Thymoquinone inhibited the chondrogenic differentiation of tendon-derived stem cells caused by tendon injury

Figure 4 Thymoquinone attenuated endoplasmic reticulum stress of tendon-derived stem cells subjected to injury conditions. A: Reverse transcription-quantitative polymerase chain reaction analysis of the expression levels of endoplasmic reticulum stress-related markers, including glucose-regulated protein 78, protein kinase RNA-like endoplasmic reticulum kinase, eukaryotic initiation factor 2α, activating transcription factor 4, and CCAAT/enhancer-binding protein homologous protein. ^bP < 0.01, compared to the control group; ^dP < 0.01, comparisons between the experimental groups; B: Western blot analysis assessing the protein expression of glucose-regulated protein 78, SOX9, and components of the protein kinase RNA-like endoplasmic reticulum kinase/eukaryotic initiation factor 2α/activating transcription factor 4/CCAAT/enhancer-binding protein homologous protein signaling pathway. The control group refers to tendon-derived stem cells (TDSCs) cultured on decellularized tendon slices with 0% strain; the control + thapsigargin group refers to TDSCs treated with thapsigargin on decellularized tendon slices with 0% strain; the injury group refers to TDSCs cultured on decellularized tendon slices with 6.4% strain; the injury + 4-phenylbutyric acid group refers to TDSCs treated with 4-phenylbutyric acid on decellularized tendon slices with 6.4% strain; the injury + thymoquinone group refers to TDSCs treated with thymoquinone on decellularized tendon slices with 6.4% strain. Ctl: Control; Ctl + Thap: Control + thapsigargin; 4-PBA: 4-phenylbutyric acid; TQ: Thymoquinone; GRP78: Glucose-regulated protein 78; PERK: Protein kinase RNA-like endoplasmic reticulum kinase; EIF2α: Eukaryotic initiation factor 2α; ATF4: Activating transcription factor 4; CHOP: CCAAT/enhancer-binding protein homologous protein.