Amerikanische Gesellschaft für Hirudotherapie

Whitmania Pigra Whitman Extracts Inhibit Lipopolysaccharide Induced Rat Vascular Smooth Muscle Cells Migration and their Adhesion Ability to THP-1 and RAW 264.7 Cells

Basic science published in J Atheroscler Thromb (2017)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportArzneimittelentwicklungLi S et al. · Journal of atherosclerosis and thrombosis, 2017

Abstract

AIM: Atherosclerosis is a kind of chronic inflammatory disease. A crucial pathology change of atherosclerosis is the migration of activated VSMCs to the intima where they interact with leukocytes by expressing adhesion molecules, including intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, monocyte chemoattractant protein-1 (MCP-1) expressed by VSMCs plays an important role in recruiting monocytes and macrophages. Leech (Whitmania pigra Whitman) is a traditional Chinese medicine to treat cardiovascular diseases including atherosclerosis, however previous research has rarely reported the molecular mechanism for its curative effect. Thus, our study focuses on the effects of leech extracts on the expression of inflammatory factors, adhesion molecules and MCP-1 in rat VSMCs. METHODS: In our present study, wound-healing assay and Boyden chamber model were applied to evaluate the anti-migration effect of LEE (Leech Enzyme Extracts) on LPS induced VSMCs. The anti-adhesion effect was assessed using DiI-labeled THP-1 and RAW264.7. RESULTS: LEE suppressed LPS-induced VSMCs migration and decreased the chemotaxis and adhesive capacity of THP-1 and RAW264.7 to LPS-stimulated VSMCs. LEE also attenuated the upregulation of a variety of pro-atherosclerotic factors by inhibiting the phosphorylation of p38 MAPK. LEE was also observed to prevent NF-κB p65 nuclear localization using immune-fluorescent staining. CONCLUSIONS: In conclusion, LEE suppresses LPS-induced upregulation of inflammatory factors, adhesion molecules and MCP-1 in rat VSMCs mainly via inhibiting the p38 MAPK/NF-κB pathways, thus partly uncovered LEE's molecular mechanisms for its therapeutic effect on atherosclerosis.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsAnimalsBlotting, WesternCell AdhesionCell MovementCells, CulturedFibrinolytic AgentsFluorescent Antibody TechniqueHumansLeechesLipopolysaccharidesMacrophagesMale

Zusammenfassung

Leech Enzyme Extracts suppress LPS-induced rat VSMC migration and reduce monocyte/macrophage adhesion via p38 MAPK/NF-kappaB pathway inhibition.

Warum dies für die Hirudotherapie relevant ist

This study examined the effects of leech enzyme extracts (LEE) from Whitmania pigra on lipopolysaccharide-induced rat vascular smooth muscle cell (VSMC) migration and adhesion, finding that LEE suppressed VSMC migration, reduced monocyte/macrophage adhesion, and attenuated pro-atherosclerotic inflammatory factors via inhibition of p38 MAPK/NF-κB pathways. These findings are relevant to ASH's domain as they partially uncover molecular mechanisms by which leech-derived preparations may exert cardiovascular protective effects, a traditional use of leech in Chinese medicine. Caveat: this is an in vitro cell culture study using rat VSMCs and cultured immune cell lines; no in vivo or clinical validation is provided, and findings may not directly translate to hirudotherapy practice.

Zitation

Whitmania Pigra Whitman Extracts Inhibit Lipopolysaccharide Induced Rat Vascular Smooth Muscle Cells Migration and their Adhesion Ability to THP-1 and RAW 264.7 Cells.

Li S et al. · Journal of atherosclerosis and thrombosis, 2017

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