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ORIGINAL ARTICLE
Anti-Inflammatory Effects of Enzymatically Hydrolyzed Pectin from Premna ligustroides Hemsl. Leaves in Gouty Rats Through NLRP3 Inflammasome Inhibition
Liling Deng 1
,
 
Rui He 2
,
 
Heng Yang 3
,
 
Geng Zhong 2
 
 
 
More details
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1
Chongqing Key Laboratory of High Active Traditional Chinese Drug Delivery System, Chongqing Engineering Research Center of Pharmaceutical Sciences, Chongqing Medical and Pharmaceutical College, Chongqing 401331, PR China
 
2
College of Food Science, Southwest University, Chongqing 400716, PR China
 
3
Research and Development Department, Mianyang Changshan Agricultural Technology Co. Ltd, Ltd, Sichuan, 621000, China
 
 
Submission date: 2025-07-04
 
 
Acceptance date: 2025-09-19
 
 
Corresponding author
Geng Zhong   

College of Food Science, Southwest University, China
 
 
 
KEYWORDS
inflammation inhibition
joint swelling
NOD-like receptor
polysaccharides
uric acid
 
TOPICS
ABSTRACT
Gout is a rheumatic inflammatory disease resulting from abnormal uric acid metabolism. This study investigated the anti-inflammatory effects and mechanisms of enzymatically hydrolyzed pectin from Premna ligustroides Hemsl. leaves (EHPPL) in gout-induced rats. Serum and organ function markers, along with ankle tissue hematoxylin-eosin staining and NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) protein expression, were analyzed. In gouty rats, EHPPL significantly reduced uric acid (from 73.38 to 54.85 μmol/L) and urea nitrogen levels (from 11.97 to 4.02 mmol/L), normalized liver and kidney functions, and decreased key inflammatory markers, including tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin (IL)-18, IL-1β, lipopolysaccharides, NLRP3, and cysteinyl aspartate specific proteinase-1. Additionally, EHPPL upregulated anti-inflammatory IL-10 levels. These effects were attributed to the inhibition of a toll-like receptor (TLR) 2/TLR4/myeloid differentiation primary response protein 88/nuclear factor-κB signaling, suggesting that EHPPL may serve as a potential dietary intervention for acute gouty arthritis.
FUNDING
This work was supported by the Natural Science Foundation Project of Chongqing (CSTB2023NSCQ-MSX0543), the Special Funding for Postdoctoral Research Projects in Chongqing (2022CQBSHTB2009), the Science and Technology Research Project of the Chongqing Municipal Education Commission (KJQN202202813), and the School level Project of Chongqing Medical and Pharmaceutical College (ygz2022103).
CONFLICT OF INTEREST
The authors declare no conflict of interest.
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