Related Experiment Video
Updated: Jun 18, 2026
Isolation of Human Endometrial Stromal Cells for In Vitro Decidualization
Published on: September 1, 2018
In vitro effects of atorvastatin on lipopolysaccharide-induced gene expression in endometriotic stromal cells
Indu Sharma1, Veena Dhawan, Nitin Mahajan
1Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Objective:
To investigate the in vitro effects of atorvastatin on lipopolysaccharide (LPS)-induced gene expression in endometrial-endometriotic stromal cells.
Design:
In vitro experimental study using flow cytometry, ELISA, semiquantitative reverse transcriptase polymerase chain reaction, and Western blot.
Setting:
Postgraduate Institute of Medical Education and Research.
Patient(S):
Twenty-five women undergoing laparoscopy (n = 10) and laparotomy (n = 15).
Intervention(S):
Endometriotic cyst wall (group I) and endometrial biopsy (group II) collection.
Main Outcome Measure(S):
The endometrial-endometriotic stromal cells were isolated from ectopic (group I) and eutopic (group II) endometrium by established methods, cultured, and stimulated with LPS (1 μg/mL), followed by atorvastatin treatment in a time- and dose-dependent manner to investigate the effects of LPS on proliferation (Ki-67) and expression of cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), receptor for advanced glycation end products (RAGE), extracellular newly identified RAGE binding protein (EN-RAGE), peroxisome proliferator activated receptor-γ (PPAR-γ), and liver X receptor-α (LXR-α) genes in endometrial-endometriotic stromal cells and on levels of insulin-like growth factor binding protein-1 (IGFBP-1) and 17β-E(2) in endometrial-endometriotic stromal cell culture supernatant.
Result(S):
Significant inhibition of Ki-67 and LPS-induced expression of inflammatory and angiogenic genes (COX-2, VEGF, RAGE, and EN-RAGE) was observed in atorvastatin-treated endometrial-endometriotic stromal cells. In contrast, a significant dose- and time-dependent increase in expression of anti-inflammatory genes (PPAR-γ and LXR-α) and levels of IGFBP-1 was observed after atorvastatin treatment in both the groups. However, atorvastatin treatment had no effect on 17β-E(2) levels in endometrial/endometriotic stromal cell culture supernatant.
Conclusion(S):
The data of the present study provide new insights for the implication of atorvastatin treatment for endometriosis in humans.
