Background Cooking oil fumes are closely related to immune response, and adipose tissue also plays an important role in immune regulation. At present, the biological effect and mechanism of inflammation of adipose tissue induced by oil fume exposure are not clear yet. Objective To investigate the inflammatory effect of different exposure duration of cooking fumes on adipose tissue in mice and explore the role of Nod-like receptor pyrin domain 3 (NLRP3)/cysteinyl aspartate specific proteinase 1 (Caspase 1)/interleukin (IL)-1β signaling pathway. Methods Forty 8-week-old female C57BL/6J mice were randomly divided into 3-day control group (CON₃ group), 7-day control group (CON₇ group), 3-day oil fume exposure group (COF₃ group), and 7-day oil fume exposure group (COF₇ group), with 10 mice in each group. The mice were exposed to oil fumes in a cooking oil fume formation and exposure equipment (COFFEE) for 20 min, followed by a 10-min pause, 1 h a day for consecutive 3 d or 7 d. General condition of mice was observed and body weight was measured every day. After exposure, blood was sampled from the eyeball. Serum levels of IL-6, IL-27, and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). The adipose tissue of mice was collected and observed after hematoxylin-eosin (HE) staining. The percentages of CD4⁺ and CD8⁺T cells in adipose tissue were detected by flow cytometry. Real-time quantitative PCR (RT-qPCR) was used to detect the expression levels of nuclear factor-κB (NF-κB), NLRP3, Caspase 1, and IL-1β in adipose tissue. Western blot was used to detect the expression levels of NLRP3, Caspase 1, and IL-1β in adipose. Results Compared with the corresponding control group, serum IL-6, IL-27, and IL-1β contents in the COF₃ group and the COF₇ group were significantly increased (P<0.05) except IL-6 in the COF₃ group, and the levels in the COF₇ group were significantly higher than those in the COF₃ group (P<0.05). Vacuolar lipid droplets in adipocytes decreased, cytoplasm shrank, and inflammatory cells infiltrated in the COF₇ group after HE staining. The flow cytometry results showed that the proportions of CD4⁺ and CD8⁺T cells in adipocytes of the COF₃ group and the COF₇ group were increased compared to the corresponding control group, with a significant increase in the COF₇ group (P<0.05), and the CD4⁺/CD8⁺T ratio also significantly increased progressively in the two groups (P<0.05). The results of RT-qPCR showed that compared with the corresponding control group, the mRNA expression levels of NF-κB, NLRP3, Caspase 1, and IL-1β in adipose tissue of mice in the COF₃ group and the COF₇ group were significantly increased (P<0.05, P<0.01). The mRNA expression levels of mice in each exposure group gradually increased over time. The Western blot results showed that compared with the corresponding control group, the protein expressions of NLRP3 and Caspase 1 in the COF₃ group were significantly increased (P<0.01), and the expression of IL-1β protein also increased but without statistical significance. The protein expressions of NLRP3, Caspase 1, and IL-1β in the COF₇ group were significantly higher than those in the CON₇ group (P<0.05, P<0.01). Conclusion Acute exposure to cooking oil fumes can induce significant inflammatory response in adipose tissue, and the effect gradually increases with the extension of exposure time. The mechanism of action may be related to the activation of NLRP3 inflammasome signaling pathway.

Objective:To investigate the global cognitive function and the function of specific cognitive domains in hypertensive patients at high risk of cardiovascular disease in China, and to explore the impact of cognition function on blood pressure control.Methods:This is a cross-sectional survey. Data were obtained from the ESPRIT study. Patients with a history of hypertension who participated in the ESPRIT study from September 2019 to July 2020 were selected. Mini-mental state examination (MMSE) was used to evaluate patients′ overall cognition and the function of each cognitive domain. According to the total MMSE score, patients were divided into the cognitive-intact group (MMSE total score=30 points), cognitive-declined group (MMSE total score<30 points, but did not reach the dementia screening threshold) and cognitive-impaired group (MMSE total score reached the dementia screening threshold). A multivariable logistic regression model was used to explore the effects of cognitive function and MMSE score on blood pressure control. The years of education were removed from the adjustment variables for sensitivity analysis. The interaction effect modeling of stratified variables and exposed variables was used for hierarchical analysis.Results:A total of 10 834 patients with hypertension at high risk of cardiovascular disease were enrolled, aged 65 (60, 69) years and 4 476 (41.3%) patients were female. There were 989 patients in cognitive-intact group, 8 676 patients in cognitive-declined group and 1 169 patients in cognitive-impaired group. The MMSE score of all included patients was (25.6±3.8) points. In the overall study population, 10.8% (1 169/10 834) of hypertensive patients had cognitive impairment, with an MMSE total score of (18.6±4.1) points. The cognitive domains with obvious impairment were recall memory (-80%), visuospatial function (-64%), attention and computation (-60%); 80.1% (8 676/10 834) of hypertensive patients did not meet the criteria for cognitive dysfunction, but had cognitive decline, and the cognitive domains with significant impairment were recall memory (-51%) and visuospatial structure (-23%). Multivariate logistic regression analysis showed that cognitive dysfunction ( OR=0.88, 95% CI: 0.72-1.08, P=0.212) and cognitive decline ( OR=0.96, 95% CI: 0.83-1.12, P=0.629) was not correlated with blood pressure control. MMSE total score and scores in each cognitive domain were not correlated with blood pressure control ( P>0.05). Sensitivity analysis showed that cognitive function was not related to blood pressure control (all P>0.05). Stratified analysis according to different frequency of medication showed that cognitive function and MMSE score were not correlated with blood pressure control ( P>0.05). Conclusion:One in ten hypertensive patients who were at high risk of cardiovascular disease have comorbid cognitive impairment. In patients with high risk of cardiovascular disease, the most affected cognitive domains were recall memory, visuospatial function, attention and calculation. Part of hypertensive patients have not reached the level of cognitive dysfunction, but have begun to show cognitive decline. Cognitive function is not an independent influencing factor on blood pressure control.

Background It is unclear if there is any combined effect of air pollutants and non-optimal temperature on metabolic syndrome, or any molecular mechanisms of related signaling pathways in the process, which requires urgent systematic research. Objective To observe the effects of combined exposure to PM_2.5 and non-optimal temperature on metabolic damage at gene and protein levels in mice, and elucidate the role of related signaling pathway in crucial organs. Methods A total of 60 six-week-old male C57BL/6J mice were randomly divided into six groups: a normal temperature-filter air group (T_N-FA), a normal temperature-concentrated PM_2.5 group (T_N-PM), a heat-filter air group (T_H-FA), a heat-concentrated PM_2.5 group (T_H-PM), a cold-filter air group (T_C-FA), and a cold-concentrated PM_2.5 group (T_C-PM). The Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) was used to provide combined exposure settings of air types [concentrated PM_2.5 and filter air (FA)] and temperatures [normal (22°C), cold (4°C), and heat (30°C)] for 4 weeks. Skeletal muscle and white adipose tissue (WAT) of the mice were sampled at the end of exposure, and transcriptomics and Western blot (WB) assay were adopted to observe selected gene and protein expression levels in the samples respectively. Results The transcriptomics results indicated that the PM_2.5 exposure enhanced the number of differentially expressed genes. Specifically, 4820 genes were differentially expressed in the T_N-PM mice compared to the T_N-FA mice at normal temperature, and 1143 genes were differentially expressed in the Tc-PM mice compared to the Tc-FA mice in the cold environment. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and the endoplasmic reticulum protein processing pathway were identified as the most significant pathways in metabolic injury resulting from combined exposure to PM_2.5 and non-optimal temperature exposure. The WB results showed that exposure to PM_2.5 in the normal temperature and the cold environments led to a significant increase in the expression of p-AKT in WAT (P<0.01, P<0.05) and a significant decrease in the expression of GLUT4 (P<0.05, P<0.01). In skeletal muscle, exposure to PM_2.5 led to a significant decrease in GLUT4 (P<0.05) in all environments, with a consistent trend of change as observed in WAT. Conclusion Cold/heat exposure might promote PM_2.5-induced metabolic disorder through suppression of the AKT/GLUT4 pathway, aggravating metabolic damage.