Pathology, research and practice · 2025
Polydatin alleviates oxidative stress and pro-inflammatory activation of alveolar macrophages in chronic cough by reducing PTGS2 levels.
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Zhao Yan, Wang Naizhu
Аннотация
BACKGROUND: Polydatin (PD) is a resveratrol derivative primarily isolated from Polygonum cuspidatum Sieb. et Zucc. with multiple pharmacological effects. This research investigates the treatment effect of polydatin (PD) on chronic cough and delves into its functional mechanism.
METHODS: Mice with chronic cough were generated through ammonia and capsaicin exposure, followed by PD treatment. Pathological alterations in the mouse lung tissues were determined using histological staining. Inflammation and oxidative stress markers were detected in the mouse serum or lung tissue samples. Mouse alveolar macrophages, MH-S, were exposed to lipopolysaccharide (LPS) to generate inflammatory cell models. The treatment effect of PD on inflammatory cytokine production and oxidative stress in cells was analyzed. Downstream targets of PD were predicted using bioinformatics tools. Prostaglandin-endoperoxide synthase 2 (PTGS2) overexpression was induced in animal and cell models to analyze its involvement in PD's effects.
RESULTS: PD treatment increased latency to cough and reduced cough frequencies of modeled mice, and it ameliorated inflammatory cell infiltration, collagen deposition, and mucus production in mouse lung tissues. Additionally, PD treatment reduced inflammatory cytokine production and oxidative stress markers both in mice and in LPS-challenged MH-S cells. PD reduced PTGS2 protein levels in mouse lung tissues and MH-S cells. Overexpression of PTGS2, introduced via lentiviral vectors, significantly counteracted the treatment effects of PD both in vivo and in vitro.
CONCLUSION: This research demonstrates that PD treatment reduces oxidative stress and pro-inflammatory activation of alveolar macrophages to ameliorate chronic cough in mice by reducing PTGS2 protein levels.
METHODS: Mice with chronic cough were generated through ammonia and capsaicin exposure, followed by PD treatment. Pathological alterations in the mouse lung tissues were determined using histological staining. Inflammation and oxidative stress markers were detected in the mouse serum or lung tissue samples. Mouse alveolar macrophages, MH-S, were exposed to lipopolysaccharide (LPS) to generate inflammatory cell models. The treatment effect of PD on inflammatory cytokine production and oxidative stress in cells was analyzed. Downstream targets of PD were predicted using bioinformatics tools. Prostaglandin-endoperoxide synthase 2 (PTGS2) overexpression was induced in animal and cell models to analyze its involvement in PD's effects.
RESULTS: PD treatment increased latency to cough and reduced cough frequencies of modeled mice, and it ameliorated inflammatory cell infiltration, collagen deposition, and mucus production in mouse lung tissues. Additionally, PD treatment reduced inflammatory cytokine production and oxidative stress markers both in mice and in LPS-challenged MH-S cells. PD reduced PTGS2 protein levels in mouse lung tissues and MH-S cells. Overexpression of PTGS2, introduced via lentiviral vectors, significantly counteracted the treatment effects of PD both in vivo and in vitro.
CONCLUSION: This research demonstrates that PD treatment reduces oxidative stress and pro-inflammatory activation of alveolar macrophages to ameliorate chronic cough in mice by reducing PTGS2 protein levels.