Tangeretin attenuates acute lung injury in septic mice by inhibiting ROS-mediated NLRP3 inflammasome activation via regulating PLK1/AMPK/DRP1 signaling axis

Liu, Yuntao; Zhang, Yuting; You, Guoxing; Zheng, Danwen; He, Zhipeng; Guo, Wenjie; Antonina, Kim; Shukhrat, Ziyadullaev; Ding, Banghan; Zan, Jie; Zhang, Zhongde

doi:10.1007/s00011-023-01819-8

Cited by 13 publications

(3 citation statements)

References 64 publications

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“…Conversely, concurrent administration of 200 mg/kg BW tangeretin led to a significant decrease in these transcript levels to 3.49–, 2.47–, and 2.94–fold, respectively ( Figure 3 F–H). The anti-inflammatory properties of tangeretin have been previously identified [ 14 , 15 , 16 ]. Therefore, our results suggest that tangeretin targets the TLR4\MyD88\NF–κB signaling pathway to inhibit the inflammatory response induced by long-term choline intake.…”

Section: Resultsmentioning

confidence: 99%

Tangeretin Mitigates Trimethylamine Oxide Induced Arterial Inflammation by Disrupting Choline–Trimethylamine Conversion through Specific Manipulation of Intestinal Microflora

Cao,

Leng,

Lin

et al. 2024

Molecules

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Previous studies have revealed the microbial metabolism of dietary choline in the gut, leading to its conversion into trimethylamine (TMA). Polymethoxyflavones (PMFs), exemplified by tangeretin, have shown efficacy in mitigating choline-induced cardiovascular inflammation. However, the specific mechanism by which these compounds exert their effects, particularly in modulating the gut microbiota, remains uncertain. This investigation focused on tangeretin, a representative PMFs, to explore its influence on the gut microbiota and the choline–TMA conversion process. Experimental results showed that tangeretin treatment significantly attenuated the population of CutC–active bacteria, particularly Clostridiaceae and Lactobacillus, induced by choline chloride in rat models. This inhibition led to a decreased efficiency in choline conversion to TMA, thereby ameliorating cardiovascular inflammation resulting from prolonged choline consumption. In conclusion, tangeretin’s preventive effect against cardiovascular inflammation is intricately linked to its targeted modulation of TMA–producing bacterial activity.

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Section: Resultsmentioning

confidence: 99%

Tangeretin Mitigates Trimethylamine Oxide Induced Arterial Inflammation by Disrupting Choline–Trimethylamine Conversion through Specific Manipulation of Intestinal Microflora

Cao,

Leng,

Lin

et al. 2024

Molecules

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“…Zhang’s group [ 48 ] identified NLRP3 as a potential therapeutic target for sepsis-induced ALI. Their research focused on the protective effects of tangeretin (TAN) on sepsis-induced ALI and its regulatory mechanism on NLRP3 inflammasomes.…”

Section: Pathogenesis Of Sepsis-induced Ali and Potential Therapeutic...mentioning

confidence: 99%

“…In a subsequent study in 2023, Pan explored the protective effects of colchicine against LPS-induced lung injury and its underlying mechanisms. It was discovered that colchicine inhibits the phosphorylation of the signal transducer and activator of transcription 3 (STAT3), which regulates the activation of NLRP3, thereby reducing the inflammatory response and apoptosis [ 47 , 48 ].…”

Section: Pathogenesis Of Sepsis-induced Ali and Potential Therapeutic...mentioning

confidence: 99%

Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment

Xu,

Xin,

Sun

et al. 2024

Pharmaceuticals

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Sepsis-induced acute lung injury (ALI), characterized by widespread lung dysfunction, is associated with significant morbidity and mortality due to the lack of effective pharmacological treatments available clinically. Small-molecule compounds derived from natural products represent an innovative source and have demonstrated therapeutic potential against sepsis-induced ALI. These natural small molecules may provide a promising alternative treatment option for sepsis-induced ALI. This review aims to summarize the pathogenesis of sepsis and potential therapeutic targets. It assembles critical updates (from 2014 to 2024) on natural small molecules with therapeutic potential against sepsis-induced ALI, detailing their sources, structures, effects, and mechanisms of action.

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The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome

Luo,

Zhuang,

et al. 2024

Clinical & Translational Med

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Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studies highlight the significant role of inflammation involved in ALI/ARDS, particularly the hyperactivation of the NOD‐like receptor thermal protein domain‐associated protein 3 (NLRP3) inflammasome in macrophages. This activation drives pulmonary inflammation by releasing inflammatory signalling molecules and is linked to metabolic reprogramming, marked by increased glycolysis and reduced oxidative phosphorylation. However, the relationship between NLRP3 inflammasome activation and macrophage glycolytic reprogramming in ALI/ARDS, as well as the molecular mechanisms regulating these processes, remain elusive. This review provides a detailed description of the interactions and potential mechanisms linking NLRP3 inflammasome activation with macrophage glycolytic reprogramming, proposing that glycolytic reprogramming may represent a promising therapeutic target for mitigating inflammatory responses in ALI/ARDS.Key points NLRP3 inflammasome activation is pivotal in mediating the excessive inflammatory response in ALI/ARDS. Glycolytic reprogramming regulates NLRP3 inflammasome activation. Therapeutic potential of targeting glycolytic reprogramming to inhibit NLRP3 inflammasome activation in ALI/ARDS.

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Tangeretin attenuates acute lung injury in septic mice by inhibiting ROS-mediated NLRP3 inflammasome activation via regulating PLK1/AMPK/DRP1 signaling axis

Cited by 13 publications

References 64 publications

Tangeretin Mitigates Trimethylamine Oxide Induced Arterial Inflammation by Disrupting Choline–Trimethylamine Conversion through Specific Manipulation of Intestinal Microflora

Tangeretin Mitigates Trimethylamine Oxide Induced Arterial Inflammation by Disrupting Choline–Trimethylamine Conversion through Specific Manipulation of Intestinal Microflora

Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment

The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome

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