Asiatic acid inhibits LPS-induced inflammatory response in endometrial epithelial cells.

Accumulating evidence indicates that asiatic acid, a natural triterpene isolated from Centella asiatica, has anti-inflammatory activity. However, the anti-inflammatory effects of asiatic acid on LPS-stimulated endometrial epithelial cells and the involved molecular pathways have not been completely elucidated. In the present study, we evaluated the effects of asiatic acid on LPS-induced inflammatory response in endometrial epithelial cells. Mouse endometrial epithelial cells were treated with asiatic acid and stimulated with LPS. ELISA was performed to measure the levels of inflammatory cytokines TNF-α, IL-1ß, and PGE2. Western blot analysis was used to test the expression of PPARγ and NF-κB. The results showed that LPS-induced inflammatory mediators TNF-α, IL-1ß, NO, and PGE2 were significantly inhibited by asiatic acid. Furthermore, LPS-induced TLR4 expression and NF-κB activation were concentration-dependently suppressed by asiatic acid. In addition, asiatic acid was found to increase the expression of PPARγ in a concentration-dependently manner. The inhibition of asiatic acid on inflammatory mediators production were prevented by PPARγ inhibitor, GW9662. Taken together, these results showed that asiatic acid exhibited its anti-inflammatory effects in endometrial epithelial cells by activating PPARγ.

Suppressive efficiency of RASSF1A in endometrial carcinoma via inhabiting estrogen receptor alpha expression and ERK pathway activation.

INTRODUCTION: Known as a tumor suppressor, the Ras association domain family 1 isoform A (RASSF1A) is implicated in many human cancers, such as endometrial carcinoma. There is little known about the tumor inhibitive effects of RASSF1A on endometrial carcinoma. The present study was designed to investigate the role of RASSF1A in HEC-1-A cells and to explore its potential mechanisms. MATERIALS AND METHODS: In this study, overexpression of RASSF1A was established by transfection the recombinant adenoviral RASSF1A in HEC-1-A cells. Cells viability was assessed by MTT assay and the apoptosis was analyzed using flow cytometry. Cell migration and invasion were measured in Transwell assay. The levels of ERα and PELP1 protein and extracellular regulated protein kinase (ERK) pathway activation were detected by Western blot. RESULTS: RASSF1A over-expression could significantly inhibit the proliferation, migration and invasion of the HEC-1-A cells in transfection with RASSF1A group compared to that in transfection with control group, also induced apoptosis and suppressed the tumor growth after injection in nude mice. Moreover, overexpression of RASSF1A could inhibit the ERK signal pathway activation and decrease the ERα and PELP1 expression. CONCLUSION: Tumor suppressive efficiency of RASSF1A is exerted through the regulation of ERK pathway activation, ERα and PELP1 expression.