Inflammation is a key contributing factor in the pathogenesis of fatty liver diseases (FLD), such as nonalcoholic fatty liver disease (NAFLD) and alcohol-associated liver diseases (ALDs). The NLRP3 inflammasome is widely present in the hepatic parenchymal and non-parenchymal cells, which are assembled and activated by sensing intracellular and extracellular danger signals resulting in the matures of IL-1β/IL-18 and pyroptosis. Moreover, the aberrant activation of the NLRP3 inflammasome is considered the main factor to drives immune outbreaks in relation to hepatic injury, inflammation, steatosis, and fibrosis. Therefore, inhibition of NLRP3 inflammasome may be a promising therapeutic target for FLD. Currently, accumulating evidence has revealed that a number of traditional Chinese medicines (TCM) exert beneficial effects on liver injury via inhibiting the NLRP3 inflammasome activation. Here, we summarized the mechanism of NLRP3 inflammasomes in the progression of FLD, and TCM exerts beneficial effects on FLD via positive modulation of inflammation. We describe that TCM is a promising valuable resource for the prevention and treatment agents against FLD and has the potential to be developed into clinical drugs.
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http://dx.doi.org/10.3389/fphar.2022.967594 | DOI Listing |
Background: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFImmunol Invest
January 2025
Traditional Chinese Medicine, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang, China.
Objective: This study investigated the mechanism of baicalin (BIA) attenuating the inflammatory response and lung injury in mycoplasma pneumoniae pneumonia (MPP) mice.
Methods: MPP mouse models were established and then treated with BIA, azithromycin, or NLRP3 inflammasome activator. Lung wet-to-dry weight (W/D) ratio were weighed.
J Neuroinflammation
January 2025
Department of Neurology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Yishan Road 600, Shanghai, 200233, China.
Background: Alzheimer's disease (AD) is a prevalent neurodegenerative disorder worldwide, and microglia are thought to play a central role in neuroinflammatory events occurring in AD. Chemerin, an adipokine, has been implicated in inflammatory diseases and central nervous system disorders, yet its precise function on microglial response in AD remains unknown.
Methods: The APP/PS1 mice were treated with different dosages of chemerin-9 (30 and 60 µg/kg), a bioactive nonapeptide derived from chemerin, every other day for 8 weeks consecutively.
J Toxicol Sci
January 2025
Laboratory of Health Chemistry, Graduate School of Pharmaceutical Sciences, Tohoku University.
A representative surfactant, benzalkonium chloride (BAC) is used as a disinfectant, but sometimes causes serious side effects, including lung disorders such as interstitial pneumonia. However, its pathogenic mechanisms remain unexplained. In this study, we identified a novel mechanism by which BAC initiates inflammatory responses that may be responsible for its side effects.
View Article and Find Full Text PDFToxicology
January 2025
School of Life Science, Liaoning University, Shenyang, 110036, China. Electronic address:
Observational studies have shown that cadmium exposure increases the risk of cardiovascular disease, but the underlying mechanism is still unclear. Atherosclerotic plaque can cause vascular obstruction, which is important for the death from cardiovascular disease. Cell damage and monocyte adhesion are two early events in atherosclerotic plaque formation that can be induced by cadmium exposure, but the mechanism remains to be determined.
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