scholarly journals Identification of ferroptosis-associated genes exhibiting altered expression in response to cardiopulmonary bypass during corrective surgery for pediatric tetralogy of fallot

2021 ◽  
Vol 104 (4) ◽  
pp. 003685042110502
Author(s):  
Hongtao Liu ◽  
Bingyong Zhang ◽  
Shaofeng Chen ◽  
Yun Zhang ◽  
Xin Ye ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiopulmonary Bypass ◽  
Tetralogy Of Fallot ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Pathway Enrichment Analysis ◽  
Corrective Surgery ◽  
Ischemia And Reperfusion Injury ◽  
Altered Expression

Background Tetralogy of Fallot (ToF) is a life-threatening congenital cardiovascular disorder. Currently, the most effective therapeutic intervention for pediatric ToF remains corrective surgery with cardiopulmonary bypass (CPB). Ferroptosis is an iron-dependent form of regulated cell death, driven by an accumulation of lipid peroxides to levels sufficient to trigger cell death. Ferroptosis was recently linked to cardiac ischemia and reperfusion injury. However, few studies have examined CPB-associated ferroptosis. Method In the current study, pediatric ToF patient pre- and post-CPB atrial biopsy gene expression profiles were downloaded from a public database, and 117 differentially expressed genes (DEGs) were identified using the Wilcoxon rank-sum test and weighted gene correlation network analysis. These were screened for ferroptosis-associated genes using the FerrDb database, thereby identifying ten genes. Finally, the construction of gene-microRNA (miRNA) and gene-transcription factor (TF) networks, in conjunction with gene ontology and biological pathway enrichment analysis, were used to inform hypotheses regarding the molecular mechanisms underlying CPB-associated ferroptosis. Results Ten genes involved in CPB-associated ferroptosis(ATF3,TNFAIP3，CDKN1A, ZFP36, JUN，SLC2A3, IL6, CXCL2, PTGS2, and DDIT3). Ferroptosis-associated genes were largely involved in myocardial inflammatory responses and may be regulated by a number of identified miRNAs and TFs, thereby suggesting modulatable pathways potentially involved in CPB-associated ferroptosis. Conclusions Results suggest that CPB precipitates ferroptosis within cardiac tissue during corrective Surgery for Pediatric Tetralogy of Fallot. These findings may ultimately help improve outcomes of corrective surgery for pediatric ToF.

scholarly journals Identification of ferroptosis-associated genes exhibiting altered expression in pulmonary arterial hypertension

2021 ◽  
Vol 18 (6) ◽  
pp. 7619-7630
Author(s):  
Fan Zhang ◽  
◽  
Hongtao Liu ◽  
Keyword(s):  
Cell Death ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Pathway Enrichment Analysis ◽  
Altered Expression ◽  
Network Analyses ◽  
Pulmonary Arterial

<abstract> <p>Pulmonary arterial hypertension (PAH) is a life-threatening illness and ferroptosis is an iron-dependent form of regulated cell death, driven by the accumulation of lipid peroxides to levels that are sufficient to trigger cell death. However, only few studies have examined PAH-associated ferroptosis. In the present study, lung samples mRNA expression profiles (derived from 15 patients with PAH and 11 normal controls) were downloaded from a public database, and 514 differentially expressed genes (DEGs) were identified using the Wilcoxon rank-sum test and weighted gene correlation network analyses. These DEGs were screened for ferroptosis-associated genes using the FerrDb database: eight ferroptosis-associated genes were identified. Finally, the construction of gene-microRNA (miRNA) and gene-transcription factor (TF) networks, in conjunction with gene ontology and biological pathway enrichment analysis, were used to inform hypotheses regarding the molecular mechanisms underlying PAH-associated ferroptosis. Ferroptosis-associated genes were largely involved in oxidative stress responses and could be regulated by several identified miRNAs and TFs. This suggests the existence of modulatable pathways that are potentially involved in PAH-associated ferroptosis. Our findings provide novel directions for targeted therapy of PAH in regard to ferroptosis. These findings may ultimately help improve the therapeutic outcomes of PAH.</p> </abstract>

scholarly journals Bioinformatics Analysis Reveals the Potential Diagnostic Biomarkers for Abdominal Aortic Aneurysm

2021 ◽  
Vol 8 ◽  
Author(s):  
Xinsheng Xie ◽  
En ci Wang ◽  
Dandan Xu ◽  
Xiaolong Shu ◽  
Yu fei Zhao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Enrichment Analysis ◽  
Aortic Aneurysms ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Abdominal Aortic

Objectives: Abdominal aortic aneurysms (AAAs) are associated with high mortality rates. The genes and pathways linked with AAA remain poorly understood. This study aimed to identify key differentially expressed genes (DEGs) linked to the progression of AAA using bioinformatics analysis.Methods: Gene expression profiles of the GSE47472 and GSE57691 datasets were acquired from the Gene Expression Omnibus (GEO) database. These datasets were merged and normalized using the “sva” R package, and DEGs were identified using the limma package in R. The functions of these DEGs were assessed using Cytoscape software. We analyzed the DEGs using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Protein–protein interaction networks were assembled using Cytoscape, and crucial genes were identified using the Cytoscape plugin, molecular complex detection. Data from GSE15729 and GSE24342 were also extracted to verify our findings.Results: We found that 120 genes were differentially expressed in AAA. Genes associated with inflammatory responses and nuclear-transcribed mRNA catabolic process were clustered in two gene modules in AAA. The hub genes of the two modules were IL6, RPL21, and RPL7A. The expression levels of IL6 correlated positively with RPL7A and negatively with RPL21. The expression of RPL21 and RPL7A was downregulated, whereas that of IL6 was upregulated in AAA.Conclusions: The expression of RPL21 or RPL7A combined with IL6 has a diagnostic value for AAA. The novel DEGs and pathways identified herein might provide new insights into the underlying molecular mechanisms of AAA.

Efferocytosis during myocardial infarction

2020 ◽  
Vol 168 (1) ◽  
pp. 1-6
Author(s):  
Chikashi Yoshimura ◽  
Akiomi Nagasaka ◽  
Hitoshi Kurose ◽  
Michio Nakaya
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Causes Of Death ◽  
Inflammatory Responses ◽  
Heart Cells ◽  
Dead Cell ◽  
Related Cell

Abstract Myocardial infarction is one of the major causes of death worldwide. Many heart cells die during myocardial infarction through various processes such as necrosis, apoptosis, necroptosis, autophagy-related cell death, pyroptosis and ferroptosis. These dead cells in infarcted hearts expose the so-called ‘eat-me’ signals, such as phosphatidylserine, on their surfaces, enhancing their removal by professional and non-professional phagocytes. Clearance of dead cells by phagocytes in the diseased hearts plays a crucial role in the pathology of myocardial infarction by inhibiting the inflammatory responses caused by the leakage of contents from dead cells. This review focuses on the rapidly growing understanding of the molecular mechanisms of dead cell phagocytosis, termed efferocytosis, during myocardial infarction, which contributes to the pathophysiology of myocardial infarction.

scholarly journals Bioinformatics-Based Study to Investigate Potential Differentially Expressed Genes and miRNAs in Hashimoto’s Thyroiditis

2021 ◽  
Author(s):  
Li Guoquan ◽  
Du Junwei ◽  
He Qi ◽  
Fu Xinghao ◽  
Ji Feihong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differentially Expressed Genes ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Treatment Options ◽  
Enrichment Analysis ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Chronic Lymphocytic Thyroiditis ◽  
Hub Genes

Abstract BackgroundHashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is a common autoimmune disease, which mainly occurs in women. The early manifestation was hyperthyroidism, however, hypothyroidism may occur if HT was not controlled for a long time. Numerous studies have shown that multiple factors, including genetic, environmental, and autoimmune factors, were involved in the pathogenesis of the disease, but the exact mechanisms were not yet clear. The aim of this study was to identify differentially expressed genes (DEGs) by comprehensive analysis and to provide specific insights into HT. MethodsTwo gene expression profiles (GSE6339, GSE138198) about HT were downloaded from the Gene Expression Omnibus (GEO) database. The DEGs were assessed between the HT and normal groups using the GEO2R. The DEGs were then sent to the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The hub genes were discovered using Cytoscape and CytoHubba. Finally, NetworkAnalyst was utilized to create the hub genes' targeted microRNAs (miRNAs). ResultsA total of 62 DEGs were discovered, including 60 up-regulated and 2 down-regulated DEGs. The signaling pathways were mainly engaged in cytokine interaction and cytotoxicity, and the DEGs were mostly enriched in immunological and inflammatory responses. IL2RA, CXCL9, IL10RA, CCL3, CCL4, CCL2, STAT1, CD4, CSF1R, and ITGAX were chosen as hub genes based on the results of the protein-protein interaction (PPI) network and CytoHubba. Five miRNAs, including mir-24-3p, mir-223-3p, mir-155-5p, mir-34a-5p, mir-26b-5p, and mir-6499-3p, were suggested as likely important miRNAs in HT. ConclusionsThese hub genes, pathways and miRNAs contribute to a better understanding of the pathophysiology of HT and offer potential treatment options for HT.

scholarly journals Tsn1-Mediated Host Responses to ToxA from Pyrenophora tritici-repentis

2009 ◽  
Vol 22 (9) ◽  
pp. 1056-1068 ◽  
Author(s):  
Tika B. Adhikari ◽  
Jianfa Bai ◽  
Steven W. Meinhardt ◽  
Suraj Gurung ◽  
Mary Myrfield ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Wheat Cultivar ◽  
Expression Profiles ◽  
Phenylpropanoid Pathway ◽  
Host Responses ◽  
Mesophyll Cells ◽  
Pyrenophora Tritici Repentis ◽  
Host Defense Response

The toxin sensitivity gene Tsn1 interacts with Ptr ToxA (ToxA), a host-selective toxin produced by the necrotrophic fungus Pyrenophora tritici-repentis. The molecular mechanisms associated with cell death in sensitive wheat cultivars following ToxA application are not well understood. To address this question, we used the Affymetrix GeneChip Wheat Genome Array to compare gene expression in a sensitive wheat cultivar possessing the Tsn1 gene with the insensitive wheat cv. Nec103, which lacks the Tsn1 gene. This analysis was performed at early timepoints after infiltration with ToxA (e.g., 0.5 to 12 h postinfiltration [hpi]); at this time, ToxA is known to internalize into mesophyll cells without visible cell death symptoms. Gene expression also was monitored at later timepoints (24 to 48 hpi), when ToxA causes extensive damage in cellular compartments and visible cell death. At both early and late timepoints, numerous defense-related genes were induced (2- to 197-fold increases) and included genes involved in the phenylpropanoid pathway, lignification, and the production of reactive oxygen species (ROS). Furthermore, a subset of host genes functioning in signal transduction, metabolism, and as transcription factors was induced as a consequence of the Tsn1–ToxA interaction. Nine genes known to be involved in the host defense response and signaling pathways were selected for analysis by quantitative real-time polymerase chain reaction, and the expression profiles of these genes confirmed the results obtained in microarray experiments. Histochemical analyses of a sensitive wheat cultivar showed that H2O2 was present in leaves undergoing cell death, indicating that ROS signaling is a major event involved in ToxA-mediated cell death. The results suggest that recognition of ToxA via Tsn1 triggers transcriptional reprogramming events similar to those reported for avirulence–resistance gene interactions, and that host-derived genes play an important role in the modulation of susceptibility to P. tritici-repentis.

scholarly journals Expression profiles of multiple genes in single neurons of Alzheimer’s disease

1998 ◽  
Vol 95 (16) ◽  
pp. 9620-9625 ◽  
Author(s):  
Nienwen Chow ◽  
Chris Cox ◽  
Linda M. Callahan ◽  
Jill M. Weimer ◽  
LiRong Guo ◽  
...  
Keyword(s):  
Single Cell ◽  
Northern Blot ◽  
Antisense Rna ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Single Neurons ◽  
Altered Expression ◽  
Rna Profiling ◽  
Multiple Messages

Many changes have been described in the brains of Alzheimer’s disease (AD) patients, including loss of neurons and formation of senile plaques and neurofibrillary tangles. The molecular mechanisms underlying these pathologies are unclear. Northern blot, dot-blot, and reverse transcription-coupled PCR analyses have demonstrated altered expression levels of multiple messages in AD brain. Because not all cells are equally affected by the disease, these methods obviously cannot study the changes in relation to disease states of individual cells. We address this problem by using antisense RNA profiling of single cells. We present expression profiles of single neurons at early and late stages of AD and describe statistical tools for data analysis. With multivariate canonical analysis, we were able to distinguish the disease state on the basis of altered expression of multiple messages. To validate this approach, we compared results obtained by this approach with results obtained by in situ hybridization analysis. When the neurofilament medium subunit was used as a marker, our results from an antisense RNA profiling revealed no change in neurofilament medium subunit expression between early- and late-stage AD, consistent with findings obtained with in situ hybridization. However, our results obtained by either analysis at the single-cell level differed from the reported decrease in AD neocortex obtained by Northern blot analysis [Kittur, S., Hoh, J., Endo, H., Tourtellotte, W., Weeks, B. S., Markesbery, W. & Adler, W. (1994) J. Geriatr. Psychiatry Neurol. 7, 153–158]. Thus, the strategy of using the single-cell antisense RNA approach to identify altered gene expression in postmortem AD brain, followed by detailed in situ hybridization studies for genes of interest, is valuable in the study of the molecular mechanisms underlying AD neuropathology.

scholarly journals Identification and Verification of Core Genes in Colorectal Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Houxi Xu ◽  
Yuzhu Ma ◽  
Jinzhi Zhang ◽  
Jialin Gu ◽  
Xinyue Jing ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Malignant Neoplasm ◽  
Gene Expression Profiles ◽  
Enrichment Analysis ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Core Genes

Colorectal cancer, a malignant neoplasm that occurs in the colorectal mucosa, is one of the most common types of gastrointestinal cancer. Colorectal cancer has been studied extensively, but the molecular mechanisms of this malignancy have not been characterized. This study identified and verified core genes associated with colorectal cancer using integrated bioinformatics analysis. Three gene expression profiles (GSE15781, GSE110223, and GSE110224) were downloaded from the Gene Expression Omnibus (GEO) databases. A total of 87 common differentially expressed genes (DEGs) among GSE15781, GSE110223, and GSE110224 were identified, including 19 upregulated genes and 68 downregulated genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was performed for common DEGs using clusterProfiler. These common DEGs were significantly involved in cancer-associated functions and signaling pathways. Then, we constructed protein-protein interaction networks of these common DEGs using Cytoscape software, which resulted in the identification of the following 10 core genes: SST, PYY, CXCL1, CXCL8, CXCL3, ZG16, AQP8, CLCA4, MS4A12, and GUCA2A. Analysis using qRT-PCR has shown that SST, CXCL8, and MS4A12 were significant differentially expressed between colorectal cancer tissues and normal colorectal tissues (P<0.05). Gene Expression Profiling Interactive Analysis (GEPIA) overall survival (OS) has shown that low expressions of AQP8, ZG16, CXCL3, and CXCL8 may predict poor survival outcome in colorectal cancer. In conclusion, the core genes identified in this study contributed to the understanding of the molecular mechanisms involved in colorectal cancer development and may be targets for early diagnosis, prevention, and treatment of colorectal cancer.

scholarly journals POS0743 GENE EXPRESSION MICROARRAY IN LUPUS NEPHRITIS BY BIOINFORMATIC ANALYSIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 623.1-623
Author(s):  
C. Wang ◽  
S. X. Zhang ◽  
S. Song ◽  
J. Qiao ◽  
R. Zhao ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Differential Expression Analysis ◽  
Deep Understanding ◽  
Enrichment Analysis ◽  
Shanxi Province ◽  
Pathway Enrichment Analysis ◽  
Ppi Network ◽  
Hub Genes

Background:Nephritis is one of the predominant causes of morbidity and mortality in patients with lupus1 2.The lack of understanding regarding the molecular mechanisms of lupus nephritis(LN) hinders the development of specific targeted therapy for this progressive disease3.Objectives:In this study, we use bioinformatics method to analyze the genes involved in regulating the potential pathogenesis of LN.Methods:The expression profile of LN(GSE104948 and GSE32591) was obtained from the GEO database.GSE104948 was a memory chip, which included 32 LN glomerular biopsy tissues and 3 glomerular tissues from living donors.GSE32591 dataset included 32 LN glomerular biopsy tissues and 15 glomerular tissues from living donors. The Oligo package was used to process the data to obtain the expression matrix files of all the related genes.P<0.05 and |log2(FC)|>2 were setted as cut-off criteria for the DEGs.Ggplot2, heatmap packages were used to DEGs visualization. Metascape online tool was used to annotating DEGs for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis performed.We used STRING online database to construct protein-protein interaction (PPI) network. Hub genes were identified by Cytoscape.Results:In differential expression analysis,357 DEGs were identified,including 248 up-regulated genes and 109 down-regulated genes (Figure 1A,B).GO enrichment showed that these DEGs were primarily enriched in biological pathways, cell localization and molecular function and revealed that LN-related genes mainly involved in immune response.KEGG pathway annotation enrichment analysis revealed these DEGs were closely associated with Staphylococcus aureus infection,Complement and coagulation cascades (Figure 1D). Fourteen hub genes(IFT3,IRF7,OAS3,GBP2,RSAD2,MX1,IFIT2,IFI6,MX2,ISF15,IFIT1,QAS2,OASL,OAS1) were identified from PPI network (Figure 1C,E).Conclusion:Illuminating the molecular mechanisms of LN was help for deep understanding of LN.References:[1]Song J, Zhao L, Li Y. Comprehensive bioinformatics analysis of mRNA expression profiles and identification of a miRNA-mRNA network associated with lupus nephritis. Lupus 2020;29(8):854-61. doi: 10.1177/0961203320925155 [published Online First: 2020/05/22].[2]Yao F, Sun L, Fang W, et al. HsamiR3715p inhibits human mesangial cell proliferation and promotes apoptosis in lupus nephritis by directly targeting hypoxiainducible factor 1alpha. Mol Med Rep 2016;14(6):5693-98. doi: 10.3892/mmr.2016.5939 [published Online First: 2016/11/24].[3]Dall’Era M. Treatment of lupus nephritis: current paradigms and emerging strategies. Curr Opin Rheumatol 2017;29(3):241-47. doi: 10.1097/BOR.0000000000000381 [published Online First: 2017/02/17].Acknowledgements:This project was supported by National Science Foundation of China (82001740), Open Fund from the Key Laboratory of Cellular Physiology (Shanxi Medical University) (KLCP2019) and Innovation Plan for Postgraduate Education in Shanxi Province (2020BY078).Disclosure of Interests:None declared

scholarly journals HOX cluster and their cofactors showed an altered expression pattern in eutopic and ectopic endometriosis tissues

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Fereshteh Esfandiari ◽  
Fereshteh Chitsazian ◽  
Masoumeh Golestan Jahromi ◽  
Raha Favaedi ◽  
Masood Bazrgar ◽  
...  
Keyword(s):  
Expression Pattern ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Critical Role ◽  
Disease Diagnosis ◽  
Altered Expression ◽  
Control Tissue ◽  
New Genes ◽  
Advanced Therapies ◽  
Altered Expression Pattern

AbstractEndometriosis is major gynecological disease that affects over 10% of women worldwide and 30%-50% of these women have pelvic pain, abnormal uterine bleeding and infertility. The cause of endometriosis is unknown and there is no definite cure mainly because of our limited knowledge about its pathophysiology at the cellular and molecular levels. Therefore, demystifying the molecular mechanisms that underlie endometriosis is essential to develop advanced therapies for this disease. In this regard, HOX genes are remarkable because of their critical role in endometrial development and receptivity during implantation, which is attributed to their ability to mediate some of the sex steroid functions during the reproductive period. Access to the expression profiles of these genes would provide the necessary information to uncover new genes for endometriosis and assist with disease diagnosis and treatment. In this study we demonstrate an altered expression pattern for the HOX clusters (A-D) and their cofactors in both eutopic and ectopic conditions compared to control tissue biopsies. Remarkably, most of the intensive changes occurred in eutopic samples from endometriosis patients compared to control tissue biopsies. Pathway analysis revealed the involvement of differentially expressed genes in cancer that correlate with an association between endometriosis and cancer. Our results suggest critical roles for the HOX cluster and their cofactors in endometriosis pathophysiology.

scholarly journals Up-regulation of FOXO1 and reduced inflammation by β-hydroxybutyric acid are essential diet restriction benefits against liver injury

2019 ◽  
Vol 116 (27) ◽  
pp. 13533-13542 ◽  
Author(s):  
Tomoyuki Miyauchi ◽  
Yoichiro Uchida ◽  
Kentaro Kadono ◽  
Hirofumi Hirao ◽  
Junya Kawasoe ◽  
...  
Keyword(s):  
Liver Injury ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Apoptotic Cell ◽  
Enzyme Level ◽  
Ischemia And Reperfusion ◽  
Hydroxybutyric Acid ◽  
Diet Restriction ◽  
Ischemia And Reperfusion Injury

Liver ischemia and reperfusion injury (IRI) is a major challenge in liver surgery. Diet restriction reduces liver damage by increasing stress resistance; however, the underlying molecular mechanisms remain unclear. We investigated the preventive effect of 12-h fasting on mouse liver IRI. Partial warm hepatic IRI model in wild-type male C57BL/6 mice was used. The control ischemia and reperfusion (IR) group of mice was given food and water ad libitum, while the fasting IR group was given water but not food for 12 h before ischemic insult. In 12-h fasting mice, serum liver-derived enzyme level and tissue damages due to IR were strongly suppressed. Serum β-hydroxybutyric acid (BHB) was significantly raised before ischemia and during reperfusion. Up-regulated BHB induced an increment in the expression of FOXO1 transcription factor by raising the level of acetylated histone. Antioxidative enzyme heme oxigenase 1 (HO-1), a target gene of FOXO1, then increased. Autophagy activity was also enhanced. Serum high-mobility group box 1 was remarkably lowered by the 12-h fasting, and activation of NF-κB and NLRP3 inflammasome was suppressed. Consequently, inflammatory cytokine production and liver injury were reduced. Exogenous BHB administration or histone deacetylase inhibitor administration into the control fed mice ameliorated liver IRI, while FOXO1 inhibitor administration to the 12-h fasting group exacerbated liver IRI. The 12-h fasting exerted beneficial effects on the prevention of liver IRI by increasing BHB, thus up-regulating FOXO1 and HO-1, and by reducing the inflammatory responses and apoptotic cell death via the down-regulation of NF-κB and NLRP3 inflammasome.

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