［Objective］This paper choosed TNF-α as an inflammatory factor to create the inflammation of tendon stem cells, and then observed the effect of PAR under this inflammatory environment. ［Methods］Tendon stem cells were isolated by collagenase and seeded in a very low cell density. The multi-differentiation of the isolated cells were confirmed by osteogenic and adipogenic induction in vitro. PAR in different concentration were added to suspress the effect of TNF-α.qPCR and western blot were used to detect the expression of osteogenic genes and proteins. Furthermore, β-catenin cell pathway was also detected by western blot. Mineral deposits of tendon stem cells were stained by Alizarin Red S in order to observe the influence of PAR under inflammatory environment. [Results] Cells isolated from human tendon tissue can be induced into osteocytes and adipocytes in vitro. qPCR showed that , compared with TNF-α group, parthenolide inhibited the expression of inflammatory related genes COX-2 and HIF-2e and fibroblastic gene Col 1α, while it significantly upregulated osteogenic genes(Run x2 and OPN) as well as tendon related gene(scleraxis)under the stimulation of TNF-i. Western Blot showed that parthenolide could increase the expression of RunX2 and β-catenin in comparison with TNF-α group. Mineral deposits detected by Alizarin Red S staining were much more in groups with PAR, whereas there were no red mineral deoposits found in control or TNF-α group. [Conclusions] Under an inflammatory environment where TNF-α created, parthenolide controled the highly expressed inflammatory response and promoted osteogenic differentiation of tendon stem cells through theβ-catenin signaling pathway.