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

Figure 6 Thymoquinone mitigated endoplasmic reticulum stress in injured rat tendons. 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; ^cP < 0.05, comparisons between the experimental groups; ^dP < 0.01, comparisons between the experimental group; B: Western blot analyses evaluating 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 tendons from rats maintained under standard cage activity conditions; the injury group refers to tendons from rats subjected to treadmill running without subsequent treatment; the injury + dimethyl sulfoxide group refers to tendons from rats subjected to treadmill running that subsequently received injections of saline solution containing dimethyl sulfoxide; the injury + thymoquinone group refers to tendons from rats subjected to treadmill running that subsequently received injections of thymoquinone. DMSO: Dimethyl sulfoxide; 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.