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Metal-Organic Frameworks-Derived Self-Supported Carbon-Based Composites pertaining to Electrocatalytic Water Breaking.
01). ② The activities of T-SOD, CAT, and GSH/GSSG in IRE were significantly increased compared with those in IR (P＜0.01). Compared with IR, the contents of 8-OHdG and MDA in IRE were significantly decreased (P＜0.01). ③ The expressions of Nrf2 and GLUT4 in gastrocnemius of IRE rats were increased than those in IR (P＜0.01). Conclusion The Nrf2 pathway was activated in gastrocnemius of rats after aerobic exercise, which promoted the activity of antioxidant enzymes, and prevented IR induced by high- glucose and high-fat diet.Objective To investigate the effects of 4-week electroacupuncture intervention on "Browning" of white fat in rats, and to explore its molecular mechanisms. Methods Twenty-four 8-week-old male SD rats were randomly divided into sedentary group (Sed), aerobic exercise group (Exe) and electroacupuncture group (ElA), 8 rats in each group. Exe group used 65% Max oxygen uptake intensity treadmill exercise, 1 h/d,6 d/w, while the ElA group used electric acupuncture to stimulate "zusanli" and "tianshu" points, 20 min/d,6 d/w, and the weight of rats was recorded every week. After 4 weeks of intervention, blood samples were collected from the apex and abdominal aorta. The wet weight of scapular fat and perirenal fat of rats was detected and the body fat and the serum levels of Irisin were determined. What's more, the expressions of adenosine 5'-monophosphate activated protein kinase-α (AMPKα), phosphorylation of adenosine 5'-monophosphate activated protein kinase-α (p-AMPKα), peroxisome proliferator activated receptor 1). Conclusion 4 weeks of electroacupuncture intervention can effectively control the weight of rats and induce "browning" of white fat, and its effect was similar to aerobic exercise, which may be release Irisin through the AMPKα-PGC-1α-FNDC5-Irisin signaling pathway, and then "crosstalk" with adipose tissue, up-regulate the expression of UCP1, and induce "browning" of white adipose tissue.Objective To investigate the changes of metabolites of teenage football players after exercise-induced fatigue. Methods Twelve male teenage football players (14～16 yrs) were selected as experimental subjects in this study. And an exercise model including aerobic and anaerobic exercise as one group exercise was established by using power bicycle completion 6 min 150 W load, 60～65 r/min of riding exercise and 30 s of riding exercise which load was the maximum speed set by the tester's weight. The rest took 1 min in the middle of one group exercise, and repeat 3 times of one group exercise, then rest for 3 min after one group exercise. The maximum oxygen uptake (VO2 max) and average anaerobic power were measured after each group exercise. Their urine samples were collected before and after the whole exercise model, and gas chromatograph-mass spectrometer (GC-MS) was used to detect the differential metabolites. Results The teenage football players had a significant decrease in anaerobic capacity after fatigue. Compared with pre-exercise, a total of 25 differential metabolites were screened out, of which 3 metabolites were significantly higher and 22 metabolites were markedly lower. The related metabolic pathways of above differential metabolites were classified as glycine-serine-threonine metabolism, tricarboxylic acid cycle, tyrosine metabolism, nitrogen metabolism and glycerophospholipid metabolism, respectively. Conclusion After exercise-induced fatigue occurs in teenage football players, the body's metabolites sarcosine, L-allothreonine, creatine, serine, succinic acid, citric acid, 4-hydroxyphenylacetic acid, hydroxylamine, and ethanolamine produce significant changes. The above-mentioned differential metabolites can be used as indicators for teenage football players' exercise-induced fatigue evaluation.Objective To investigate the changes of pyroptosis-related proteins in the hippocampus of insulin-resistant mice and the regulation of resistance training on pyroptosis-related proteins. Methods Six-week-old male C57BL/6J mice were randomly divided into control group (C, n=12) and high-fat diet group (HFD, n=26) for normal or high-fat diet for 12 weeks. Subsequently, according to the results of glucose tolerance test (GTT) and insulin tolerance test (ITT), the rats fed with high-fat diet were divided into insulin resistance group (IR, n=10) and resistance exercise group (RT, n=10) as well as to maintain high-fat diet. At the same time, mice in the RT group were subjected to resistance training. After 12 weeks, all mice were sacrificed after anesthesia, brain was removed and hippocampus was exfoliated, and the expressions of pyroptosis-related proteins were detected by Western blot. Results Compared with the C group, NF-κB, the NLRP3 inflammasome proteins, their downstream pyroptosis-related proteins GSDMD-N and GSDMD as well as inflammation factors IL-1β and IL-18 in hippocampus of IR group were significantly increased (P＜0.05), and the expression levels of SIRT1 and p-AMPK protein were significantly decreased (P＜0.05). Compared with the IR group, NF-κB, the NLRP3 inflammasome proteins, their downstream pyroptosis-related proteins GSDMD-N and GSDMD as well as inflammation factors IL-1β and IL-18 in hippocampus of RT group were significantly decreased (P＜0.05), and the expression levels of SIRT1 and p-AMPK protein were significantly increased (P＜0.01). Conclusion NLRP3 inflammasome in the hippocampus of insulin-resistant mice is activated, which mediates pyroptosis in the hippocampus. Twelve weeks of resistance training can effectively inhibit the activation of NLRP3 inflammasome and decrease pyroptosis and improve inflammation in the hippocampus.Objective To evaluate the neuroprotective effects of linagliptin, a dipeptidyl peptidase-4(DPP-4) inhibitor, on cerebral ischemia/reperfusion(I/R) injury in mice. Methods BALB/c mice were randomly divided into Sham group, I/R group and linagliptin (2.5, 5 and 10 mg/kg) +I/R group, 8 mice in each group. The mice in the linagliptin group were administrated by gavage 3 weeks before I/R. Etrumadenant mw I/R injury model was induced by MCAO, neurological deficit scores(n=8) and infarct volume(n=4) were assessed 24 h following reperfusion. Forty-eight hours following reperfusion, mice were euthanized, the contents of glutathione (GSH), malondialdehyde (MDA), phosphoinositide 3 kinase (PI3K), phosphoprotein kinase B (p-Akt) and rapamycin target protein (mTOR) in brain tissue were measured (n=4). Results Compared with the I/R group, the neurological deficit score and infarct volume were significantly decreased in the linagliptin pretreatment group after 24 h reperfusion (P＜0.05); the MDA content in the brain was significantly decreased (P＜0.
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