Endogenous hydrogen sulphide attenuates NLRP3 inflammasome-mediated neuroinflammation by suppressing the P2X7 receptor after intracerebral haemorrhage in rats

Zhao, Hengli; Pan, Pengyu; Yang, Yang; Ge, Hongfei; Chen, Weixiang; Qu, Jie; Shi, Jiandang; Cui, Gaoyu; Liu, Xin; Feng, Hua; Chen, Yujie

doi:10.1186/s12974-017-0940-4

Cited by 107 publications

(80 citation statements)

References 37 publications

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“…Studies have shown that oral administration of uridine can increases synaptic membranes and dendritic spines in rodents, signi cantly elevated striatal dopamine, tyrosine hydroxylase (TH) activity in 6-OHDA model [41]. S-adenosine methionine can reduce microglial aggregation and neuroin ammatory by increasing plasma hydrogen sulphide [42], which play neuroprotective role in central nervous system. Therefore, the decrease of Prevotella_copri will participate in the occurrence and progression of PD by leading loss of dopaminergic neurotransmission and neuroprotective effect.…”

Section: Discussionmentioning

confidence: 99%

Metagenomic analysis of gut microbiota in Parkinson's disease patients from Central China

Zhang

Zhao

Fang

et al. 2020

Preprint

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Background: Parkinson's disease (PD) is one of the most common neurodegenerative diseases, pathologic and epidemiologic studies suggest that gut microbiota may play important roles in the occurrence and progression of Parkinson's disease. However, the alterations in fecal microbiome in PD patients from Central China has not been investigated. Therefore, in this case-control study, we characterised the gut microbial community of 46 PD patients and compared it to those of healthy spouses by using metagenomic shotgun sequencing. Correlation between altered microbiota and clinical features were examined, functional pathways of gut microbiota were estimated, and potential biomarker were explored for further understaning of gut microbiota in PD. Results: Microbial communities in the feces of PD patients were notably different from those of healthy spouses at species level. Gut microbiota of patients was characterized by depletion of Prevotella_copri and Bacteroides_fragilis, while the Bacteroides_stercoris and Escherichia_coli were markedly elevated. Correlation analysis found that most identified species were negatively correlated with disease clinical features. In particular, Prevotella_copri was negatively correlated with age and UPDRS Ⅲ score. Random forest model indicated that 6 species including Prevotella_copri had good predictive value for disease. Functional analyses of the metagenomes revealed differences in microbiota metabolism. Pathways associated with superpathway of thiamin diphosphate biosynthesis, 4-aminobutanoate degradation, glucose-1-phosphate degradation and methylphosphonate degradation were significant increase in patients, while pathways associated with aromatic amino acid biosynthesis, chorismate biosynthesis, thiamin formation and pyrimidine deoxyribonucleosides salvage were significantly decrease. Functional pathways of Prevotella_copri were mainly concentrated in UMP biosynthesis, S-adenosyl-L-methionine cycle and guanosine ribonucleotides de novo biosynthesis. Conclusion: Our findings confirmed changes of gut microbiota in Chinese patients with PD. Altered microbiota had correlation with the clinical characteristics of disease, which may used as potential biomarkers. Different functional pathways of gut microbiota in PD patients will help to improve our understanding of the mechanism in disease, and targeting on gut microbiota may be one of the new therapeutic choices of PD in the future.

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Section: Discussionmentioning

confidence: 99%

Metagenomic analysis of gut microbiota in Parkinson's disease patients from Central China

Zhang

Zhao

Fang

et al. 2020

Preprint

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“…Supplementing taurine can upregulate the content of H 2 S and reduce neutrophil infiltration and glial activation, downregulate the expression of inflammatory mediators and P2X7R, and reduce the inflammatory response, thereby improving the condition of WMI . Previous study also demonstrated that endogenous H 2 S reduces NLRP3‐mediated neuroinflammation by inhibiting the P2X7 receptor in rats with ICH . Another study showed that curcumin could inhibit neuroinflammation and alleviate WMI after ICH .…”

Section: Repair or Recovery Mechanism And Strategymentioning

confidence: 98%

“…28,29 Zhao et al found that ICH could significantly reduce the production of endogenous hydrogen sulfide (H 2 S) in the brain and that H 2 S weakened the inflammatory damage mediated by NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) through the purinergic P2X7 receptor (P2X7R) signaling pathway. 30 Wang et al reported that microglia also closely interact with the endothelial cells. ICH induced damage to the endothelial cells, resulting in a large number of CXC chemokine ligand (CXCL).…”

Section: Pathophys I Ology Of Wmi Af Ter Ichmentioning

confidence: 99%

“…47 Previous study also demonstrated that endogenous H 2 S reduces NLRP3-mediated neuroinflammation by inhibiting the P2X7 receptor in rats with ICH. 30,48 Another study showed that curcumin could inhibit neuroinflammation and alleviate WMI after ICH. 49 In addition, increasing the expression of procedural death protein 1 and procedural death ligand 1 can induce microglial polarization by regulating neuroimmunity and alleviate inflammatory response after ICH.…”

Section: Reducing Neuroinflammationmentioning

confidence: 99%

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White matter repair and treatment strategy after intracerebral hemorrhage

et al. 2019

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The predilection site of intracerebral hemorrhage (ICH) is in the basal ganglia, which is rich in white matter (WM) fiber bundles, such as cerebrospinal tract in the internal capsule. ICH induced damage to this area can easily lead to severe neurological dysfunction and affects the prognosis and quality of life of patients. At present, the pathophysiological mechanisms of white matter injury (WMI) after ICH have attracted researchers' attention, but studies on the repair and recovery mechanisms and therapy strategies remain rare. In this review, we mainly summarized the WM recovery and treatment strategies after ICH by updating the WMI‐related content by reviewing the latest researches and proposing the bottleneck of the current research.

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“…According to previous reports [27][28][29][30] and the results of MTT assay (Supplementary Figure S1), we selected glucose, SAMe, NaHS and resveratrol at a concentration of 85 mM, 0.2 mM, 250 μM and 10 μM to treat HT-22 cells, respectively, and divided them into the following ve groups: control group (25 mM glucose), high glucose (HG) group (85 mM glucose), HG + NaHS group (85 mM glucose + 250 μM NaHS), HG + SAMe group (85 mM glucose + 0.2 mM SAMe) and HG + resvertatrol (RES) group (85 mM glucose + 10 μM resveratrol).…”

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

Hydrogen Sulfide Ameliorates High Glucose-induced Inflammation Through SIRT1-mTOR/NF-κB Signaling Pathway in HT-22 cells

et al. 2020

Preprint

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Background: Hyperglycemia-induced neuroinflammation promotes the progression of diabetic encephalopathy (DE). Hydrogen sulfide (H2S) exerts anti-inflammatory and neuroprotective activities against neurodegenerative diseases. However, its role in hyperglycemia-induced neuronal inflammation has not been investigated. Herein, we examined the effects and its related signaling pathway of H2S on inflammatory response in high glucose-treated HT-22 cells.Methods: A hippocampal neuronal cell line, HT-22, was used as an in vitro model to explore the function of H2S on inflammatory response triggered by high glucose. A dicyanoisophorone-based near-infrared fluorescent probe (NIR-NP) was synthesized to detect H2S levels in HT-22 cells. Western blotting, immunofluorescence and real time-qPCR were carried out to study the mechanism of action for H2S.Results: We found that high glucose (85 mM) decreased the level of endogenous H2S and the expression of cystathionine-β-synthase (CBS) which is the main enzyme for H2S production in the brain. Sodium hydrosulfide (NaHS, a H2S donor) or S-adenosylmethionine (SAMe, an allosteric activator of CBS) administration restored high glucose-induced downregulation of CBS and H2S levels. Importantly, high glucose upregulated the level of pro-inflammatory factors (IL-1β, IL-6, TNF-α) in HT-22 cells. Treatment with NaHS or SAMe alleviated this enhanced transcription of these pro-inflammatory factors, suggesting that H2S might ameliorate high glucose-induced inflammation in HT-22 cells. We also found that high glucose reduced SIRT1 protein levels. SIRT1 reduction elevated the level of p-mTOR, p-NF-κB and pro-inflammatory factors, which were restored by resveratrol (a SIRT1 agonist). These results suggested that SIRT1 might be an upstream mediator of mTOR/NF-κB signaling pathway. Furthermore, NaHS or SAMe treatment reversed the expression of SIRT1, mTOR and NF-κB under high glucose conditions.Conclusions: Our study revealed that high glucose decreased CBS to reduce the production of H2S, which in turn decreased the expression of SIRT1. The reduction of SIRT1 activated mTOR/NF-κB signaling to promote inflammation. Given that promoting H2S production using NaHS or SAMe can reverse high glucose-induced inflammatory response, our study might shed light on the prophylactic treatment of DE.

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Endogenous hydrogen sulphide attenuates NLRP3 inflammasome-mediated neuroinflammation by suppressing the P2X7 receptor after intracerebral haemorrhage in rats

Cited by 107 publications

References 37 publications

Metagenomic analysis of gut microbiota in Parkinson's disease patients from Central China

Metagenomic analysis of gut microbiota in Parkinson's disease patients from Central China

White matter repair and treatment strategy after intracerebral hemorrhage

Hydrogen Sulfide Ameliorates High Glucose-induced Inflammation Through SIRT1-mTOR/NF-κB Signaling Pathway in HT-22 cells

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