Protective effect and mechanism of loganin and morroniside on acute lung injury and pulmonary fibrosis

Background: Loganin and morroniside are two iridoid glycosides with anti-inflammatory, antioxidant and antitumor effects. Whether they have effect on acute lung injury and pulmonary fibrosis are still unknown.& nbsp;Purpose: To explore the potential effects of loganin and morroniside against acute lung cancer and pulmonary fibrosis, and the underlying molecular mechanism.& nbsp;Study design and methods: Cell and animal models of acute lung injury were established by the induction of LPS. After intervention with loganin and morroniside, the pathological symptom of lung tissue was assessed, pro-inflammatory factors in cells and lung tissues were detected, NF-kappa B/STAT3 signaling pathway related proteins were detected by western blotting. Mice pulmonary fibrosis model was induced by bleomycin, pathological symptom was assessed by HE and Masson staining. Fibrosis related indicators were detected by qPCR or western blot. CD4+/CD8+ was detected by flow cytometry.& nbsp;Results: Loganin and morroniside relieved the pathological symptom of lung tissue in acute lung injury, pro-inflammatory factors such as IL-6, IL-1 beta, TNF-alpha mRNA were inhibited. Expression of p-p65 and STAT3 in lung tissues were also downregulated. In addition, loganin and morroniside downregulated the expression of collagen fiber, hydroxyproline and TGF-beta 1, collagen I and alpha-SMA mRNA in lung tissues of pulmonary fibrosis model. This study proved that loganin and morroniside have protective effect on acute lung injury and pulmonary fibrosis, and may provide theoretical basis for the development of new clinical drugs.

Automated summary

This study found that loganin and morroniside have a protective effect against acute lung injury and pulmonary fibrosis by inhibiting the expression of pro-inflammatory factors and regulating the NF-κB/STAT3 signaling pathway. In addition, they also suppressed the expression of fibrosis-related indicators in the pulmonary fibrosis model.