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Curcumin alleviates LPS-induced WI-38 cell inflammation injury by regulating PTGS2 expression.
Hongli Xiao1, Wangsheng Ma1, Lin Zha1
1Department of Pediatrics, Puren Hospital, Wuhan University of Science and Technology, No.1 Benxi Street, Heping Avenue, Qingshan District, Wuhan City, 430081, Hubei, China.
Curcumin (CUR) protects against lipopolysaccharide (LPS)-induced infantile pneumonia in WI-38 cells by downregulating prostaglandin endoperoxide synthase 2 (PTGS2). This natural compound may offer a therapeutic strategy for infantile pneumonia by reducing inflammation and oxidative stress.
Area of Science:
- Cell Biology
- Pharmacology
- Immunology
Background:
- Infantile pneumonia is a significant cause of morbidity and mortality in young children.
- Curcumin (CUR), a natural polyphenol, possesses anti-inflammatory and antioxidant properties.
- This study investigates CUR's effects on lipopolysaccharide (LPS)-induced cellular damage relevant to infantile pneumonia.
Purpose of the Study:
- To explore the therapeutic potential of Curcumin (CUR) in a cellular model of infantile pneumonia.
- To elucidate the molecular mechanisms underlying CUR's protective effects against LPS-induced cellular injury.
- To identify key molecular targets of CUR in the context of infantile pneumonia.
Main Methods:
- Cell viability, proliferation, and apoptosis were assessed using CCK8, EdU, and flow cytometry.
- Inflammation and oxidative stress markers (IL-6, IL-1β, TNF-α, MDA, SOD) were measured via ELISA.
- Network pharmacology, molecular docking, and in vitro experiments were employed to predict and validate therapeutic targets, including PTGS2.
Main Results:
- LPS treatment impaired WI-38 cell viability, proliferation, and SOD levels while increasing apoptosis, IL-6, IL-1β, TNF-α, and MDA.
- CUR treatment reversed LPS-induced cellular damage, restoring cell vitality and function.
- CUR exerted its protective effects by downregulating prostaglandin endoperoxide synthase 2 (PTGS2) expression, which was confirmed by molecular docking and knockdown experiments.
Conclusions:
- Curcumin (CUR) effectively attenuates lipopolysaccharide (LPS)-induced injury in WI-38 cells.
- The primary mechanism involves the downregulation of prostaglandin endoperoxide synthase 2 (PTGS2).
- CUR demonstrates potential as a therapeutic agent for infantile pneumonia by modulating PTGS2 expression and reducing inflammation.
