kg/mice/day), (4) SPSPE-2X (1.98 g/kg/mice/day), and (5) SPSPE-5X (4.95 g/kg/mice/day). A sample or an equal volume of liquid was fed orally for four consecutive weeks. Grip strength and swimming exhaustion tests were used as exercise performance assessments. After 10 and 90 min of unloaded swimming, biochemical parameters of fatigue were evaluated. We found that supplementation with SPSPE for four consecutive weeks could significantly improve mice’s grip strength, exercise endurance performance, and glycogen content (p < 0.05), and significantly reduced post-exercise fatigue biochemical parameters, such as lactate, blood ammonia (NH3), blood urea nitrogen (BUN) concentration, and muscle damage index creatine kinase (CK) activity (p < 0.05). In summary, supplementation with SPSPE for 4 weeks could effectively improve exercise performance, reduce sports fatigue, and accelerate fatigue recovery. In addition, it did not cause any physiological or histopathological damage.

Effectiveness of human-origin Lactobacillus plantarum PL-02 in improving muscle mass, exercise performance and anti-fatigue

Gut microbiota is very important for energy metabolism and regulation, which in turn affect the health and physiological functions of the host, and provide energy required for exercise. Supplementation with probiotics may be one of the ways to change the gut microbiota. In recent years, many studies have shown that probiotic supplementation can effectively improve sports performance. In this study, we screened Lactobacillus plantarum (PL-02), a probiotic of human-origin, from the intestines of 2008 Olympic women's 48 kg weightlifting gold medalist and explored the role of PL-02 in improved exercise endurance performance, reduced fatigue biochemical parameters, and changes in body composition. Male Institute of Cancer Research (ICR) mice were assigned to 0, 2.05 × 109, 4.10 × 109 and 1.03 × 1010 CFU/kg/day groups and were fed by oral gavage once daily for 4 weeks. The results showed that 4 weeks of PL-02 supplementation could significantly increase muscle mass, muscle strength and endurance performance, and hepatic and muscular glycogen storage. Furthermore, PL-02 could significantly decrease lactate, blood urea nitrogen (BUN), ammonia, and creatine kinase (CK) levels after exercise (p < 0.05). We believe that PL-02 can be used as a supplement to improve exercise performance and for its anti-fatigue effect.

Effects of Long-Term Exposure to L-Band High-Power Microwave on the Brain Function of Male Mice.

Currently, the impact of electromagnetic field (EMF) exposure on the nervous system is an increasingly arousing public concern. The present study was designed to explore the effects of continuous long-term exposure to L-band high-power microwave (L-HPM) on brain function and related mechanisms. Forty-eight male Institute of Cancer Research (ICR) mice were exposed to L-HPM at various power densities (0.5, 1.0, and 1.5 W/m2) and the brain function was examined at different time periods after exposure. The morphology of the brain was examined by hematoxylin-eosin (HE) and deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. Furthermore, cholinergic markers, oxidative stress markers, and the expression of c-fos were evaluated to identify a “potential” mechanism. The results showed that exposure to L-HPM at 1.5 W/m2 can cause generalized injuries in the hippocampus (CA1 and CA3) and cerebral cortex (the first somatosensory cortex) of mice, including cell apoptosis, cholinergic dysfunction, and oxidative damage. Moreover, the deleterious effects were closely related to the power density and exposure time, indicating that long-term and high-power density exposure may be detrimental to the nervous system.

Lycopene Alleviates Titanium Dioxide Nanoparticle-Induced Testicular Toxicity by Inhibiting Oxidative Stress and Apoptosis in Mice.

The research was carried out to investigate the possible ameliorative effect of lycopene on TiO2 NPs-induced male reproductive toxicity and explore the possible mechanism. Ninety-six healthy male Institute of Cancer Research (ICR) mice were equally divided into eight groups (control group, 50mg/kg TiO2 NPs group, 5mg/kg LYC group, 20mg/kg LYC group, 40mg/kg LYC group, 50mg/kg TiO2 NPs + 5mg/kg LYC group, 50mg/kg TiO2 NPs + 20mg/kg LYC group, 50mg/kg TiO2 NPs + 40mg/kg LYC group), and the mice were treated by intragastric administration every day for 30days in this research. Sperm parameters, testicular histopathology, oxidant and antioxidant enzymes, and cell apoptosis-related protein expression in the testicular tissue were analyzed. The results showed that TiO2 NPs exposure significantly decreased sperm count and motility, and TiO2 NPs also increased sperm malformation in the epididymis; these characteristics were improved when co-administration with LYC. Testicular histopathological lesions like disorder of germ cells arrange, detachment, atrophy, and vacuolization were observed after TiO2 NPs exposure, and these abnormalities were effectively ameliorated by co-administration with LYC. Oxidative stress was induced by TiO2 NPs exposure as evidenced by increased the level of MDA and decreased the activity of SOD as well as the level of anti-O2-, and these alterations were effectively prevented by co-administration with LYC. LYC also alleviated TiO2 NPs-induced germ cell apoptosis by inhibiting mitochondrial apoptotic pathway, as shown by the upregulation of Bcl-2, the downregulation of Bax, Cleaved Caspase 3, and Cleaved Caspase 9. LYC could ameliorate TiO2 NPs-induced testicular damage via inhibiting oxidative stress and apoptosis, which could be used to alleviate the testicular toxicity associated with TiO2 NPs intake.

High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery.

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.