The influence of Life's Essential 8 on the link between socioeconomic status and depression in adults: a mediation analysis.

BACKGROUND: Individuals with low socioeconomic status (SES) are at a higher risk of developing depression. However, evidence on the role of cardiovascular health (CVH) in this chain is sparse and limited. The purpose of this research was to assess the mediating role of Life's Essential 8 (LE8), a recently updated measurement of CVH, in the association between SES and depression according to a nationally representative sample of adults. METHODS: Data was drawn from the National Health and Nutrition Examination Survey (NHANES) in 2013-2018. Multivariate logistic regression analysis was applied to analyze the association of SES (measured via the ratio of family income to poverty (FIPR), occupation, educational level, and health insurance) and LE8 with clinically relevant depression (CRD) (evaluated using the Patient Health Questionnaire (PHQ-9)). Multiple linear regression analysis was performed to analyze the correlation between SES and LE8. Mediation analysis was carried out to explore the mediating effect of LE8 on the association between SES and CRD. Moreover, these associations were still analyzed by sex, age, and race. RESULTS: A total of 4745 participants with complete PHQ-9 surveys and values to calculated LE8 and SES were included. In the fully adjusted model, individuals with high SES had a significantly higher risk of CRD (odds ratio = 0.21; 95% confidence interval: 0.136 to 0.325, P < 0.01) compared with those with low SES. Moreover, LE8 was estimated to mediate 22.13% of the total association between SES and CRD, and the mediating effect of LE8 varied in different sex and age groups. However, the mediating effect of LE8 in this chain was significant in different sex, age, and racial subgroups except for Mexican American (MA) individuals. CONCLUSION: The results of our study suggest that LE8 could mediate the association between SES and CRD. Additionally, the mediating effect of LE8 in this chain could be influenced by the race of participants.

Effect of low-frequency noise exposure on cognitive function: a systematic review and meta-analysis.

BACKGROUND: Low-frequency noise may cause changes in cognitive function. However, there is no established consensus on the effect of low-frequency noise on cognitive function. Therefore, this systematic review and meta-analysis aimed to explore the relationship between low-frequency noise exposure and cognitive function. METHODS: We conducted a systematic review and identified original studies written in English on low-frequency noise and cognition published before December 2022 using the PsycINFO, PubMed, Medline, and Web of Science databases. The risk of bias was evaluated according to established guidelines. A random-effects meta-analysis was performed where appropriate. To explore the association between low-frequency noise exposure and cognitive function, we reviewed eight relevant studies. These studies covered cognitive functions grouped into four domains: attention, executive function, memory, and higher-order cognitive functions. The data extraction process was followed by a random-effects meta-analysis for each domain, which allowed us to quantify the overall effect. RESULTS: Our analysis of the selected studies suggested that interventions involving low-frequency noise only had a negative impact on higher-order cognitive functions (Z = 2.42, p = 0.02), with a standardized mean difference of -0.37 (95% confidence interval: -0.67, -0.07). A moderate level of heterogeneity was observed among studies (p = 0.24, I2 = 29%, Tau2 = 0.03). CONCLUSIONS: Our study findings suggest that low-frequency noise can negatively impact higher-order cognitive functions, such as logical reasoning, mathematical calculation, and data processing. Therefore, it becomes important to consider the potential negative consequences of low-frequency noise in everyday situations, and proactive measures should be taken to address this issue and mitigate the associated potential adverse outcomes.

Dexmedetomidine Improves Anxiety-like Behaviors in Sleep-Deprived Mice by Inhibiting the p38/MSK1/NFκB Pathway and Reducing Inflammation and Oxidative Stress.

(1) Background: Sleep deprivation (SD) triggers a range of neuroinflammatory responses. Dexmedetomidine can improve sleep deprivation-induced anxiety by reducing neuroinflammatory response but the mechanism is unclear; (2) Methods: The sleep deprivation model was established by using an interference rod device. An open field test and an elevated plus maze test were used to detect the emotional behavior of mice. Mouse cortical tissues were subjected to RNA sequence (RNA-seq) analysis. Western blotting and immunofluorescence were used to detect the expression of p38/p-p38, MSK1/p-MSK1, and NFκBp65/p- NFκBp65. Inflammatory cytokines were detected using enzyme-linked immunosorbent assay (ELISA); (3) Results: SD triggered anxiety-like behaviors in mice and was closely associated with inflammatory responses and the MAPK pathway (as demonstrated by transcriptome analysis). SD led to increased expression levels of p-p38, p-MSK1, and p-NFκB. P38 inhibitor SB203580 was used to confirm the important role of the p38/MSK1/NFκB pathway in SD-induced neuroinflammation. Dexmedetomidine (Dex) effectively improves emotional behavior in sleep-deprived mice by attenuating SD-induced inflammatory responses and oxidative stress in the cerebral cortex, mainly by inhibiting the activation of the p38/MSK1/NFκB pathway; (4) Conclusions: Dex inhibits the activation of the p38/MSK1/NFκB pathway, thus attenuating SD-induced inflammatory responses and oxidative stress in the cerebral cortex of mice.

Impacts of complex electromagnetic radiation and low-frequency noise exposure conditions on the cognitive function of operators.

Background: Both electromagnetic radiation (EMR) and low-frequency noise (LFN) are widespread and influential environmental factors, and operators are inevitably exposed to both EMR and LFN within a complex exposure environment. The potential adverse effects of such exposure on human health must be considered seriously. This study aimed to investigate the effects of EMR and LFN on cognitive function as well as their interaction effect, which remain unclear. Methods: Sixty young male college students were randomly grouped and experiments were conducted with a 2 × 2 factorial design in a shielded chamber. Mental workload (MWL) levels of the study subjects were measured and assessed using the NASA-task load index (TLX) subjective scale, an n-back task paradigm, and the functional near-infrared spectroscopy (fNIRS) imaging technique. Results: For the 3-back task, the NASA-TLX subjective scale revealed a statistically significant main effect of LFN intensity, which enhanced the subjects' MWL level (F = 8.716, p < 0.01). Behavioral performance revealed that EMR intensity (430.1357 MHz, 10.75 W/m2) and LFN intensity (0-200 Hz, 72.9 dB) had a synergistic interaction effect, and the correct response time was statistically significantly prolonged by the combined exposure (F = 4.343, p < 0.05). The fNIRS imaging technique revealed a synergistic interaction effect between operational EMR intensity and operational LFN intensity, with statistically significant effects on the activation levels in the left and right dorsolateral prefrontal cortex (DLPFC). The mean ß values of DLPFC were significantly increased (L-DLPFC F = 5.391, p < 0.05, R-DLPFC F = 4.222, p < 0.05), and the relative concentrations of oxyhemoglobin in the DLPFC were also significantly increased (L-DLPFC F = 4.925, p < 0.05, R-DLPFC F = 9.715, p < 0.01). Conclusion: We found a statistically significant interaction effect between EMR (430.1357 MHz, 10.75 W/m2) and LFN (0-200 Hz, 72.9 dB) when simultaneously exposing subjects to both for 30 min. We conclude that exposure to this complex environment can cause a statistically significant increase in the MWL level of operators, and even alterations in their cognitive function.

Tibial fracture surgery in elderly mice caused postoperative neurocognitive disorder via SOX2OT lncRNA in the hippocampus.

Increasing evidence indicates the major role of mitochondrial function in neurodegenerative disease. However, it is unclear whether mitochondrial dynamics directly affect postoperative neurocognitive disorder (PND). This study aimed to analyze the underlying mechanisms of mitochondrial dynamics in the pathogenesis of PND. Tibial fracture surgery was performed in elderly mice to generate a PND model in vivo. Cognitive behavior was evaluated 3 days post-surgery using novel object recognition and fear conditioning. A gradual increase in the SOX2OT mRNA level and decrease in the SOX2 mRNA level were noted, with impaired cognitive function, in the mice 3 days after tibial surgery compared with mice in the sham group. To evaluate the role of SOX2OT in PND, SOX2OT knockdown was performed in vitro and in vivo using lentivirus transfection in HT22 cells and via brain stereotactic injection of lentivirus, respectively. SOX2OT knockdown reduced apoptosis, inhibited oxidative stress, suppressed mitochondrial hyperdivision, attenuated surgery-induced cognitive dysfunction, and promoted downstream SOX2 expression in elderly mice. Furthermore, Sox2 alleviated mitochondrial functional damage by inhibiting the transcription of mitochondrial division protein Drp1. Our study findings indicate that SOX2OT knockout alleviates surgery-induced mitochondrial fission and cognitive function defects by upregulating the expression of Sox2 in mice, resulting in the inhibition of drp1 transcription. Therefore, regulation of the SOX2/Drp1 pathway may be a potential mechanism for the treatment of patients with PND.

The role of periodontitis in the link between alpha-tocopherol intake and cognitive performance: A mediation analysis in older adults.

Background: Epidemiological evidence on alpha (α)-tocopherol intake and cognitive performance in older individuals is controversial and the effect of periodontitis in this chain is sparse and limited. The goal of this study was to characterize the association between α-tocopherol intake and cognitive performance and the mediating role of periodontitis in a nationally representative sample of older adults. Methods: Data from the National Health and Nutrition Examination Survey (NHANES), 2011-2014, were used. Multivariate logistic regression analysis was performed to explore the association of α-tocopherol intake, periodontal measures (mean attachment loss [AL] and mean probing depth [PD]), and clinical periodontitis defined by the European Workshop in Periodontology with poor cognitive performance evaluated by Consortium to Establish a Registry for Alzheimer's disease (CERAD); the animal fluency test (AFT); and the Digit Symbol Substitution test (DSST) and the correlation between α-tocopherol intake and clinical periodontitis. Multiple linear regression analysis was used to explore the relationship between α-tocopherol intake and periodontal measures. Mediation analysis was used to test the effects of periodontal measures on the association between α-tocopherol intake and cognitive measures. Results: A total of 1,749 older participants (≥60 years of age) with complete periodontal diagnosis, dietary retrospective survey, and cognitive tests were included. In the fully adjusted model, the odds ratio (OR) with 95% confidence interval (CI) of CERAD score, AFT score and DSST score were 0.214 (0.137-0.327), 0.378 (0.241-0.585) and 0.298 (0.169-0.512) for the highest versus lowest tertile of α-tocopherol intake, respectively. And participants with clinical periodontitis were more likely to exhibit lower DSST score (OR = 1.689; 95 CI%: 1.018-2.771) than those without periodontitis. Mean AL (OR = 1.296; 95 CI%: 1.102-1.524) and PD (OR = 1.667; 95 CI%: 1.18-2.363) were negatively correlated with DSST, and were estimated to mediate 9.1 and 8.2% of the total association between α-tocopherol intake and cognitive performance, respectively. Conclusion: Finding of the present study suggested that participants with low α-tocopherol intake were at higher risk for developing cognitive decline. Moreover, periodontitis mediated the association between α-tocopherol intake and cognitive performance.

Irisin Protects Cerebral Neurons from Hypoxia/Reoxygenation via Suppression of Apoptosis and Expression of Pro-Inflammatory Cytokines.

BACKGROUND: Ischemic stroke is a major health issue that causes high incidents of morbidity and mortality worldwide. Irisin is an excise-induced protein that has exhibited pleiotropic properties. Accumulating evidence reveals its critical roles in the regulation of various cellular functions, including nervous system functions. This study aims to disclose the effect of irisin on rat cerebral neurons suffering from hypoxia/reoxygenation (H/R) treatment and to explore the potential underlying molecular mechanisms. METHODS: The percentage of rat cerebral neuron cell death was determined by flow cytometry analysis and MTT assay. The expression levels of target genes were measured by western blotting and real-time quantitative reverse transcription PCR assay. RESULTS: Our results demonstrated that irisin treatment substantially reduced H/R-induced apoptosis of rat cerebral neurons. Further investigation revealed that irisin treatment markedly decreased mitogen-activated protein kinase (MAPK) signaling pathway activation and suppressed pro-informatory cytokine expression in cerebral neurons with H/R challenge. Finally, we showed that the neuroprotective effect and anti-inflammatory effect of irisin were comparable with three MAPK signaling inhibitors. CONCLUSION: Irisin exerts profound neuroprotective and anti-inflammatory effects on H/R-stimulated cerebral neurons by inhibiting the MAPK signaling activation. Therefore, irisin may serve as a potential drug for the treatment of patients with ischemic stroke.

Irisin Protects Brain against Ischemia/Reperfusion Injury through Suppressing TLR4/MyD88 Pathway.

BACKGROUND: Inflammatory response exerts an important role in ischemia/reperfusion (I/R) injury. TLR4 and myeloid differentiation factor 88 (MyD88) are key components in inflammation and are involved in the cerebral I/R injury. Irisin is a skeletal muscle-derived myokine produced after exercise, which was found to suppress inflammation. In this study, we investigated whether irisin could protect the brain from I/R injury through the TLR4/MyD88 pathway. METHODS: Male Sprague Dawley rats (20 months, 190 ∼ 240 g) were pretreated with irisin at 10, 50, or 100 mg/kg for consecutive 3 days and then subjected to surgery of middle cerebral artery occlusion or sham operation. Infarct size and neuron loss were measured to evaluate brain damage. The mRNA and protein levels of TLR4 and MyD88 were measured by in situ hybridization and immunohistochemistry, respectively. NF-κB activation was assessed by electrophoretic mobility shift assay. Neurological function was evaluated by neurobehavior score test and passive avoidance test. RESULTS: Irisin could reduce neuronal damage and neurofunctional impairment after I/R injury. This effect was mediated by downregulating the TLR4/MyD88 and inhibiting NF-κB activation. CONCLUSION: Irisin plays a beneficial effect in I/R injury through regulating the TLR4/MyD88 pathway.

[Electromagnetic pulse irradiation up-regulates methyl-CpG-binding protein 2 (MeCP2) and down-regulates neurogenin 2 in rat hippocampus].

Objective To investigate the alterations in hippocampus neuron morphology, the expression of neurogenin 2 (Ngn2) and methyl-CpG-binding protein 2 (MeCP2) in hippocampus after electromagnetic pulse (EMP) irradiation. Methods Adult healthy male SD rats were randomly divided into control group, EMP 7-day group, and EMP 14-day group (n=12). Hippocampus neuron morphology was tested by HE staining; the expression of Ngn2 and MeCP2 were measured by Western blotting and fluorescent immunohistochemistry; the protein levels of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95) were measured by Western blotting. Results Compared with the control group, the number of pyramidal cells in the EMP 7-day group and EMP 14-day group was reduced, the neuron boundary was blurred, and the nuclear outline was blurred. Compared with the EMP 7-day group, the hippocampus neuron structure in the EMP 14-day group was more severely damaged. Compared with the control group, the expression of Ngn2, BDNF, and PSD95 significantly decreased, while the expression of MeCP2 increased in the EMP 14-day group and EMP 7-day group. Conclusion EMP exposure leads to the pathological damage of hippocampus neurons in rats, increases MeCP2 expression and decreases Ngn2, PSD95, BDNF expression.

MicroRNA-665-3p attenuates oxygen-glucose deprivation-evoked microglial cell apoptosis and inflammatory response by inhibiting NF-κB signaling via targeting TRIM8.

Microglial inflammation induced by ischemic stroke aggravates brain damage. MicroRNAs (miRNAs) have emerged as pivotal regulators in ischemic stroke-induced inflammation in microglial cells. miR-665-3p has been reported as a critical inflammation-associated miRNA. However, whether miR-665-3p participates in regulating microglial inflammation during ischemic stroke is underdetermined. This study investigated the potential role of miR-665-3p in stroke-induced inflammation in microglial cells using a cellular model of oxygen-glucose deprivation (OGD)-stimulated microglial cells in vitro. We found that miR-665-3p expression was decreased in microglial cells exposed to OGD treatment. Functional experiments demonstrated that the overexpression of miR-665-3p attenuated OGD-induced apoptosis and inflammation in microglial cells. Notably, tripartite motif 8 (TRIM8) was identified as a target gene of miR-665-3p. TRIM8 expression was induced by OGD treatment in microglial cells and the knockdown of TRIM8 protected microglial cells from OGD -induced cytotoxicity and inflammation. Moreover, TRIM8 knockdown or miR-665-3p overexpression blocked OGD-induced activation of nuclear factor (NF)-κB signaling in microglial cells. In addition, TRIM8 overexpression partially reversed the miR-665-3p overexpression-mediated inhibitory effect on OGD-induced inflammation in microglial cells. Taken together, these results indicate that miR-665-3p up-regulation protects microglial cells from OGD-induced apoptosis and inflammatory response by targeting TRIM8 to inhibit NF-κB signaling.

Astragaloside IV Exerts Cognitive Benefits and Promotes Hippocampal Neurogenesis in Stroke Mice by Downregulating Interleukin-17 Expression via Wnt Pathway.

BACKGROUND: Stroke remains a leading cause of adult disability and the demand for stroke rehabilitation services is growing, and Astragaloside IV (As IV), a primary bioactive compound of Radix Astragali : Astragalus mongholicus Bunge (Fabaceae), may be a promising stroke therapy. METHODS: To access the effect of As IV on adult mice after ischemic stroke, a photochemical ischemia model was established on C57BL/6 mice, which were intravenously administered As IV for three consecutive days later. And then the cognitive benefits and hippocampal neurogenesis were evaluated by Morris Water Maze (MWM) test, Golgi staining, and immunohistochemical staining in vivo and in vitro. Furthermore, to find out the underlying mechanism, interleukin-17 (IL-17) knockout (KO) mice were used, through RNA sequence (RNA-seq) analysis and immunohistochemistry. Then the mechanism of neurogenesis promoted by As IV was observed by western blot both in vivo and in vitro. Specifically, As IV, recombinant mouse IL-17A and IL-17F, and Wingless/integrated (Wnt)-expressing virus was administered respectively in neural stem cells (NSCs), and then their diameters and protein expression of Nestin, IL-17, and Wnt pathway relevant protein, were measured in vitro. RESULTS: Administering As IV resulted in significant amelioration of stroke-induced cognitive deficits. And more hippocampal neurons with normal morphology, significant increments in the length of the apical dendrites, and the density of their spines were observed in As IV-treated mice. Furthermore, the immunohistochemistry staining of DCX/BrdU and Sox2/Nestin showed As IV could promote hippocampal neurogenesis and NSC proliferation after ischemic stroke, as well as in vitro. For the mechanism underlying, IL-17 expression was downregulated significantly by As IV treatment and knocking out IL-17 was associated with nervous regeneration and synapse repair according to the analysis of RNA-seq. Consistent to As IV treatment, knocking out IL-17 showed some promotion on hippocampal neurogenesis and proliferation of NSCs, with activating Wnt pathway after stoke. Finally, in vitro, NSCs' diameters and protein expression of Nestin, IL-17, and Wnt pathway were regulated by either administering As IV or inhibiting IL-17. CONCLUSION: As IV stimulates hippocampal neurogenesis after stroke, thus potentially facilitates brain to remodel and repair by downregulating IL-17 expression via Wnt pathway.

Effects of remote ischemic preconditioning on prognosis in patients with lung injury: A meta-analysis.

OBJECTIVE: A number of trials have shown that remote ischemic preconditioning (RIPC) could reduce lung injury of patients suffering cardiovascular surgery, pulmonary transplantation surgery and thoracic surgery with one-lung ventilation. However, there is still a controversy over the lung protection of RIPC in patients who suffers different types of surgery. We undertook meta-analysis of the randomized controlled trials to evaluate the effect of remote ischemic preconditioning on clinical outcomes of patients with lung injury. DESIGN: Systematic review and meta-analysis. SETTING: Perioperative care areas. PATIENTS: Adults and infants suffering cardiovascular surgery with lung injury. INTERVENTION: Remote ischemic preconditioning. MEASUREMENTS: The literatures were selected complying with the inclusive and exclusive criteria from the following databases as PubMed, Embase, Medline, Chinese Biomedical Literature and Journal Databases, Chinese Academic and VIP journal full-text Databases. Inclusion criteria includes: (1) Human clinical randomized and controlled trial; (2) the article we included is a clinical randomized controlled study; (3) the article discusses the effect of RIPC on lung injury of patients; (4) the primary evaluation indicators of the inclusive studies included postoperative intensive care unit stay time and mechanical ventilation time; (5) published in the form of full text, any language; (6) the type of operation is cardiovascular surgery; (7) there is no serious COPD, ARDS, respiratory failure and other lung diseases. Articles were excluded if they reported none of the outcomes as follows: postoperative intensive care unit stay time and mechanical ventilation time, human clinical controlled trails, pulmonary protection of RIPC, prospective clinical controlled trials. Two independent reviewers screened abstracts and titles, and selected records following full-text review. Software RevMan5.3 and STATA 12.0 were adopted to perform Meta-analysis. RESULT: The search finally includes10 studies of 708 patients, 352 patients in RIPC group and 356 patients in control group. The baseline characteristics of patients are no differences in two groups (P > 0.05). Compared with control group, RIPC significantly reduced the duration of ICU (P < 0.05) and mechanical ventilation time (P < 0.05) in RIPC group. In addition, the serum TNF-α and MDA concentration 24 h after operation in RIPC group are significantly lower than control group (P < 0.05). However, there are no significant differences between RIPC group and control group in terms of serum IL-6, IL-8 concentrations, A-aDO2, PaO2/FiO2 and respiratory index 24 h after operation. CONCLUSION: RIPC can decrease pulmonary inflammatory responses, reduce the duration of ICU and mechanical ventilation time, and improve the clinical outcomes of patients with lung injury.

α7 Nicotinic Acetylcholine Receptor Mediates the Neuroprotection of Remote Ischemic Postconditioning in a Rat Model of Asphyxial Cardiac Arrest.

BACKGROUND: Remote ischemic postconditioning (RIPost) has been shown to reduce the ischemia-reperfusion injury of the heart and brain. However, the protection mechanisms have not yet been fully elucidated. We have observed that RIPost could alleviate the brain injury after cardiac arrest (CA). The aim of this study was to explore whether α7 nicotinic acetylcholine receptor (α7nAChR) mediates the neuroprotection of RIPost in a rat model of asphyxial CA. MATERIALS AND METHODS: Asphyxial CA model was induced by occlusion of the tracheal tube for 8 min and resuscitated later. RIPost produced by three cycles of 15-min occlusion and 15-min release of the right hind limb by a tourniquet was performed respectively at the moment and the third hour after restoration of spontaneous circulation. The α7nAChR agonist PHA-543613 and the antagonist methyllycaconitine (MLA) were used to investigate the role of α7nAChR in mediating neuroprotective effects. RESULTS: Results showed that α7nAChR was decreased in hippocampus and cortex after resuscitation, whereas RIPost could attenuate the reduction. The use of PHA-543613 provided neuroprotective effects against cerebral injury after CA. Furthermore, RIPost decreased the levels of neuron-specific enolase, inflammatory mediators, the number of apoptotic cells, and phosphorylation of nuclear factor-κB while increased the phosphorylation of signal transducer and activator of transcription-3. However, the above effects of RIPost were attenuated by α7nAChR antagonist methyllycaconitine. CONCLUSIONS: Neuroprotection of RIPost was related with the activation of α7nAChR, which could suppress nuclear factor-κB and activate signal transducer and activator of transcription-3 in a rat asphyxial CA model.

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway.

Electromagnetic pulse (EMP) is a unique type of electromagnetic radiation, and EMP exposure causes a series of biological effects. The nervous system is sensitive to EMP. We studied the neuroprotective effects of isoflurane preconditioning against EMP exposure and used hematoxylin-eosin staining (HE) to observe the effects of electromagnetic pulse and isoflurane preconditioning on neurons. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of caspase-3, CD11b, TLR4, and NFκBp65. We found that after EMP exposure, the number of abnormal neurons had increased, and the expression of caspase-3, CD11b, TLR4, and NFκBp65 had also increased. Isoflurane preconditioning can reverse the above phenomenon. Moreover, we found that isoflurane preconditioning can reduce neuronal apoptosis and improve cognitive impairment induced by EMP. These findings indicate that isoflurane preconditioning can protect neurons in the cerebral cortex from EMP exposure, alleviate the inflammatory reaction and cell apoptosis, and improve cognitive impairment induced by EMP. These effects may occur through the downregulation of the TLR4/NFκB signaling pathway and the inhibition of microglial activation.

Isoflurane preconditioning ameliorates electromagnetic pulse-induced neural damage by shifting microglia polarization toward anti-inflammatory phenotype via upregulation of SOCS1.

With the speedy technological advances during the past few decades, human exposure to the electromagnetic field (EMF) has become increasingly common. Exposure to EMF may induce neural injuries and dysfunction of various organs, likely involving neuroinflammation and activation of microglial cells. Isoflurane preconditioning (IP) is shown to provide neuroprotection in various neurological diseases by inhibiting excessive neuroinflammatory responses. Brain samples harvested from rats exposed to electromagnetic pulse (EMP) with or without IP were subjected to qPCR, Western blot assay, and immunohistochemistry to determine the expression of pro-inflammatory/anti-inflammatory microglia markers and a variety of pro- and anti-inflammatory mediators. Suppressor of cytokine signaling 1 (SOCS1) siRNA was used in cultured N9 microglia cells to examine the roles of SOCS1 in the effect of IP. In both in vivo and in vitro experiments, EMP-exposed microglia were predominantly pro-inflammatory microglia, accompanied by increased expression of pro-inflammatory cytokines and chemokines, and activation of TLR4 pathway, leading to neuronal death. IP reversed the changes induced by EMP and switched the activated microglia to an anti-inflammatory phenotype. SOCS1 siRNA abolished the beneficial effects of IP. IP ameliorates EMP-induced neural injuries by shifting microglia polarization from pro-inflammatory to anti-inflammatory phenotype via upregulation of SOCS1.