Acteoside attenuates acute lung injury following administration of cobra venom factor to mice

Background: Acteoside, a water-soluble active constituent of diverse valuable medicinal vegetation, has shown strong anti-inflammatory property. However, studies on the anti-inflammatory property of acteoside in complement-induced acute lung injury (ALI) are limited. Therefore, this study aims to evaluate the antiinflammatory activity of acteoside in cobra venom factor (CVF)-stimulated human microvascular endothelial cells (HMEC) and in ALI mice model. Methods: In this study, we investigated the effects of acteoside (20, 10, and 5 mu g/mL) in vitro in CVF induced HMECs and the activity of acteoside (100, 50, and 20 mg/kg/day bodyweight) in vivo in CVF induced ALI mice. Each eight male mice were orally administered acteoside or the positive drug PDTC (100 mg/kg/day) for 7 days before CVF (35 mu g/kg) injection. After injection for 1 h, the pharmacological effects of acteoside were investigated by spectrophotometry, pathological examination, enzyme-linked immunosorbent assay, and immunohistochemistry.Results: In vitro, acteoside (20, 10, and 5 mu g/mL) reduced the protein expression of adhesion molecules and proinflammatory cytokines and transcriptional activity of NF-Kappa B (P < 0.01). In vivo studies showed that acteoside dose-dependently alleviated lung histopathologic lesion, inhibited the production of the protein content of BALF, leukocyte cell number, lung MPO activity, and expression levels of IL-6, TNF-alpha, and ICAM-1, and suppressed the C5b-9 deposition and NF-Kappa B activation in CVF-induced acute lung inflammation in mice (P < 0.05, 0.01).Conclusion: This study demonstrates that acteoside exerts strong anti-inflammatory activities in the CVF-induced acute lung inflammation model and suggests that acteoside is a potential therapeutic agent for complementrelated inflammatory diseases.

Automated summary

This study demonstrates the strong anti-inflammatory activity of acteoside in the CVF-induced acute lung inflammation model, suggesting it as a potential therapeutic agent for complement-related inflammatory diseases.