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Abstract Objective Recent studies reported that hydrogen sulfide (H 2 S) is an effective agent for the prevention and treatment of acute lung injury (ALI). But the underlying mechanisms have not been understood clearly. In this study, we explored the possible mechanism from the perspective of autophagy regulation. Methods A mouse model of ALI and alveolar type II epithelial cells (MLE-12 cells) injury was induced using lipopolysaccharide (LPS). Expression of Beclin 1 and the conversion of LC3I to LC3II were detected to evaluate the activity of autophagy. Lung histopathological changes, wet/dry (W/D) ratio, pro-inflammatory cytokines TNF-α, IL-1β and protein content in bronchoalveolar lavage fluid (BALF), cell viability and lactic dehydrogenase (LDH) in the culture medium were determined to evaluate the severity of ALI. The activity of PI3K/Akt/mTOR pathway was detected to explore the possible mechanisms involved in the regulation of autophagy by H 2 S. Results The expression of Beclin 1 and the conversion of LC3I to LC3II were significantly increased after LPS treatment and reversed by H 2 S both in vivo and in vitro. Lung histopathological changes, W/D ratio, TNF-α, IL-1β and protein content in BALF induced by LPS were effectively ameliorated by H 2 S and autophagy inhibitor 3-methyladenine. The in vitro results showed that H 2 S and 3-methyladenine also attenuated LPS-induced cell viability decrease and LDH release. Furthermore, H 2 S effectively reversed LPS-induced PI3K/Akt/mTOR signaling pathway inhibition. Conclusion Autophagy inhibition through PI3K/Akt/mTOR pathway was involved in H 2 S prevention of LPS-induced ALI in mice. Highlights • Autophagy activation is an important pathogenesis of LPS-induced ALI in mouse. • H 2 S can inhibit the activation of autophagy in ALI induced by LPS. • H 2 S and 3-MA ameliorated LPS-induced ALI both in vivo and in vitro. • H 2 S inhibit the activation of autophagy through PI3K/Akt/mTOR pathway. [ABSTRACT FROM AUTHOR]

Highlights: [•] Arctigenin enhanced cholesterol efflux in oxLDL-loaded THP-1 macrophages. [•] The expression of ABCA1, ABCG1 and apoE was upregulated in arctigenin-treated cells. [•] Arctigenin promoted the expression of PPAR-γ and LXR-α. [•] Inhibition of PPAR-γ or LXR-α reversed arctigenin-mediated biological effects. [•] Arctigenin promotes cholesterol efflux via activation of PPAR-γ/LXR-α/ABCA1 pathway. [Copyright &y& Elsevier]

Abstract Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-β1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-β1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-β1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC. Highlights • FPPS expression is significantly correlated with TNM stage and metastasis of non-small cell lung cancer. • Inhibition or knockdown of FPPS blocks TGF-β1-induced cell invasion and EMT. • FPPS expression is induced by TGF-β1. • FPPS mediates TGF-β1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. [ABSTRACT FROM AUTHOR]