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Published on: July 6, 2019
Cardamonin protects septic mice from acute lung injury by preventing endothelial barrier dysfunction
Zhifeng Wei1, Jian Yang, Yu-Feng Xia
1State Key Laboratory of Natural Medicines, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, People's Republic of China.
Insights
Cardamonin, a natural compound, protects against sepsis-induced acute lung injury (ALI) by strengthening blood vessel barriers. It achieves this by inhibiting the P38 signaling pathway, reducing inflammation and improving survival rates in mice.
Area of Science:
- Pharmacology
- Immunology
- Molecular Biology
Background:
- Sepsis is a life-threatening condition associated with high mortality.
- Acute lung injury (ALI) is a common and severe complication of sepsis.
- Cardamonin, a flavone from Alpinia katsumadai, shows anti-inflammatory potential.
Purpose of the Study:
- To investigate the protective effects of cardamonin against experimental sepsis-induced ALI.
- To elucidate the molecular mechanisms underlying cardamonin's action on endothelial barrier function.
Main Methods:
- In vivo studies using septic mouse models treated with cardamonin (30 and 100 mg/kg).
- In vitro assays using rat lung microvascular endothelial cells and RAW 264.7 macrophage cells.
- Assessment of survival rates, ALI severity, lung microvascular leak, serum cytokine levels, and P38 phosphorylation.
Main Results:
- Cardamonin significantly increased survival rates and alleviated ALI and lung microvascular leak in septic mice.
- It reduced serum levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
- In vitro, cardamonin inhibited LPS-induced endothelial permeability and selectively downregulated P38 phosphorylation in endothelial and macrophage cells.
Conclusions:
- Cardamonin demonstrates significant protective effects against sepsis-induced ALI.
- Its mechanism involves preventing endothelium barrier dysfunction through selective inhibition of P38 activation.
- Cardamonin holds promise as a therapeutic agent for managing sepsis-related lung injury.
Abstract:
Cardamonin, a flavone compound isolated from Alpinia katsumadai Heyata seeds, has been reported to possess anti-inflammatory and anticoagulative activities, and it might be beneficial for management of sepsis. This study was conducted to examine the protective effects of cardamonin on experimental sepsis and resultant acute lung injury (ALI). Cardamonin (30 and 100 mg/kg) significantly elevated the survival rate of septic mice, alleviated ALI and lung microvascular leak, and lowered the serum levels of proinflammatory cytokines TNF-α, IL-1β, and IL-6. In vitro, it (25 and 50 µM) concentration dependently inhibited endothelium permeability and downregulated phosphorylation of P38 in rat lung microvascular endothelial cells induced by lipopolysaccharide (LPS). P38 inhibitor inhibited the endothelium permeability. In RAW 264.7 macrophage cells, cardamonin also showed selective inhibition of P38 phosphorylation induced by LPS. These results indicate that cardamonin can protect septic mice from ALI by preventing endothelium barrier dysfunction via selectively inhibiting P38 activation.