Green tea polyphenols inhibit TBBPA-induced lung injury via enhancing antioxidant capacity and modulating the NF-κB pathway in mice.

Tetrabromobisphenol A (TBBPA) is a global pollutant. When TBBPA is absorbed by the body through various routes, it can have a wide range of harmful effects on the body. Green tea polyphenols (GTPs) can act as antioxidants, resisting the toxic effects of TBBPA on animals. The effects and mechanisms of GTP and TBBPA on oxidative stress, inflammation and apoptosis in the mouse lung are unknown. Therefore, we established in vivo and in vitro models of TBBPA exposure and GTP antagonism using C57 mice and A549 cells and examined the expression of factors related to oxidative stress, autophagy, inflammation and apoptosis. The results of the study showed that the increase in reactive oxygen species (ROS) levels after TBBPA exposure decreased the expression of autophagy-related factors Beclin1, LC3-II, ATG3, ATG5, ATG7 and ATG12 and increased the expression of p62; oxidative stress inhibits autophagy levels. The increased expression of the pro-inflammatory factors IL-1ß, IL-6 and TNF-α decreased the expression of the anti-inflammatory factor IL-10 and activation of the NF-κB p65/TNF-α pathway. The increased expression of Bax, caspase-3, caspase-7 and caspase-9 and the decreased expression of Bcl-2 activate apoptosis-related pathways. The addition of GTP attenuated oxidative stress levels, restored autophagy inhibition and reduced the inflammation and apoptosis levels. Our results suggest that GTP can attenuate the toxic effects of TBBPA by modulating ROS, reducing oxidative stress levels, increasing autophagy and attenuating inflammation and apoptosis in mouse lung and A549 cells. These results provide fundamental information for exploring the antioxidant mechanism of GTP and further for studying the toxic effects of TBBPA.

High-fat diet disrupts the gut microbiome, leading to inflammation, damage to tight junctions, and apoptosis and necrosis in Nyctereutes procyonoides intestines.

Given the burgeoning Nyctereutes procyonoides breeding industry and its growing scale, it is imperative to investigate the impact of high-fat diets on the health of these animals. This study involved 30 male Nyctereutes procyonoides of comparable weights (3 kg ±0.5), randomly assigned to either a control group or a high-fat diet group (n = 15 each). The latter group was fed a mixture of lard and basal diet in a 2:5 ratio, establishing a high-fat diet model in Nyctereutes procyonoides. This diet induced diarrhea and histopathological changes in the Nyctereutes procyonoides. Analysis of the small intestine contents using 16S rRNA sequencing revealed a high-fat diet-induced disruption in the gut microbiota. Specifically, Escherichia-Shigella emerged as the biomarker in the high-fat diet group (P = 0.049), while Vagococcus was prevalent in the control group (P = 0.049), indicating a significant increase in harmful bacteria in the high-fat diet group. Furthermore, this disrupted gut flora correlated with inflammation and oxidative stress, as evidenced by marked increases in TNF-α (P < 0.01), IL-1ß (P < 0.05), and IL-6 (P < 0.05) levels, measured via q-PCR, Western blot, and oxidative stress assays. In addition, q-PCR analysis revealed significant upregulation of apoptosis and necrosis markers, including Bax, Caspase3, Caspase9, Caspase12, RIPK3, and RIPK1 (P < 0.01 to P < 0.001), and a concurrent downregulation of the anti-apoptotic gene Bcl-2 (P < 0.01) in the high-fat diet group, consistent with protein expression trends. These findings suggest that a high-fat diet alters the gut microbiome toward a more harmful bacterial composition, escalating inflammatory responses and intestinal tissue permeability, culminating in intestinal cell apoptosis and necrosis.IMPORTANCEThis study examines the impact of high-fat diets on Nyctereutes procyonoides. Our research established a Nyctereutes procyonoides model on a high-fat diet, revealing significant health impacts, such as diarrhea, histological anomalies, and alterations in the gut microbiota. These findings emphasize the importance of preventing health issues and promoting sustainable industry growth. They highlight the significant impact of diet on gut microbiota and overall animal health.

Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp.

Microplastics (MPs), a new class of pollutant that threatens aquatic biodiversity, are becoming increasingly prevalent around the world. Fish growth may be severely inhibited by microplastics, resulting in severe mortality. Exposure to microplastics increases the likelihood of intestinal injuries, but the underlying mechanisms remain equivocal. The objective of this study was to investigate the potential toxic mechanisms underlying microplastic-induced intestinal injury in fish and to assist researchers in identifying novel therapeutic targets. In this study, a model of carp exposed to microplastics was established successfully. Histological observation showed that exposure to polyethylene microplastics caused damage to the intestinal mucosal surface and a significant increase in goblet cells, which aggregated on the surface of the mucosa. The mucosal layer was observed to fall off. Lymphocytes in the intestinal wall proliferated and aggregated. TUNEL staining showed that apoptosis occurred in the group exposed to microplastics. The qPCR results showed that the expression of Ferroptosis apoptotic factors COX-2 and ACSL4 was upregulated, while the expression of TFRC, FIH1, SLC7A11, and GPX4 was downregulated. The NF-κB pathway (p-p65, IκBα), inflammatory cytokines (TNF-α, IL-8, IL-6) and apoptosis genes (Bax, Caspase3) were upregulated. Semi-quantitative detection of related proteins by Western blotting was consistent with the gene expression results. In addition, the ELISA assay showed that lipid peroxidation and inflammatory cytokines (TNF-α, IL-1ß, IL-6) were increased in the microplastic exposed group. To conclude, lipid peroxidation induced by microplastics activates the NF-κB pathway and causes ferroptosis, ultimately resulting in intestinal damage and cellular apoptosis.

Zinc deficiency causes oxidative stress, endoplasmic reticulum stress, apoptosis and inflammation in hepatocytes in grass carp.

A lack of the trace element zinc (Zn) in freshwater environments causes slow growth and malnutrition and affects the normal biological functions of organisms. In this study, a Zn deficiency model of grass carp hepatocytes was established with TPEN. Acetylcysteine (NAC) was used as an inhibitor. TPEN was added to L8824 cell culture medium, and LDH, AST, ALT, and AKP activities were enhanced in a Zn-deficient environment, leading to abnormal hepatopancreas function. Fluorescence microscopy showed an increase in ROS levels, and antioxidant enzyme activity assays revealed that SOD, CAT, GSH-PX, and T-AOC activities were decreased, indicating oxidative stress caused by Zn deficiency. The RT‒PCR results showed that the mRNA expression of GRP78, PERK, EIF2α, ATF4, and Chop was increased due to the addition of TPEN. Calcium kits showed increased Ca2+ levels. The RT‒PCR results showed that the mRNA expression levels of Caspase-12, Caspase-9, Caspase-3, and PARP apoptotic were increased due to the addition of TPEN. RT‒PCR and ELISA showed that the expression levels of interleukin-1ß (IL-1ß), interleukin-8 (IL-8), tumour necrosis factor (TNF-α), and inducible nitric oxide synthase (iNOS) were increased. This led to the conclusion that Zn deficiency in the freshwater environment caused inflammation and apoptosis in hepatocytes in grass carp. For the first time, apoptosis caused by endoplasmic reticulum stress in grass carp hepatocytes due to Zn deficiency was studied in the context of Ca2+. The present study provided some insight into the adverse effects of Zn deficiency in freshwater environments on fish.

Selenium deficiency induced inflammation and apoptosis via NF-κB and MAPKs pathways in muscle of common carp (Cyprinus carpio L.).

Selenium (Se), one of the essential trace elements of fish, regulates immune system function and maintains immune homeostasis. Muscle is the important tissue that generate movement and maintain posture. At present, there are few studies on the effects of Se deficiency on carp muscle. In this experiment, carps were fed with dietary with different Se content to successfully establish a Se deficiency model. Low-Se dietary led to the decrease of Se content in muscle. Histological analysis showed that Se deficiency resulted in muscle fiber fragmentation, dissolution, disarrangement and increased myocyte apoptosis. Transcriptome revealed a total of 367 differentially expressed genes (DEGs) were screened, including 213 up-regulated DEGs and 154 down-regulated DEGs. Bioinformatics analysis showed that DEGs were concentrated in oxidation-reduction process, inflammation and apoptosis, and were related to NF-κB and MAPKs pathways. Further exploration of the mechanism showed that Se deficiency led to excessive accumulation of ROS, decreased the activity of antioxidant enzymes, and also resulted in increased expression of the NF-κB and MAPKs pathways. In addition, Se deficiency significantly increased the expressions of TNF-α, IL-1ß and IL-6, and the pro-apoptotic factors BAX, p53, caspase-7 and caspase-3, while decreased the expressions of anti-apoptotic factors Bcl-2 and Bcl-xl. In conclusion, Se deficiency reduced the activities of antioxidant enzymes and led to excessive accumulation of ROS, which caused oxidative stress and affected the immune function of carp, leading to muscle inflammation and apoptosis.

Prevalence of gastrointestinal symptoms and their association with psychological problems in youths.

BACKGROUND: Gastrointestinal symptoms and psychological problems are common in youths, which can negatively affect their lives on physical, mental, and social levels. This cross-sectional study aimed to determine the prevalence of gastrointestinal symptoms in youths and further explore their association with psychological problems. METHODS: Self-reported data on gastrointestinal symptoms and psychological problems in 692 sophomores who majored in education in a high vocational school and 310 recruits who were undergoing basic training in an army in China were retrospectively collected. The self-reported data included demographics, gastrointestinal symptoms, and Symptom Checklist 90 (SCL-90) used for the assessment of psychological problems. Gastrointestinal symptoms surveyed included nausea, emesis, abdominal pain, acid regurgitation, eructation, heartburn, anorexia, abdominal bloating, diarrhea, constipation, hematemesis, and hematochezia. Logistic regression analysis was performed to identify the independent risk factors associated with gastrointestinal symptoms. Odds ratios (ORs) with 95% confidence intervals (CI) were calculated. RESULTS: The prevalence of gastrointestinal symptoms was 36.7% (n=254) and 15.5% (n=48) in the sophomores and recruits, respectively. Participants with gastrointestinal symptoms had a significantly higher prevalence of total SCL-90 score beyond 160 than those without gastrointestinal symptoms in both sophomores (19.7% vs. 3.2%, P<0.001) and recruits (10.4% vs. 1.1%, P<0.001). Total SCL-90 score beyond 160 was independently associated with gastrointestinal symptoms in both sophomores (OR =5.467; 95% CI: 2.855-10.470; P<0.001) and recruits (OR =6.734; 95% CI: 1.226-36.999; P=0.028). CONCLUSIONS: Gastrointestinal symptoms may be common and strongly associated with psychological problems in youths. Prospective studies should be required to explore the impact of the correction of psychological problems on the improvement of gastrointestinal symptoms.

Working memory function in patients with major depression disorder: A narrative review.

Working memory (WM) deficits are recognized as serious cognitive impairment in patients with major depressive disorder (MDD). This review aims to clarify the effects of impaired WM function in patients with MDD and explore non-invasive and effective treatments that can be adopted in clinical practice. This review (1) synthesizes extant literature examining brain function and brain areas in terms of WM in individuals with depression, (2) utilizes the outcomes of the studies presented in this review to discuss the effects of impaired WM function on cognitive processing in individuals with depression, (3) integrates the treatments explored in current studies and (4) provides some suggestions for future research. We found that (1) central executive (CE) components affect the processing of WM, and this might be one of the factors influencing cognitive biases, as it is implicated in repetitive negative thinking and rumination; (2) the left dorsal anterior cingulate cortex (dACC), the left dorsolateral prefrontal cortex (DLPFC) and the regions of the default mode network (DMN) play a vital role in CE functioning; and (3) psychotherapy, cognitive training, exercise and physical therapy can be used as complementary treatments for MDD.

Psychological resilience and related influencing factors in patients diagnosed with major depressive disorder in remission: A cross-sectional study.

WHAT IS KNOWN ON THE SUBJECT?: Recurrence is common in patients diagnosed with major depressive disorder (MDD). Psychological resilience has been shown to be a protective factor against recurrence of depression. It has important clinical nursing significance to analyse the influencing factors of psychological resilience in major depressive disorder in remission (MDDR) patients. WHAT THE PAPER ADDS TO EXISTING KNOWLEDGE?: There are few previous studies on the influencing factors of psychological resilience in patients diagnosed with MDDR. We found the education levels, personal monthly income, social support, well-being and self-efficacy were influencing factors of psychological resilience in patients diagnosed with MDDR. WHAT ARE THE IMPLICATIONS FOR PRACTICE?: According to the factors affecting the psychological resilience of patients diagnosed with MDDR, targeted clinical nursing is helpful to prevent the recurrence of depression. Nurses should strengthen the nursing of patients with <12 years of education, and patients with personal monthly income less than 5000 RMB. In addition, nurses should cultivate patients' awareness of social support and identity, cultivate their ability to strive for social support, cultivate interpersonal skills and positive emotional experience to improve subjective well-being and carry out self-efficacy training to improve psychological resilience by enhancing patients' internal protective factors. ABSTRACT: AIM: Psychological resilience is closely related to recurrence of depression. There are few previous studies on the influencing factors of psychological resilience in patients diagnosed with major depressive disorder in remission (MDDR). Here, we investigated the current status of resilience in patients diagnosed with MDDR and its influencing factors. METHODS: A descriptive cross-sectional study was conducted from June 2019 to April 2021. One hundred and forty-two patients diagnosed with MDDR were recruited from the Department of Psychiatry and Psychology of the General Hospital of Northern Theater Command. Demographic information, social support, well-being, self-efficacy and psychological resilience were collected using self-reported questionnaires. RESULTS: The psychological resilience of MDDR patients was lower than that of the healthy Chinese adults in China. Multiple logistic regression analysis showed that education, personal monthly income, social support, well-being and self-efficacy were associated with psychological resilience. Receiver operating characteristic (ROC) curve analysis further confirmed that social support, well-being and self-efficacy were associated with psychological resilience. CONCLUSION: The psychological resilience of MDDR patients was lower than that of the general population in China. The education levels, personal monthly income, social support, well-being and self-efficacy were influencing factors of psychological resilience. IMPLICATIONS FOR PRACTICE: According to the factors affecting the psychological resilience of patients diagnosed with MDDR, targeted clinical nursing is helpful to prevent the recurrence of depression.

Polyethylene microplastics trigger cell apoptosis and inflammation via inducing oxidative stress and activation of the NLRP3 inflammasome in carp gills.

Microplastics cause varying degrees of damage to aquatic organisms. Exposure to microplastics contaminated water, the gills are among the first tissues, after the skin, to be affected by microplastics. As an essential immune organ, prolonged stimulation by microplastics disrupts immune function not only in the gills but throughout the body, yet the underlying mechanisms remain elusive. A model of gill injury from exposure to polyethylene (PE) microplastics was developed in this study. H&E staining revealed that polyethylene microplastics caused gill inflammation, vascular remodeling, and mucous cell proliferation. An increase in collagen indicates severe tissue damage. Additional analysis showed that polyethylene microplastics profoundly exacerbated oxidative stress in the gills. TUNEL assay demonstrated cell apoptosis induced by polyethylene microplastic. The mRNA levels were subsequently quantified using RT-PCR. The results showed that polyethylene microplastics increased the expression of the nuclear factor-κB (NF-κB) pathway (NF-κB p65, IKKα, IKKß) and apoptosis biomarkers (p53, caspase-3, caspase-9, and Bax). Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasomes, which is an influential component of innate immunity, were overactive. What's more, the pro-inflammatory factors (TNF-α, IFN-γ, IL-2, IL-6, IL-8, IL-1ß) that induce immune disorder also increased significantly, while the anti-inflammatory factors (IL-4, IL-10) decreased significantly. These results suggested that oxidative stress acted as an activation signal of apoptosis triggered by the NF-κB pathway and activating the NLRP3 inflammasome to promote inflammatory immune responses. The present study provided a different target for the prevention of toxin-induced gill injury under polyethylene microplastics.

Intensive rTMS for treatment-resistant depression patients with suicidal ideation: An open-label study.

The advantages of intensive repetitive transcranial magnetic stimulation (rTMS) protocol are in the possible acute effect of the stimulation and in the possible reduction in the time required to achieve remission in depression. Here, we investigated the antidepressant effects and antisuicidal effects of a more intensive rTMS protocol for treatment-resistant depression (TRD) patients with suicidal ideation. Thirty-one outpatients were included in this study, including 22 military veterans and 9 non- militaries. The rTMS treatment consisted of 25 sessions, each session lasting 30 min (60 trains of 50 pulsations, 110 % resting motor threshold intensity) for a total of 3000 pulse. The total amount of stimulation (750,000 pulses) applied by our rTMS protocol was equivalent to that of a 5-week standard rTMS protocol. We found a significant effect of time on the 17-item Hamilton Depression Rating Scale (HAMD-17) scores and the Sheehan Disability Scale (SDS) scores. There was no difference in change in the HAMD-17 scores and SDS scores between the military veteran group and the non-military group between baseline and the week 4 assessment time point. The response rate of depression was 64.52 %, and the remission rate of depression was 51.61 % at day 5. 48.39 % and 35.48 % at week 4, respectively. All patients (100 %) met response criteria of suicidal ideation, and the remission rate was 87.09 % at day 5. The response rate was 83.87 % %, and the remission rate was 77.42 % at week 4. The accelerated high-dose rTMS treatment was well tolerated by all patients. Our intensive rTMS protocol is preliminarily safe and feasible. The TRD patients with suicidal ideation could benefit from much shorter exposure to this protocol with more efficacy in comparison with conventional rTMS protocol. In addition, intensive rTMS offers a promising treatment for military veteran populations.

Electroacupuncture Prevents the Depression-Like Behavior by Inhibiting the NF-κB/NLRP3 Inflammatory Pathway in Hippocampus of Mice Subjected to Chronic Mild Stress.

BACKGROUND: The precise physiological mechanisms of acupuncture in the treatment of depression are still unknown. This study aimed to observe the effects of electroacupuncture (EA) on depression-like behavior of mouse in chronic mild stress (CMS) model and explore the underlying mechanism. METHODS: The depression model was established by using CMS method for 6 weeks. After the third week of the CMS paradigm, EA treatment was performed daily for 15 min over a period of 3 weeks. The antidepressant-like effects of EA were evaluated using the sucrose preference test and the forced swimming test (FST). The protein levels of the nuclear factor-kappa B (NF-κB), p-NF-κB, inhibitor of NF-κB, p-IκBα, NOD-like receptor protein 3, interleukin (IL)-6, IL-1ß, IL-18, and tumor necrosis factor-α (TNF-α) in hippocampus of mice were detected. RESULTS: Sucrose preference was decreased after 6 weeks of CMS and the effects of CMS was reversed by EA. CMS increased immobility time and decreased latency to the first immobility in the FST test, but these effects were reversed by EA. CMS-induced nuclear entry of NF-κB (nuclear/cytoplasmic ratio of NF-κB) with an increase in protein levels of p-NF-κB and p-IκBα in the hippocampus. The CMS also increased NLRP3 levels in the hippocampus. However, these effects were reversed by EA. In addition, the levels of IL-6, IL-1ß, IL-18, and TNF-α in the hippocampus were increased by CMS, and these effects of stress were reversed by EA. CONCLUSION: EA prevented CMS-induced depressive-like behaviors by inhibiting NF-κB/NLRP3 inflammatory pathway.

JSH-23 prevents depressive-like behaviors in mice subjected to chronic mild stress: Effects on inflammation and antioxidant defense in the hippocampus.

Nuclear factor-kappa B (NF-κB), which is reported to play an important role in the pathogenesis of depression, also has a central role in the genesis and progression of inflammation. Here, we have targeted the nuclear translocation of NF-κB using 4-methyl-N1-(3-phenyl-propyl)-benzene-1,2-diamine (JSH-23) to elucidate its role in depression. We investigated the antidepressant-like effects of JSH-23 in the chronic mild stress (CMS) mouse model, which is a valid, reasonably reliable, and useful model of depression. The antidepressant-like effects of JSH-23 were evaluated using the sucrose preference test (SPT) and the forced swimming test (FST). We also assessed inflammatory markers [interleukin (IL)-6 and tumor necrosis factor-α (TNF-α)] and components of antioxidant defense [superoxide dismutase (SOD) and nuclear factor erythroid-2-related factor 2 (Nrf 2)] in the hippocampus. Fluoxetine, a classical antidepressant, was used in this study as a positive control. Administration of JSH-23 significantly prevented the decreased sucrose preference in the SPT and prevented the increased immobility time in the FST caused by CMS, but had no effect on locomotor activity. Expression of NF-κB p65 protein in the hippocampus was decreased, and elevated levels of IL-6 and TNF-α were reduced, after JSH-23 administration. In addition to its anti-inflammatory effect, JSH-23 treatment increased the expression of SOD and Nrf 2 in the hippocampus, suggesting that it strengthens antioxidant defense. The current study demonstrated that inhibiting the NF-κB signaling cascade using JSH-23 prevented depressive-like behaviors by decreasing inflammation and improving antioxidant defense in the hippocampus. We concluded that NF-κB activation plays an important role in the pathophysiology of depression and that targeting NF-κB signaling may provide a novel and effective therapy for depression. Additional preclinical studies and clinical trials are, however, needed to further elucidate the effects of this therapeutic strategy.

Plasma rotation in the Peking University Plasma Test device.

Some preliminary results of plasma rotations in a linear plasma experiment device, Peking University Plasma Test (PPT) device, are reported in this paper. PPT has a cylindrical vacuum chamber with 500 mm diameter and 1000 mm length, and a pair of Helmholtz coils which can generate cylindrical or cusp magnetic geometry with magnitude from 0 to 2000 G. Plasma was generated by a helicon source and the typical density is about 1013 cm-3 for the argon plasma. Some Langmuir probes, magnetic probes, and one high-speed camera are set up to diagnose the rotational plasmas. The preliminary results show that magnetic fluctuations exist during some plasma rotation processes with both cylindrical and cusp magnetic geometries, which might be related to some electromagnetic processes and need further studies.

2D profile of poloidal magnetic field diagnosed by a laser-driven ion-beam trace probe (LITP).

Based on large energy spread of laser-driven ion beam (LIB), a new method, the Laser-driven Ion-beam Trace Probe (LITP), was suggested recently to diagnose the poloidal magnetic field (Bp) and radial electric field (Er) in toroidal devices. Based on another property of LIB, a wide angular distribution, here we suggested that LITP could be extended to get 2D Bp profile or 1D profile of both poloidal and radial magnetic fields at the same time. In this paper, we show the basic principle, some preliminary simulation results, and experimental preparation to test the basic principle of LITP.

[Effect of three-step acupuncture combined with small dosage antipsychotic in treating incipient schizophrenia].

OBJECTIVE: To explore the clinical efficacy and safety of three-step acupuncture (TSA) combined with small dosage antipsychotic in treating incipient schizophrenia (IS). METHODS: Sixty IS patients were randomly assigned to the test group and the control group equally. Patients in the test group received the combined therapy of TSA and antipsychotic, while patients in the control group were treated by full-dose antipsychotic, all for 8 weeks. The clinical efficacy was assessed by the positive and negative syndrome scale (PANSS), and the adverse reaction was evaluated by treatment emergent symptom scale (TESS). RESULTS: The clinical efficacy in the two groups showed insignificant difference at the end of the 8-week treatment (P > 0.05), but the total scores of PANSS evaluated at the end of the 2nd and 4th week in the test group (74.26 +/- 9.54, 56.33 +/- 10.12) were significantly higher than those in the control group (85.56 +/- 9.73, 70.57 +/- 9.62), respectively (P < 0.05), furthermore, TESS analysis showed that the incidence of adverse reactions in nervous system and autonomic nervous system in the test group were also lesser than in the control group (P < 0.05). CONCLUSION: The combined therapy of TSA and small dose antipsychotic shows an efficacy equivalent to that of full-dose antipsychotic, but with shorter initiation time and less side effects.