Indomethacin inhibits PGE2, regulates inflammatory response, participates in adipogenesis regulation, and improves success rate of fat transplantation in C57/B6 mice
Purpose: To investigate the effect of indomethacin on prostaglandin E2, regulation of inflammation and adipogenesis, and success of fat transplantation in mice.
Methods: The mice were randomly divided into 4 groups: group A (free fat group), group B (free fat + stromal vascular fragments group (SVF)), group C (free fat + 200 μM indomethacin group), and group D (free fat + 200 μM indomethacin + SVF group), with 21 mice in each group. Expression levels of adipogenic genes CEBP-α, FABP4 and LPL in each group were determined. Changes in PGE2 level in transplanted adipose tissue, and changes in the expression of NF-κB in apoptotic stem cells induced by different pro-inflammatory treatments were assayed.
Results: Compared with group B, the expression levels of adipogenic genes CEBP-α, FABP4 and LPL significantly decreased in groups A, C and D, with group A as the lowest (p < 0.05). Compared with the indomethacin treatment group, the level of inhibition of PGE2 in mice adipose tissue in the indomethacin-free group increased significantly (p < 0.01). The expression of NF-κB in the adipose stem cells from the indomethacin-treated group was significantly lower than that in the indomethacin-treated group after pretreatment with IL-17 or INF-γ + TNF-α.
Conclusion: Indomethacin regulates adipogenesis by inhibiting the production of COX2 metabolite, PGE2. It also regulates the local microenvironment, inhibits the inflammatory process, and protects various stem cells. Therefore, it may improve the success rate of fat transplantation
