Reactive oxygen species mediate TNF-α-induced inflammatory response in bone marrow mesenchymal cells | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 8، دوره 22، شماره 11، بهمن 2019، صفحه 1296-1301 اصل مقاله (673.88 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2019.37893.9006 | ||
| نویسندگان | ||
| Liuzhong Wu1، 2؛ Yaping Pan* 1 | ||
| 1Department of Periodontics, School of Stomatology, China Medical University, Liaoning Province, China | ||
| 2Department of Periodontics, Shenyang Stomatological Hospital, Shenyang, Liaoning Province, China | ||
| چکیده | ||
| Objective(s): It is generally believed that the inflammatory response in bone marrow mesenchymal stem cells (BMSCs) transplantation leads to poor survival and unsatisfactory effects, and is mainly mediated by cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α). In this study, we explored the mechanisms underlying the TNF-α-induced inflammatory response in BMSCs. Materials and Methods: We treated BMSCs with TNF-α (1 and 10 ng/ml) for 5 days. The expression levels of key inflammatory mediators were evaluated by Real-time PCR. Intracellular ROS level was measured by using a 2, 7-dichlorofluorescein diacetate (DCF-DA). Results: We found that TNF-α treatment dramatically increased the expression levels of some key inflammatory mediators, including IL-6, IL-1β, IFN-γ and transforming growth factor β (TGF-β). Moreover, TNF-α induced intracellular oxidative stress by elevating intracellular reactive oxygen species (ROS) level, which is due to the increase of lipid peroxidation, the reduction of antioxidant Glutathione (GSH) levels and the inhibition of many antioxidant enzyme activities in BMSCs. Interestingly, 5 µM curcumin, a ROS scavenger, dramatically lowered the TNF-α-induced inflammatory response in BMSCs. In addition, TNF-α induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK), p38 and their down-stream transcription factors nuclear factor kappa B (NF-κB) pathway. Conclusion: ROS mediated the TNF-α-induced inflammatory response via MAPK and NF-κB pathway, and may provide a novel strategy to prevent the inflammatory-dependent impairments in BMSCs. | ||
| کلیدواژهها | ||
| BMSCs؛ Inflammation response؛ MAPK؛ NF-κB؛ Oxidative stress؛ TNF-α | ||
| مراجع | ||
|
| ||
|
آمار تعداد مشاهده مقاله: 1,381 تعداد دریافت فایل اصل مقاله: 951 |
||