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Background: This work elucidated the effect of honokiol (HKL) on hippocampal neuronal mitochondrial function in Alzheimer's disease (AD). Methods: APP/PS1 mice were used as AD mice models and exposed to HKL and 3‐TYP. Morris water maze experiment was performed to appraise cognitive performance of mice. Hippocampal Aβ+ plaque deposition and neuronal survival was evaluated by immunohistochemistry and Nissl staining. Hippocampal neurons were dissociated from C57BL/6 mouse embryos. Hippocampal neuronal AD model was constructed by Aβ oligomers induction and treated with HKL, CsA and 3‐TYP. Neuronal viability and apoptosis were detected by cell counting kit‐8 assay and TUNEL staining. mRFP–eGFP–LC3 assay, MitoSOX Red, dichlorodihydrofluorescein diacetate, and JC‐1 staining were performed to monitor neuronal autophagosomes, mitochondrial reactive oxygen species (ROS), neuronal ROS, and mitochondrial membrane potential. Autophagy‐related proteins were detected by Western blot. Results: In AD mice, HKL improved cognitive function, relieved hippocampal Aβ1–42 plaque deposition, promoted hippocampal neuron survival, and activated hippocampal SIRT3 expression and mitochondrial autophagy. These effects of HKL on AD mice were abolished by 3‐TYP treatment. In hippocampal neuronal AD model, HKL increased neuronal activity, attenuated neuronal apoptosis and Aβ aggregation, activated SIRT3 and mitochondrial autophagy, reduced mitochondrial and neuronal ROS, and elevated mitochondrial membrane potential. CsA treatment and 3‐TYP treatment abrogated the protection of HKL on hippocampal neuronal AD model. The promotion of mitochondrial autophagy by HKL in hippocampal neuronal AD model was counteracted by 3‐TYP. Conclusions: HKL activates SIRT3‐mediated mitochondrial autophagy to mitigate hippocampal neuronal damage in AD. HKL may be effective in treating AD. [ABSTRACT FROM AUTHOR]

Objective: To explore the correlation between air pollution and the onset of depression and anxiety disorders, to draw more comprehensive and integrated conclusions, and to provide recommendations for maintaining mental health and developing policies to reduce mental health risks caused by air pollution. Methods: Meta-analysis of cohort study articles exploring the relationship between air pollution and depression or anxiety disorders included in Pubmed, Web Of Science, CNKI, and Wan Fang database before October 31, 2022, and subgroup analysis of the association between air pollution and depression and anxiety disorders regarding the air pollutants studied, the study population, and Publication bias analysis and sensitivity analysis. Results: A total of 25 articles meeting the criteria were included in this study, including 23 articles examining the relationship between air pollution and depression and 5 articles examining the relationship between air pollution and anxiety disorders. The results of the meta-analysis were based on the type of pollutant and showed that there was a high degree of heterogeneity among the studies on the relationship between air pollution and depression and a significant heterogeneity among the studies on PM2.5 and the risk of anxiety disorders (I 2 = 71%, p <.01), so a random-effects model was selected for the analysis. CO, O3, and SO2 and depression onset had combined RR values of 1.10 (1.00, 1.20), 1.06 (0.87, 1.29), 1.17 (1.06, 1.31), 1.19 (0.90, 1.58), 1.03 (0.99, 1.07), and 1.09 (0.97, 1.24), respectively, and PM2.5 and anxiety The combined RR value for morbidity was 1.10 (0.99, 1.22). The results of sensitivity analysis showed that the combined results were stable and reliable. The results of Egger regression method test showed that none of them had significant publication bias (p >.05). Limitation: Combined exposure to air pollutants on depression and anxiety, further studies by other researchers are needed in the future. Conclusions: PM2.5 and NO2 exposure, especially long-term exposure, may be associated with the onset of depression, and no association was found for the time being between PM10, CO, O3, SO2 exposure and depression and PM2.5 exposure and anxiety disorders. [ABSTRACT FROM AUTHOR]

Effects of short-term exposure to ambient air pollution on systemic immunological and inflammatory biomarkers in rural population have not been adequately characterized. From May to July 2021, 5816 participants in rural villages of northern Henan Province, China, participated in this cross-sectional study. Blood biomarkers of systemic inflammation were determined including peripheral white blood cells (WBC), eosinophils (EOS), basophils (BAS), monocytes (MON), lymphocytes (LYM), neutrophils (NEU), neutrophil-lymphocyte ratio (NLR), and serum high-sensitivity C-reactive protein (hs-CRP). The concentrations of ambient fine particulate matter (PM 2.5 ), PM 10 , nitrogen dioxide (NO 2 ), carbon monoxide (CO), and ozone (O 3 ) were assessed up to 7 days prior to the blood draw. A generalized linear model was used to analyze the associations between air pollution exposure and the above-mentioned blood biomarkers. Significantly positive associations were revealed between PM 2.5 , CO and WBC; CO, O 3 and LYM; PM 2.5 , PM 10 , SO 2 , CO and NEU; PM 2.5 , PM 10, SO 2 , CO and NLR; PM 2.5 , PM 10 , SO 2 , NO 2 , CO, O 3 and hs-CRP. Meanwhile, negative associations were found between SO 2 and WBC; PM 2.5 , PM 10 , NO 2 , CO, or O 3 and EOS; PM 2.5 , SO 2 , or CO and BAS; SO 2 , NO 2 or O 3 and MON; PM 2.5 , PM 10 , SO 2 , or NO 2 and LYM. Moreover, men, individuals with normal body mass index (BMI), current smokers, and those older than 60 years were found vulnerable to air pollution effects. Taken together, short-term exposure to air pollution was associated with systemic inflammatory responses, providing insight into the potential mechanisms for air pollution-induced detrimental systemic effects in rural residents., (© 2024. The Author(s).)