Objective:To investigate the effects of pulsed electromagnetic field(PEMF)on sevoflurane-induced cognitive dysfunction in elderly rats and also explore its related mechanism.Methods:Thirty elderly male rats were randomly divided into the control group,sevoflurane treatment group(SEV),and sevoflurane+PEMF treatment group(SEV+PEMF).Rats in the sevoflurane group and sevoflurane+PEMF group passively inhaled 2.5％sevoflurane for 4 h,while rats in the SEV+PEMF group were stimulated with 2 mT,15 Hz PEMF for 14 d(2 h/day).The cognitive function of rats was evaluated via the Morris water maze testing.The serum concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1β),IL-6,neuron specific enolase(NSE),and β amyloid protein(Aβ),as well as the levels of nerve growth factor(NGF)and brain-derived neurotrophic factor(BDNF)in hippocampal tissue,were de-termined via ELISA.Western blot was used to detect the expression of autophagy-related biomarkers in rat hippocampal tissue.Secondly,30 elderly male rats were randomly divided into three groups:SEV group,SEV+PEMF group,and SEV+3-MA(the autophagy inhibitor)+PEMF group.The Morris water maze experiment was used to evaluate the change of PEMF-induced improvement of cognitive function sevoflurane-inhaled elderly rats following the autophagy inhi-bition.Results:PEMF inhibited sevoflurane-induced increase in escape latency and overall swimming distance,as well as the decrease in the number of crossing target quadrant(P＜0.05);PEMF decreased the levels of serum Aβ and NSE in elderly rats inhaled with sevoflurane(P＜0.05),decreased the levels of TNF-α,IL-1β,and IL-6(P＜0.05),increased the levels of NGF and BDNF in hippocampal tissue(P＜0.05),inhibited neuronal apoptosis in hip-pocampal tissue and increased its autophagy level(P＜0.05).Following inhibition of autophagy with 3-MA,the im-provement of PEMF on the decreased learning and memory ability induced by sevoflurane in elderly rats was significantly inhibited(P＜0.05).Conclusion:PEMF can effectively inhibit sevoflurane-induced cognitive dysfunction in elderly rats by regulating the autophagy of hippocampal neuronal cells.

Objective To investigate the ameliorative effect and the related mechanism of rotating magnetic fields(RMF)on sevoflurane(SEV,a commonly used inhalational anesthetics in clinics)-induced cognitive impairments in elderly rats.Methods The cognitive functions of 24 elderly male SD rats which were allocated into 3 experimental groups(Control group,SEV group,and SEV+RMF group;n=8 per group)were assessedviawater maze testing,and the damage and repair of hippocampal neurons were detected using ELISA and Western blotting assays.Water maze testing was also conducted on additional 24 elderly male SD rats which were randomized into 3 groups(SEV group,SEV+RMF group,and SEV+autophagy inhibitor+RMF group;n=8 per group)for assessing their cognitive functions.Results Compared with SEV group,RMF intervention significantly reduced the escape latency and swimming distance in water maze test(P<0.01),while increasing the number of platform crossovers(P<0.001).RMF downregulated the serum levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in SEV-treated rats(P<0.001),and led to remarkable reductions in both serum neuron-specific enolase and β-amyloid protein levels(P<0.001).Moreover,RMF upregulated the expressions of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons(P<0.001),suppressed the expression of apoptotic protein caspase-3 and autophagy related protein p62 in the hippocampus,and upregulate the expression of autophagy related protein Beclin-1(P<0.001).However,the administration of autophagy inhibitor 3-MA abolished the ameliorative effects of RMF on SEV-induced cognitive impairments in elderly rats(P<0.001).Conclusion RMF can effectively improves SEV-induced cognitive dysfunction in elderly rats,and this neuroprotective effect is mediated by the autophagy activation in hippocampal neurons.

Objective: To explore the relationship between school sports environment and physical activity levels of middle school students, so as to provide theoretical and empirical support for optimizing school sports environment and enhance adolescent physical activity. Methods: Using multi-stage random cluster sampling, from September to December 2023, 1 329 junior and senior high school students from Xuancheng City of Anhui Province, Lianyungang City of Jiangsu Province, Wuhan City of Hubei Province, Qiqihar City and Suihua City of Heilongjiang Province, and Shenzhen City of Guangdong Province were selected. The International Physical Activity Questionnaire-Short Form (IPAQ-SF) assessed students physical activity levels, and the questionnaire on the characteristics of school sports environment was developed to evaluate the factors of school sports environment. Multivariate ordered Logistic regression was performed to analyze the correlation between school sports environment factors and physical activity levels, and the analytic hierarchy process determined the weight of key influencing factors. Results: The results showed that weekly vigorous physical activity time was [60 (25, 90)] minutes, moderate physical activity time was [60 (30, 90)] minutes, light physical activity time was [105 (40, 200)] minutes, and sedentary behavior time was [ 3 300 (2 100, 4 500)] minutes, only 10.53% of the students met World Health Organization physical activity recommendations, and 89.69% of the students averaged >8 h daily sedentary time. Multivariate ordered Logistic regression showed that adequate sports equipment significantly promoted physical activity across all intensities and reduced sedentary time ( OR = 4.97, 11.54, 4.03, 0.11); diverse sports activities improved vigorous and moderate physical activity while reducing sedentary time ( OR =4.20, 14.06, 0.17); and peer encouragement was associated with increased low-intensity physical activities and decreased sedentary time ( OR =10.40, 0.15)( P <0.05). The analytic hierarchy process weighting analysis identified the top three influential factors related to physical activity among middle school students: sufficient sports equipment, varied physical education activities, frequent peer encouragement, the influence weight accounts for 23.55% , 14.18% and 11.77% of the total, respectively. Conclusion Key school sports environmental factors for adolescent physical activity level include ensuring adequate sports equipment and class availability, diversifying activity content, fostering peer support, and cultivating an active sports culture and a comprehensive approach encourage students participation in extracurricular physical activities.

The incomplete degradation of tumour cells by macrophages(Mφ)is a contributing factor to tumour progression and metastasis,and the degradation function of Mφ is mediated through phagosomes and lysosomes.In our preliminary experiments,we found that overactivation of NADPH oxidase 2(NOX2)reduced the ability of Mφ to degrade engulfed tumour cells.Above this,we screened out liquiritin from Glycyrrhiza uralensis Fisch,which can significantly inhibit NOX2 activity and inhibit tumours,to elucidate that suppressing NOX2 can enhance the ability of Mφ to degrade tumour cells.We found that the tumour environment could activate the NOX2 activity in Mφ phagosomes,causing Mφ to produce excessive reactive oxygen species(ROS),thus prohibiting the formation of phagolysosomes before degradation.Conversely,inhibiting NOX2 in Mφ by liquiritin can reduce ROS and promote phagosome-lysosome fusion,therefore improving the enzymatic degradation of tumour cells after phagocytosis,and subse-quently promote T cell activity by presenting antigens.We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox,blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox,thereby inhibiting the activity of NOX2.This study elucidates the specific mechanism by which Mφ cannot degrade tumour cells after phagocytosis,and indicates that liquiritin can promote the ability of Mφ to degrade tumour cells by suppressing NOX2.

Objective To investigate the effect of dexmedetomidine(Dex)on bone loss in tail-suspended rats and primarily explore its regulatory mechanism on bone metabolism.Methods A total of 30 male rats were randomly divided into a control group,a model group,and a Dex group,with 10 animals in each group.Rat model of osteoporosis was established by hind limb suspension for 4 weeks.Dex at a dose of 10 μg/kg was given intraperitoneally,once every other day from the day of tail suspension.And equal amount of normal saline was given to the control and model group.Bone histological staining was used to observe the trabecular bone area fraction.Biomechanical three-point bending test was employed to measure the maximum load,stiffness,and fracture energy.Dual calcein/alizarin red fluorescence labeling and tartrate resistant acid phosphatase(TRAP)staining were applied respectively to detect the mineral apposition rate and bone formation rate as well as the number of osteoclasts on bone surfaces.Secondly,after primary osteoblasts were isolated from the tibiae of tail-suspended rats and then treated with 1 nmol/L Dex,the proportion of alkaline phosphatase(ALP)-positive osteoblasts and the activity of the enzyme were detected by ALP staining and activity test.qRT-PCR was applied to measure the expression of osteogenic activity-related factors,including osteocalcin(Ocn),Runt related transcription factor 2(Runx2),Osterix protein(Osx),and type 1 collagen(Col1).Results The animal experiments revealed that Dex treatment significantly increased the tibial trabecular bone area fraction,inhibited the decrease in bone mechanical strength,and enhanced the mineralization deposition rate and new bone formation rate of trabecular bone in the tail-suspended rats(all P＜0.001).The in vitro experiments showed that Dex treatment obviously improved ALP activity and the number of ALP-positive osteoblasts in primary osteoblasts isolated from tail-suspended rats(P＜0.01),and up-regulated the expression levels of osteogenic differentiation-related genes,such as Ocn,Runx2,Osx and Col1(P＜0.01).Conclusion Dex exerts anti-bone loss effect in tail-suspended rats,which may be associated with its stimulation on osteoblast-mediated bone formation.

The incomplete degradation of tumour cells by macrophages (Mϕ) is a contributing factor to tumour progression and metastasis, and the degradation function of Mϕ is mediated through phagosomes and lysosomes. In our preliminary experiments, we found that overactivation of NADPH oxidase 2 (NOX2) reduced the ability of Mϕ to degrade engulfed tumour cells. Above this, we screened out liquiritin from Glycyrrhiza uralensis Fisch, which can significantly inhibit NOX2 activity and inhibit tumours, to elucidate that suppressing NOX2 can enhance the ability of Mϕ to degrade tumour cells. We found that the tumour environment could activate the NOX2 activity in Mϕ phagosomes, causing Mϕ to produce excessive reactive oxygen species (ROS), thus prohibiting the formation of phagolysosomes before degradation. Conversely, inhibiting NOX2 in Mϕ by liquiritin can reduce ROS and promote phagosome-lysosome fusion, therefore improving the enzymatic degradation of tumour cells after phagocytosis, and subsequently promote T cell activity by presenting antigens. We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox, blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox, thereby inhibiting the activity of NOX2. This study elucidates the specific mechanism by which Mϕ cannot degrade tumour cells after phagocytosis, and indicates that liquiritin can promote the ability of Mϕ to degrade tumour cells by suppressing NOX2.

Objective:To explore whether LBP3 exerts anti-tumor effects by promoting production of short-chain fatty acids(SCFAs)by intestinal microbiota and regulating function of polymorphonuclear myeloid-derived suppressor cells(PMN-MDSC).Methods:A subcutaneous H22 liver cancer model was employed to assess anti-tumor activity of LBP3 and its regulatory effects on PMN-MDSC.Pseudo-sterile tumor-bearing mouse model was used to investigate role of intestinal microbiota in tumor suppression of LBP3.Fecal microbiota transplantation(FMT)was conducted to explore immune regulatory role of LBP3-modulated flora.Serum SCFAs levels in tumor-bearing mice were quantified using liquid chromatography-mass spectrometry,and effect of SCFAs butyrate on arginase 1(Arg-1)expression was evaluated in vitro.Results:Both low-dose(125 mg/kg)and high-dose(250 mg/kg)LBP3 signifi-cantly inhibited tumor growth in H22 tumor-bearing mice,also led to a marked reduction in proportion of PMN-MDSC in both spleen and tumor,a reduced proportion of Treg in lymphoid tissues,a decrease in Arg-1 level within tumor,infiltration of CD8+T cells into tumor was significantly enhanced.However,these effects of LBP3 were did not observed in pseudo-sterile mice,while the above changes could be reproduced after fecal supernatant transplantation in high-dose LBP3 treatment group,suggesting a crucial role for gut microbiota.Furthermore,co-expression of Ly6G and SCFA receptor GPR43 in tumor was also observed.LBP3 treatment resulted in increased levels of SCFAs,particularly butyrate,in both blood and tumor tissues.In vitro,butyrate was shown to inhibit Arg-1 expression in MSC-2 cells,further supporting hypothesis that SCFAs mediate immune-modulatory effects of LBP3.Conclusion:LBP3 exerts its anti-tumor effects by promoting SCFA production,which subsequently inhibits function of PMN-MDSC.This highlights LBP3's potential as an immunomodulatory agent in cancer therapy.

Objective:To investigate the effects of pulsed electromagnetic field(PEMF)on sevoflurane-induced cognitive dysfunction in elderly rats and also explore its related mechanism.Methods:Thirty elderly male rats were randomly divided into the control group,sevoflurane treatment group(SEV),and sevoflurane+PEMF treatment group(SEV+PEMF).Rats in the sevoflurane group and sevoflurane+PEMF group passively inhaled 2.5％sevoflurane for 4 h,while rats in the SEV+PEMF group were stimulated with 2 mT,15 Hz PEMF for 14 d(2 h/day).The cognitive function of rats was evaluated via the Morris water maze testing.The serum concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1β),IL-6,neuron specific enolase(NSE),and β amyloid protein(Aβ),as well as the levels of nerve growth factor(NGF)and brain-derived neurotrophic factor(BDNF)in hippocampal tissue,were de-termined via ELISA.Western blot was used to detect the expression of autophagy-related biomarkers in rat hippocampal tissue.Secondly,30 elderly male rats were randomly divided into three groups:SEV group,SEV+PEMF group,and SEV+3-MA(the autophagy inhibitor)+PEMF group.The Morris water maze experiment was used to evaluate the change of PEMF-induced improvement of cognitive function sevoflurane-inhaled elderly rats following the autophagy inhi-bition.Results:PEMF inhibited sevoflurane-induced increase in escape latency and overall swimming distance,as well as the decrease in the number of crossing target quadrant(P＜0.05);PEMF decreased the levels of serum Aβ and NSE in elderly rats inhaled with sevoflurane(P＜0.05),decreased the levels of TNF-α,IL-1β,and IL-6(P＜0.05),increased the levels of NGF and BDNF in hippocampal tissue(P＜0.05),inhibited neuronal apoptosis in hip-pocampal tissue and increased its autophagy level(P＜0.05).Following inhibition of autophagy with 3-MA,the im-provement of PEMF on the decreased learning and memory ability induced by sevoflurane in elderly rats was significantly inhibited(P＜0.05).Conclusion:PEMF can effectively inhibit sevoflurane-induced cognitive dysfunction in elderly rats by regulating the autophagy of hippocampal neuronal cells.

Objective To investigate the ameliorative effect and the related mechanism of rotating magnetic fields(RMF)on sevoflurane(SEV,a commonly used inhalational anesthetics in clinics)-induced cognitive impairments in elderly rats.Methods The cognitive functions of 24 elderly male SD rats which were allocated into 3 experimental groups(Control group,SEV group,and SEV+RMF group;n=8 per group)were assessedviawater maze testing,and the damage and repair of hippocampal neurons were detected using ELISA and Western blotting assays.Water maze testing was also conducted on additional 24 elderly male SD rats which were randomized into 3 groups(SEV group,SEV+RMF group,and SEV+autophagy inhibitor+RMF group;n=8 per group)for assessing their cognitive functions.Results Compared with SEV group,RMF intervention significantly reduced the escape latency and swimming distance in water maze test(P<0.01),while increasing the number of platform crossovers(P<0.001).RMF downregulated the serum levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in SEV-treated rats(P<0.001),and led to remarkable reductions in both serum neuron-specific enolase and β-amyloid protein levels(P<0.001).Moreover,RMF upregulated the expressions of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons(P<0.001),suppressed the expression of apoptotic protein caspase-3 and autophagy related protein p62 in the hippocampus,and upregulate the expression of autophagy related protein Beclin-1(P<0.001).However,the administration of autophagy inhibitor 3-MA abolished the ameliorative effects of RMF on SEV-induced cognitive impairments in elderly rats(P<0.001).Conclusion RMF can effectively improves SEV-induced cognitive dysfunction in elderly rats,and this neuroprotective effect is mediated by the autophagy activation in hippocampal neurons.

Objective:To explore whether LBP3 exerts anti-tumor effects by promoting production of short-chain fatty acids(SCFAs)by intestinal microbiota and regulating function of polymorphonuclear myeloid-derived suppressor cells(PMN-MDSC).Methods:A subcutaneous H22 liver cancer model was employed to assess anti-tumor activity of LBP3 and its regulatory effects on PMN-MDSC.Pseudo-sterile tumor-bearing mouse model was used to investigate role of intestinal microbiota in tumor suppression of LBP3.Fecal microbiota transplantation(FMT)was conducted to explore immune regulatory role of LBP3-modulated flora.Serum SCFAs levels in tumor-bearing mice were quantified using liquid chromatography-mass spectrometry,and effect of SCFAs butyrate on arginase 1(Arg-1)expression was evaluated in vitro.Results:Both low-dose(125 mg/kg)and high-dose(250 mg/kg)LBP3 signifi-cantly inhibited tumor growth in H22 tumor-bearing mice,also led to a marked reduction in proportion of PMN-MDSC in both spleen and tumor,a reduced proportion of Treg in lymphoid tissues,a decrease in Arg-1 level within tumor,infiltration of CD8+T cells into tumor was significantly enhanced.However,these effects of LBP3 were did not observed in pseudo-sterile mice,while the above changes could be reproduced after fecal supernatant transplantation in high-dose LBP3 treatment group,suggesting a crucial role for gut microbiota.Furthermore,co-expression of Ly6G and SCFA receptor GPR43 in tumor was also observed.LBP3 treatment resulted in increased levels of SCFAs,particularly butyrate,in both blood and tumor tissues.In vitro,butyrate was shown to inhibit Arg-1 expression in MSC-2 cells,further supporting hypothesis that SCFAs mediate immune-modulatory effects of LBP3.Conclusion:LBP3 exerts its anti-tumor effects by promoting SCFA production,which subsequently inhibits function of PMN-MDSC.This highlights LBP3's potential as an immunomodulatory agent in cancer therapy.