Methylallyl sulfone attenuates inflammation, oxidative stress and lung injury induced by cigarette smoke extract in mice and RAW264.7 cells.

In this study, we revealed that methylallyl sulfone (AMSO2), the metabolite of active organosulfur compounds, had anti-inflammatory and antioxidant effect in a cigarette smoke extract (CSE)-induced lung injury model. Firstly, histological analysis showed that the CSE group exhibited lung injury compared with the control, which was alleviated by AMSO2. Secondly, we estimated its anti-inflammatory capacity. The results indicated that pretreatment with AMSO2 significantly decreased CSE-elevated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in serum. Thirdly, AMSO2 also showed antioxidant properties through enhancing activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as reducing the level of malondialdehyde (MDA) and myeloperoxidase (MPO). Finally, we elucidated that AMSO2 alleviated inflammation and oxidative stress probably via suppressing ERK/p38 MAPK and inhibiting NF-κB expressions. In conclusion, we proposed that AMSO2 protected against the development of CSE-induced lung injury by reducing inflammatory cytokine levels and augmenting antioxidant activity via ERK/p38 MAPK and NF-κB pathways.

Protective effect of methylallyl sulfone in the development of cigarette smoke extract-induced apoptosis in rats and HFL-1 cells.

Although the organosulfur compounds from garlic have shown diverse pharmacological activities, the prototype drug was almost undetectable in vivo. As known, methylallyl sulfone (AMSO2) is the main metabolite of some active organosulfur compounds derived from garlic. The purpose of this article was to study the protective effect of AMSO2 on cigarette smoke extract (CSE) induced cell apoptosis in lungs in vivo and in vitro. The male rats were injected intraperitoneally with 900 µL of 100% CSE 3 times for three successive weeks. The rats from treatment groups were injected intraperitoneally with AMSO2 (50 mg/kg/day or 100 mg/kg/day) or DEX (1 mg/kg/day) for 21 days. We observed that pretreatment of AMSO2 effectively reversed apoptosis and oxidative stress in rats induced by CSE. Moreover, CSE-induced apoptosis in the HFL-1 cells was significantly suppressed by pretreated AMSO2 (400 µM) and DEX (0.1 mg/mL). Mechanistic studies suggested that this activity may arise from its effects on the regulation of p38 MAPK, Nrf-2 and Bcl-2/Bax signaling pathways. Overall, the metabolite of active organosulfur compounds AMSO2 might be a potential candidate for the treatment of CSE-induced apoptosis in rats.