The effect of indoor air filtration on biomarkers of inflammation and oxidative stress: a review and meta-analysis of randomized controlled trials.

Improvement of indoor air quality is beneficial for human health. However, previous studies have not reached consistent conclusions regarding the effects of indoor air filtration on inflammation and oxidative stress. This study aims to determine the relationship between indoor air filtration and inflammation and oxidative stress biomarkers. We conducted an electronic search that evaluated the association of indoor air filtration with biomarkers of inflammation and oxidative stress in five databases (PubMed, Cochrane Library, EMBASE, Web of Science, and Scopus) from the beginning to April 23, 2023. Outcomes included the following markers: interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), malondialdehyde (MDA), 8-hydroxy-2deoxyguanosine (8-OHdG), and 8-iso-prostaglandinF2α (8-isoPGF2α). We extracted data from the included studies according to the system evaluation and the preferred reporting item for meta-analysis (PRISMA) guidelines and used the Cochrane risk of bias tool to assess bias risk. Our meta-analysis included 15 studies with 678 participants to assess the combined effect size. The meta-analysis demonstrated that indoor air filtration could have a marked reduction in IL-6 (SMD: -0.275, 95% CI: -0.545 to -0.005, p = 0.046) but had no significant effect on other markers of inflammation or oxidative stress. Subgroup analysis results demonstrated a significant reduction in 8-OHdG levels in the subgroup with < 1 day of duration (SMD: -0.916, 95% CI: -1.513 to -0.320; p = 0.003) and using filtrete air filter (SMD: -5.530, 95% CI: -5.962 to -5.099; p < 0.001). Our meta-analysis results depicted that indoor air filtration can significantly reduce levels of inflammation and oxidative stress markers. Considering the adverse effects of air pollution on human health, our study provides powerful evidence for applying indoor air filtration to heavy atmospheric pollution.

Flaxseed oil attenuates PFOS-induced testicular damage by regulating RNA alternative splicing.

Background: Perfluorooctane sulfonate (PFOS) is a persistent, widely present environmental pollutant, and its toxicity to male reproduction has gradually attracted attention. Flaxseed oil (FO) is a dietary oil abundant in α-linolenic acid and has been demonstrated to possess multiple health benefits. However, whether FO protects against PFOS-induced testicular injury and its mechanism remain unclear. Methods: C57/BL6 mice were gavaged with different concentrations of FO or PFOS (10 mg kg-1) for 28 days. Blood and testicular tissues were collected for histopathology, proteomics, and biochemical and molecular analyses. Results: Our results showed that FO supplementation significantly attenuated PFOS-induced testicular injury, as indicated by histopathological changes, decreased oxidative stress level, increased sperm count, decreased rate of sperm malformation, and improved functional markers of spermatogenesis. Proteomic analysis showed that differentially expressed proteins were notably enriched in spliceosome pathways. Machine learning algorithms were used to screen the hub gene, and PRPF3 and PUF60 proteins were found to be important for FO to exert protective benefits to testicular injury. Western blot results confirmed that FO supplementation could increase the protein expression of PRPF3 and decrease the protein expression of PUF60 in PFOS-exposed mice. Conclusions: This study revealed that FO can alleviate PFOS-induced testicular dysfunction by regulating RNA alternative splicing. The spliceosome-related proteins PRPF3 and PUF60 may be the potential targets for FO to alleviate PFOS-induced testicular injury. FO supplementation may be an effective dietary intervention to prevent adverse effects of PFOS on testes.

Exposure to volatile organic compounds and growth indicators in adolescents: Unveiling the association and potential intervention strategies.

Environmental pollutant is considered to be one of the important factors affecting adolescent growth. However, the effects of volatile organic compounds (VOCs) exposure on adolescent growth have not been assessed. Data from the National Health and Nutrition Examination Survey (NHANES) 2011-2018 was used to examine the associations between VOCs exposure and adolescent growth indicators through three statistical models. The mediating effect of bone mineral density (BMD) on these associations was examined. The potential pathways and key targets were identified by the network pharmacology analysis methods. This study included 746 adolescents. Three statistical methods consistently showed a negative correlation between VOCs exposure and adolescent growth indicators. Furthermore, BMD mediated the relationship between VOCs exposure and adolescent growth indicators, with mediated proportion ranging from 4.3 % to 53.4 %. Network pharmacology analysis found a significant enrichment in IL-17 signaling pathway. Moreover, the adverse effects of VOCs exposure on adolescent growth were observed to significantly attenuate in adolescents with high serum vitamin D levels. Our results suggested that VOCs exposure was an adverse factor affecting adolescent growth, with BMD playing a significant regulatory role, and IL-17 signaling pathway was the underlying mechanism. Vitamin D supplementation may be a viable strategy to prevent VOCs exposure from affecting adolescent growth.

Harnessing Reconstructed Macrophage Modulation of Infiltration-Excluded Immune Microenvironments To Delineate Glioma Infiltrative Region.

High invasiveness of glioma produces residual glioma cells in the brain parenchyma after surgery and ultimately causes recurrence. Precise delineation of glioma infiltrative region is critical for an accurate complete resection, which is challenging. The glioma-infiltrating area constitutes infiltration-excluded immune microenvironments (I-E TIMEs), which recruits endogenous or adoptive macrophages to the invasive edge of glioma. Thus, combined with immune cell tracing technology, we provided a novel strategy for the preoperative precise definition of the glioma infiltration boundary, even satellite-like infiltration stoves. Herein, the biomimetic probe was constructed by internalizing fluorophore labeled PEGylated KMnF3 nanoparticles into bone-marrow-derived macrophages using magnetic resonance imaging (MRI)/fluorescence imaging (FI). The biomimetic probe was able to cross the blood-brain barrier and home to the orthotopic glioma infiltrates including satellite stove under MRI and FI tracing, which was validated using hematoxylin and eosin staining, indicating its excellent performance in distinguishing the margins between the glioma cell and normal tissues. This study guides the precise definition of glioma infiltration boundaries at the cellular level, including the observation of any residual glioma cells after surgery. Thus, it has the potential to guide surgery to maximize resection and predict recurrence in the clinic.

The Effects of Sesamin Supplementation on Obesity, Blood Pressure, and Lipid Profile: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Aims: Sesamin, the main lignin constituent of sesame, plays a pivotal role in regulating physical state. Some studies have evidenced that the supplementation of sesamin may decrease cardiovascular disease risk. The goal of this systematic review was to summarize evidence of the effects of sesamin supplementation on obesity, blood pressure, and lipid profile in humans by performing a meta-analysis of randomized controlled trials. Data Synthesis: Five databases (PubMed, Cochrane Library, EMBASE, Web of Science, and Scopus) were searched electronically from inception to July 2021 to identify randomized controlled trials that assessed the impact of sesamin on obesity, blood pressure, and lipid profile. Weighted mean difference (WMD) and standard deviation (SD) were used to present the major outcomes. Conclusions: Seven trials (n = 212 participants) were included in the overall analysis. Results showed that sesamin supplementation caused a great reduction in TC (WMD: -10.893 mg/dl, 95% CI: -19.745 to -2.041, p = 0.016), LDL-c (WMD: -8.429 mg/dl, 95% CI: -16.086 to -0.771, p = 0.031), and SBP (WMD: -3.662 mmHg, 95% CI: -6.220 to -1.105, p = 0.005), whereas it had no effect on HDL-c, TG, DBP, or weight. Subgroup analysis showed that duration, parallel design, and unhealthy status can affect TC, LDL-c, and SBP evidently. We did not discover a strong link between indicators' changes and duration of supplementation. Sesamin can be used as an obtainable dietary supplement to improve blood pressure and blood lipids, and further as a health product to prevent cardiovascular diseases.

Sesamin attenuates PM2.5-induced cardiovascular injury by inhibiting ferroptosis in rats.

Objective: This study aimed to elucidate the pharmacological effects of sesamin (Ses) and its mechanism of action towards PM2.5-induced cardiovascular injuries. Method: Forty Sprague Dawley (SD) rats were randomly divided into five groups: a saline control group; a PM2.5 exposure group; and low-, middle-, and high-dose Ses pretreatment groups. The SD rats were pretreated with different concentrations of Ses for 21 days. Afterward, the rats were exposed to ambient PM2.5 by intratracheal instillation every other day for a total of three times. The levels of inflammatory markers, including tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß), and interleukin-6 (IL-6), and indicators related to oxidative responses, such as total superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA), were measured in the blood and heart. The expression of ferroptosis-related proteins in heart tissues was determined via western blot and immunohistochemistry. Results: Ses pretreatment substantially ameliorated cardiovascular injuries in rats as evidenced by the decrease in the pathological score and collagen area. The decreased levels of SOD, GSH, and GSH-Px in the heart and serum were inhibited by Ses. In addition, Ses not only notably increased the activity of antioxidant enzymes but also reduced the levels of MDA, CK, LDH, CK-MB, IL-6, TNF-α, IL-1ß, and IL-6. Furthermore, Ses pretreatment upregulated the expression levels of GPX4, SLC7A11, TFRC, and FPN1 and inhibited the expression levels of FTH1 and FTL. Conclusion: Ses pretreatment could ameliorate PM2.5-induced cardiovascular injuries perhaps by inhibiting ferroptosis. Therefore, Ses pretreatment may be a novel strategy for the prevention and treatment of PM2.5-induced cardiovascular injury.