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High-intensity interval training (HIIT) has proven to be a time-saving and efficient exercise strategy. Compared with traditional aerobic exercise, it can provide similar or even better health benefits. In recent years, a number of studies have suggested that HIIT could be used as a potential exercise rehabilitation therapy to improve cognitive impairment caused by obesity, diabetes, stroke, dementia and other diseases. HIIT may be superior to regular aerobic exercise. This article reviews the recent research progress on HIIT with a focus on its beneficial effect on brain cognitive function and the underlying mechanisms. HIIT may become an effective exercise for the prevention and/or improvement of brain cognitive disorder.

The aim of the present study was to observe the expression of pyroptosis- and inflammation-related proteins in the hippocampus of mice with insulin resistance (IR) after aerobic exercise, and to explore the possible mechanism of exercise to improve IR. C57BL/6J male mice of 6 weeks old were randomly fed with normal diet (n = 12) and high-fat diet (HFD) (n = 26) for 12 weeks respectively. Glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed to determine whether IR occurred in HFD mice. Then the mice were randomly divided into control group (n = 12), IR group (n = 10) and IR + aerobic exercise group (AE, n = 10). Mice in AE group performed a 12-week progressive speed treadmill training after being adapted to the treadmill for one week. After the intervention, the expression of pyroptosis- and inflammation-related proteins in hippocampus was detected by Western blot. The results showed that compared with control group, NFκB, Nod-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing CARD (ASC), pyroptosis-related proteins like pro-Caspase-1, gasdermin D (GSDMD), GSDMD-N, and inflammatory factors IL-1β, IL-18 were significantly increased. The inflammasome-related protein NIMA-related kinase 7 (NEK7) and pyroptosis-related protein Caspase-1 showed an increasing trend, but there was no significant difference. Compared with the IR group, progressive speed treadmill training significantly reduced the expression of NFκB, NLRP3, NEK7, ASC, pro-Caspase-1, GSDMD, GSDMD-N, IL-1β, and IL-18 in the hippocampus of mice with IR. These results suggested 12-week progressive speed treadmill training can significantly reduce the expression of pyroptosis-related proteins and inflammatory factors in the hippocampus of mice with IR, and inhibit pyroptosis.

To investigate the effects of supplement of corn peptides plus aerobic exercise on fat loss and blood lipid profile in obese rats resulted from high fat diet and the mechanism:the role of adipose triglyceride lipase (ATGL) and lipoprotein lipase (LPL).One hundred and fifty male SD rats (4 weeks age) were randomly divided into control group (C,①Compared with obesity control group, the body weight and the masses of perirenal fat and epididymal fat in exercise group and corn peptides+exercise group were decreased obviously, with more obvious decrease in the corn peptides+exercise group compared with the exer-cise group. No difference was found in the rats of corn peptides group and casein group. ②Compared with obesity control group, the plasma TG was decreased in exercise group, and the plasma levels of TG and TC were reduced in the rats of corn peptides+exercise group, while they remained unchanged in the rats of corn peptides group and casein group. The plasma levels of HDL and LDL had no significant difference a-mong groups. ③The protein levels of ATGL in livers and LPL in adipose tissues were significantly increased in the rats of exercise group and corn peptides+exercise group, with more obvious in the latter group. No difference was shown in the rats of corn peptides group and casein group compared with obesity control group.Significant decrease of body weight, perirenal fat and epididymal fat as well as plasma TG, TC were induced by 4-week aerobic exercise or supplement of corn peptides plus exercise, with more obvious effects induced by corn pep-tides plus exercise than exercise, while no effect was induced by corn peptides alone, which may be related to the enhancements of the protein levels of ATGL in livers and LPL in adipose tissues.

Exercise can increase neurogenesis and affect gene expression in the brains of adult rats. Little is known about how exercise intensity affects neurogenesis and associated gene expression in juvenile rats. Here, we show that exercise influenced neurogenesis and mRNA expression of brain derived neurotrophic factor (BDNF), N-methyl-d-aspartate receptor type 1 (NMDAR1), vascular endothelial growth factor (VEGF) and fetal liver kinase-1 (Flk-1) in the hippocampus of 5 weeks old rats in an intensity-dependent manner. One week of low- or moderate-intensity exercise in a treadmill running task enhanced neurogenesis in the dentate gyrus of hippocampus. The low-, but not the high-, intensity exercise paradigm resulted in significantly increased expression of BDNF, NMDAR1, and Flk-1 mRNA. Gene expression levels in the low-intensity exercise group were greater than the high-intensity group for these four molecules.

LINGO-1 is a transmembrane receptor expressed primarily in the central nervous system (CNS) and plays an important role in myelination. Recent studies have indicated that it is also involved in oligodendrocyte precursor cell (OPC) survival and differentiation; however, the downstream signaling pathway underlying OPC development is unknown. In our previous study, we found that LINGO-1 is associated with WNK1 in mediating Nogo-induced neurite extension inhibition by RhoA activation. In an effort to identify the role of LINGO-1-WNK1 in OPCs, we first confirmed that WNK1 is also expressed in OPCs and co-localized with LINGO-1, which suppresses WNK1 expression by RNA interference-attenuated Nogo66-induced inhibition of OPC differentiation. Furthermore, we mapped the WNK1 kinase domain using several fragmented peptides to identify the key region of interaction with LINGO-1. We found that a sequence corresponding to the D6 peptide is necessary for the interaction. Finally, we found that using the TAT-D6 peptide to introduce D6 peptide into primary cultured OPC inhibits the association between LINGO-1 and WNK1 and significantly attenuates Nogo66-induced inhibition of OPC differentiation. Taken together, our results show that WNK1, via a specific region on WNK1 kinase domain, interacts with LINGO-1, thus mediating Nogo66-inhibited OPC differentiation.

Nongenomic mechanisms of corticosterone (B) inhibition of nicotine (Nic)-induced calcium influx were investigated in PC12 cells. Corticosterone could rapidly inhibit the Ca2+ influx induced by Nic, and BSA-conjugated B had a similar inhibitory effect. The inhibition of Nic-induced Ca2+ influx by B could be mimicked by protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) and reversed by PKC inhibitors, chelerythrine chloride and Go6976. When PC12 cells were pretreated with pertussis toxin, the inhibitory effect of B on Nic-induced Ca2+ influx was blocked. Both B and BSA-conjugated B could activate PKC activity, with the maximal responses at 10(-9) and 10(-7) M at 37 C, respectively. The dose-response curve was bell shaped. At 25 C, however, the dose-response curve considerably shifted to the right, and B was most potent at 10(-5) M. The time course showed that PKC activity was highest at 5 min of B's action. The results suggest that B might act via putative membrane receptors and inhibit the Ca2+ influx induced by Nic through the pertussis toxin-sensitive G protein-PKC pathway and that PKC plays an important role in the mechanisms of glucocorticoid nongenomic action.

To analyse the mechanism of corticosterone on the elevation of cytosolic free calcium ([Ca2+]i) induced by high-K+ in pheochromocytoma PC12 cells,The [Ca2+]i was real-time checked by fluorescence image system.(1) When the cells were preincubated at 37 degrees C for 5 min in the presence of various concentration corticosterone and stimulated with 55 mmol/L KCl , an inhibitory effect of corticosterone on delta[Ca2+]i was observed in a concentration-dependent manner. (2) When PC12 cells were preincubated with various concentration of B-BSA at 37 degrees C for 5 min and stimulated with 55 mmol/L KCl, an inhibitory effect of B-BSA on delta[Ca2+]i was observed, which is also concentration-dependent manner. (3) The inhibitory effect of corticosterone and B-BSA could not be antagonized by RU38486 at 10(-4) mol/L. (4) cycloheximide could not block the inhibitory effect of corticosterone after pretreating cells at 10(-5) mol/L at 37 degrees C for 3 hours.It is obvious that the locus of corticosterone action is on the plasmic membrane. The inhibitory effect of corticosterone is independent of protein synthesis and intracellular glucocorticoid receptor. The effect of corticosterone on [Ca2+]i is nongenomic action in PC12 cells.

To investigate the effect of treadmill running on the ability of learning in young rats, male Sprague-Dawley rats (5 weeks of age) were used for the experiment. Animals were randomly divided into the control and running groups (n=15 in each group). The rats in running group were made run on a motor-driven treadmill for 1 week at a speed of 2 m/min for the first 5 min, at a speed of 5 m/min for the next 5 min, then at a speed of 8 m/min for the last 20 min. Then the Morris water maze was used to observe learning and memory ability of rats in both groups. The tests consisted of place navigation and spatial probe test. We found that, in place navigation training, the latency of rats in running group was less than that in control group (P0.05); and from the third training session on, there was significant difference between the rats in control and running groups in swimming velocity (P0.01); furthermore, it was observed that the rats in running group had stronger motivation and more exact orientation in searching for platform, which could be indicated by the index of turn angle and angular velocity. In spatial probe test, there was no significant difference between the two groups in swimming velocity, percentage of swimming distance and frequency of crossing platform in D quadrant, where the platform situated (P0.05). These findings suggest that low speed treadmill running can enhance the ability of learning in young rats.

To observe the influence of tumor necrosis factor-alpha (TNF-alpha) on differentiation of rat mesencephalic neural stem cells (NSCs), the numbers of neurons, astrocytes and oligodendrocytes generated from NSCs were analyzed after differentiation for 3 days by using immunocytochemistry technique. The results show that: (1) TNF-alpha enhanced the proportions of neurons and oligodendrocytes in progeny of NSCs; and (2) TNF-alpha induced the proliferation of oligodendrocytes derived from NSCs, but the proliferation of astrocytes was not influenced by TNF-alpha. We conclude that the TNF-alpha could influence the application of NSCs.

Glucocorticoids (GCs) are routinely believed to work solely through genomic mechanisms. Recent evidence indicates that GCs can act at the membrane to exert rapid nongenomic effects on various tissues and cells. To ascertain whether nongenomic effects of GCs exist on the allergic asthma reaction, Hartley guinea pigs were sensitized with ovalbumin and challenged with the same antigen given by aerosol. Some animals received inhaled budesonide (3 mg/ml suspended in Hydroxypropyl methylcellulose vehicle) for 5 minutes before ovalbumin challenge; Other animals received saline or blank vehicle as control. We measured the changes of lung resistance and dynamic lung compliance, the pulmonary function used to evaluate allergic asthma severity. Inhaled budesonide inhibited allergic reaction within 10 minutes, which would preclude genomic-mediated responses that normally takes several hours to occur. This study infers for the first time that rapid nongenomic effect of GCs exists on allergic asthma reaction, and provides a new way to investigate nongenomic mechanism of GCs. Further study would raise the possibility of new therapeutic strategies for allergic disease including asthma.

There are numerous parallels between the heamatolymphopoietic and nervous systems in terms of the mechanisms regulating their development. We proposed that neural stem cells (NSCs) may respond to the microenvironmental signals provided by bone marrow stromal cells (BMSCs) which regulate the differentiation and maturation of hematolymphopoietic stem cells. First, we isolated and proliferated BMSCs from the femur and tibia, and NSCs from the midbrain of Sprague-Dawley (SD) rats, and then investigated the effects of BMSCs on the differentiation of NSCs into neurons, astrocytes and oligodendrocytes by directly plating neurospheres on BMSC monolayers in serum-free conditions. The results confirmed that BMSCs induced NSCs to differentiate selectively into neurons. The percentage of neurons significantly increased in 7 days in vitro co-cultures of NSCs and BMSCs as compared to NSCs cultures alone. When the duration of the cultures was extended to 12 days in vitro, BMSCs enhanced the survival of neurons derived from these NSCs; our investigation then focused on the underlying mechanism for this effect of BMSCs. NSCs were cultured with BMSC conditioned-medium and co-cultured with membrane fragments of live BMSCs or paraformaldehyde fixed BMSCs, the inducing activity of BMSCs was solely detectable in BMSC conditioned-medium, indicating that soluble factors secreted by BMSCs were responsible for its effect on the neuronal differentiation of NSCs. Therefore, BMSCs may provide a powerful tool for therapeutic neurological applications.

Objective. To examine the effect of electromagnetic fields (EMF) (20 Hz, 8 mT; 5 Hz, 8 mT) on the neuron-orientated differentiation of neural stem cells (NSCs) from midbrains of new-bom rats. Method. Differentiated NSCs were exposed to EMF for 2 x 15 min per day lasting for I d, 5 d, or 10 d. The sham-exposure controls were correspondingly established. Cells were fixed and processed for immunofluorescent staining using the antibody against neuron-specific marker MAP2, then the percentage of MAP2+ cells was calculated. Result. The two EMFs promoted the differentiation of a neuronal fate in different ways. Both of them came into effect even after 1 d exposure. When cells exposed to the 20 Hz EMF, the percentage of neuron-orientated cells gradually increased with longer-term exposure and the most significant effect appeared in 10 d group while that happened in 5 d group under the condition of 5 Hz EMF. The effect contrasted horizontally, significant differences between the two EMFs were observed only at 10 d groups, 20 Hz EMF having more favorable effect than 5 Hz EMF. Conclusion. 20 Hz and 5 Hz EMF could promote the differentiation of midbrain NSCs to a neuronal phenotype in different ways, suggesting that the physical induction might be another strategy to manipulate the differentiation of NSCs.

We report here a new example in which glucocorticoids (GCs) acted in a rapid, nongenomic way. In rat B103 neuroblastoma cells, 5-hydroxytryptamine (5-HT) was found to evoke an immediate rise in intracellular free calcium concentration ([Ca(2+)](i)). Pre-incubation of B103 cells for 5 min with corticosterone (B) or bovine serum albumin-conjugated corticosterone (B-BSA) concentration-dependently (10(-4)-10(-8) M) inhibited the peak increments in [Ca(2+)](i). Cortisol and dexamethasone had a similar effect, while deoxycorticosterone and cholesterol were ineffective. This rapid inhibitory effect of corticosterone could be mimicked by protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) and abolished completely by PKC inhibitors Ro31-8220 or GF-109203X. Neither pertussis toxin (PTX) nor nuclear GC receptor (GR) antagonist RU38486 influenced the rapid action of B. Our results suggest that GCs can modulate the 5-HT-induced Ca(2+) response in B103 cells in a membrane-initiated, nongenomic, and PKC-dependent manner.

To investigate the mechanism underlying the norepinephrine-induced elevation in intracellular calcium concentration ([Ca2+]i) in C6 glioma cells.Measurement of [Ca2+]i was carried out using the dual-wavelength fluorescence method with fura-2 as the indicator.Norepinephrine was found to induce concentration-dependent increases in [Ca2+ ]i through alpha1-adrenoreceptors. The [Ca2+]i elevations were extracellular-calcium independent and not influenced by the treatment of pertussis toxin. Pretreatments with either U73122 or thapsigargin abolished the subsequent cellular calcium responses to norepinephrine. Preincubation with phorbol 12-myristate 13-acetate (PMA) significantly reduce d the [Ca2+]i elevations, while protein kinase C inhibitors Ro31-8220 or GF-109203X completely blocked the inhibitory action of PMA. However, drugs either activating or inhibiting the function of protein kinase A had no effect on the [Ca2+]i elevations.Norepinephrine induces calcium mobilization from internal stores by activation of phospholipase C in C6 cells. The [Ca2+]i elevation is negatively regulated by the activation of protein kinase C.

The effect of glucocorticoid(GC) on peak cytosolic free calcium net increment (delta[Ca2+]i) induced by high-K+ was detected with MiraCal Image System. The main results were as follows: (1) Corticosterone(B) could inhibit delta[Ca2+]i in a time-dependent and concentration-dependent manner. (2) The inhibitory effect of B could be mimicked by bovine-serum albumin conjugated corticosterone (B-BSA) also in a dose-dependent manner. (3) G-protein inhibitor, either PTX or GDP beta S significantly reduced the inhibitory effect of B and B-BSA on delta[Ca2+]i (4) PMA, a stimulator for protein kinase C(PKC), could inhibit delta[Ca2+]i. (5) Although the inhibitors of PKC, chelerythrine chloride and bisindolylamide I per se had no influence on delta[Ca2+]i, but they significantly antagonized the inhibitory effect of B and B-BSA on delta[Ca2+]i. It is postulated that GC inhibit delta[Ca2+]i induced by high-K+ through a membrane mechanism and by a pathway involving G-protein and PKC.