Non-coding RNAs as a Critical Player in the Regulation of Inflammasome in Inflammatory Bowel Diseases; Emphasize on lncRNAs DOI

H. Abed,

Enwa Felix Oghenemaro,

Aziz Kubaev

et al.

Cell Biochemistry and Biophysics, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 19, 2024

Language: Английский

Anti-Inflammatory Role of the Klotho Protein and Relevance to Aging DOI Creative Commons
Gérald J. Prud’homme, Qinghua Wang

Cells, Journal Year: 2024, Volume and Issue: 13(17), P. 1413 - 1413

Published: Aug. 24, 2024

The α-Klotho protein (hereafter Klotho) is an obligate coreceptor for fibroblast growth factor 23 (FGF23). It produced in the kidneys, brain and other sites. Klotho insufficiency causes hyperphosphatemia anomalies. Importantly, it associated with chronic pathologies (often age-related) that have inflammatory component. This includes atherosclerosis, diabetes Alzheimer's disease. Its mode of action these diseases not well understood, but inhibits or regulates multiple major pathways. has a membrane form soluble (s-Klotho). Cytosolic postulated characterized. s-Klotho endocrine properties are incompletely elucidated. binds to FGF receptor 1c (FGFR1c) widely expressed (including endothelial cells). also attaches FGF23, FGF23/Klotho FGFRs. Thus, might be roaming FGF23 coreceptor, functions. Notably, (cell-bound soluble) counteracts inflammation appears mitigate related aging (inflammaging). NF-κB NLRP3 inflammasome. inflammasome requires priming by produces active IL-1β, pores cell death (pyroptosis). In accord, countered injury induced toxins, damage-associated molecular patterns (DAMPs), cytokines, reactive oxygen species (ROS). blocks TGF-β Wnt ligands, which lessens fibrotic Low loss muscle mass (sarcopenia), as occurs diseases. counters inhibitory effects myostatin on muscle, reduces inflammation, improves repair following injury. inhibition factors may protective diabetic retinopathy age-related macular degeneration (AMD). review examines functions especially potential applications.

Language: Английский

Citations

10

Anti-Neuroinflammatory Effects of Prenylated Indole Alkaloids from the Antarctic Fungus Aspergillus sp. Strain SF-7367 DOI Creative Commons
Zhiming Liu,

Chi–Su Yoon,

Thao Quyen Cao

et al.

Molecules, Journal Year: 2025, Volume and Issue: 30(2), P. 294 - 294

Published: Jan. 13, 2025

Inflammation has always been considered a trigger or consequence of neurodegenerative diseases, and the inhibition inflammation in central nervous system can effectively protect nerve cells. Several studies have indicated that various natural products inhibit neuroinflammation. Among these, Antarctic fungal metabolites pharmacological activities developmental value. Therefore, this study aimed to evaluate anti-neuroinflammatory activity an fungus belonging Aspergillus (strain SF-7367). Secondary SF-7367 were isolated using high-performance liquid chromatography followed by validation their anti-inflammatory effects lipopolysaccharide-stimulated BV2 microglia RAW264.7 macrophages. Chemical analysis from strain revealed five known compounds: epideoxybrevianamide E (1), brevianamide V/W (2), K (3), Q (4), R (5). these compounds, showed significant against both cell types. Results Western blotting molecular docking could regulate activation nuclear factor kappa-light-chain-enhancer activated B (NF-κB) signaling. This indicates present sp. SF-7367) inflammatory responses reducing lipopolysaccharide-induced translocation NF-κB (p65). These findings suggest are candidate agents for treating diseases.

Language: Английский

Citations

1

Inflammasomes in Alzheimer’s Progression: Nrf2 as a Preventive Target DOI Creative Commons

Rubén López-Hernández,

María Magdalena de la Torre-Álamo,

Borja García‐Bueno

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 121 - 121

Published: Jan. 21, 2025

Current knowledge about Alzheimer’s disease highlights the accumulation of β-amyloid plaques (Aβ1–42) and neurofibrillary tangles composed hyperphosphorylated Tau, which lead to loss neuronal connections. Microglial activation release inflammatory mediators play a significant role in progression pathology. Recent advances have identified involvement inflammasomes, particularly NOD-like receptor NLR family pyrin domain containing 3 (NLRP3), whose promotes proinflammatory cytokines triggers pyroptosis, exacerbating neuroinflammation. Aggregates Aβ1–42 Tau been shown activate these while apoptosis-associated speck-like protein (ASC) components form aggregates that further accelerate Aβ aggregation. Defects autophagic clearance inflammasomes also implicated disease, contributing sustained inflammation. This review explores strategies counteract inflammation Alzheimer’s, emphasizing degradation ASC specks inhibition NLRP3 inflammasome activation. Notably, nuclear factor erythroid 2-related 2 (Nrf2) transcription emerges as promising therapeutic target due its dual mitigating oxidative stress directly inhibiting formation. By reducing inflammasome-driven inflammation, Nrf2 offers potential for addressing neuroinflammatory aspects disease.

Language: Английский

Citations

1

Immune Response in Traumatic Brain Injury DOI Creative Commons
Eder Cáceres,

Juan Olivella,

Mario Di Napoli

et al.

Current Neurology and Neuroscience Reports, Journal Year: 2024, Volume and Issue: 24(12), P. 593 - 609

Published: Oct. 29, 2024

Abstract Purpose of Review This review aims to comprehensively examine the immune response following traumatic brain injury (TBI) and how its disruption can impact healing recovery. Recent Findings The is now considered a key element in pathophysiology TBI, with consequences far beyond acute phase after injury. A delicate equilibrium crucial for healthy When this disrupted, chronic inflammation imbalance lead detrimental effects on survival disability. Summary Globally, imposes substantial burden terms both years life lost lived Although epidemiology exhibits dynamic trends over time across regions, TBI disproportionally affects younger populations, posing psychosocial financial challenge communities families. Following initial trauma, primary succeeded by an inflammatory response, primarily orchestrated innate system. inflammasome plays pivotal role during stage, catalyzing programmed cell death pathways up-regulation cytokines transcription factors. These events trigger activation differentiation microglia, thereby intensifying systemic level facilitating migration cells edema. initially originated brain, monitored our autonomic nervous Through vagus nerve adrenergic cholinergic receptors various peripheral lymphoid organs cells, bidirectional communication regulation between systems established.

Language: Английский

Citations

7

Oridonin exerts anticonvulsant profile and neuroprotective activity in epileptic mice by inhibiting NLRP3-mediated pyroptosis DOI Creative Commons
Ting Zhao,

Xuefei Zhang,

Xiaoxiao Cui

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 134, P. 112247 - 112247

Published: May 16, 2024

Epilepsy is a chronic disabling disease poorly controlled by available antiseizure medications. Oridonin, bioactive alkaloid with anti-inflammatory properties and neuroprotective effects, can inhibit the increased excitability of neurons caused glutamate accumulation at cellular level. However, whether oridonin affects neuronal it has antiepileptic potential not been reported in animal models or clinical studies. Pentylenetetrazol was injected into mice to create model epilepsy. Seizure severity assessed using Racine scale, duration latency seizures were observed. Abnormal discharge detected electroencephalography, calcium imaging. Damage hippocampal evaluated Hematoxylin-Eosin Nissl staining. The expression NOD-like receptor thermal protein domain associated 3 (NLRP3) inflammasome other pyroptosis-related proteins determined western blotting immunofluorescence. A pyroptosis established supernatant BV2 cells treated lipopolysaccharide adenosine triphosphate stimulate neurons. Oridonin (1 5 mg/kg) reduced damage, seizures, shortened fully kindled epilepsy mice. decreased abnormal during epileptic episodes suppressed excitability. In vitro experiments showed that alleviated HT22 exerts effects inhibiting through NLRP3/caspase-1 pathway It also reduces vitro, suggesting its as therapy for

Language: Английский

Citations

6

Qingzhuan dark tea Theabrownin alleviates hippocampal injury in HFD-induced obese mice through the MARK4/NLRP3 pathway DOI Creative Commons
Yining Lei, Yong Chen, Shuo Zhang

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(5), P. e26923 - e26923

Published: Feb. 28, 2024

Feeding on a high-fat diet (HFD) results in obesity and chronic inflammation, which may have long-term effects neuroinflammation hippocampal injury. Theabrownin, biologically active compound derived from the microbial fermentation of Qingzhuan dark tea, exhibits anti-inflammatory properties lipid-lowering effects. Nevertheless, its potential neuroprotection has yet to be investigated. Consequently, this study aims investigate neuroprotective Theabrownin extracted as well therapeutic mechanisms.

Language: Английский

Citations

5

TXNIP Regulates NLRP3 Inflammasome-Induced Pyroptosis Related to Aging via cAMP/PKA and PI3K/Akt Signaling Pathways DOI

Xiaoshuang Xi,

Rong Zhang,

Yijia Chi

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(10), P. 8051 - 8068

Published: March 9, 2024

Language: Английский

Citations

5

The role of quercetin in NLRP3-associated inflammation DOI

Jiaqi Wu,

Tongtong Lv, Yü Liu

et al.

Inflammopharmacology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 22, 2024

Language: Английский

Citations

5

Natural products target pyroptosis for ameliorating neuroinflammation: A novel antidepressant strategy DOI
Guangheng Zhang,

Ruirui Shang,

Xia Zhong

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: 138, P. 156394 - 156394

Published: Jan. 14, 2025

Language: Английский

Citations

0

The role of NLRP3 inflammasome-mediated pyroptosis in astrocytes during hyperoxia-induced brain injury DOI
Qiao Liu, Yan Tan,

Zhanwei Zhang

et al.

Inflammation Research, Journal Year: 2025, Volume and Issue: 74(1)

Published: Jan. 25, 2025

Language: Английский

Citations

0