Salidroside regulates the expressions of IL-6 and defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 6، دوره 22، شماره 1، فروردین 2019، صفحه 31-37 اصل مقاله (806.01 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2018.26994.6602 | ||
| نویسندگان | ||
| Jiawen Wang؛ Yibin Pan؛ Yongqing Cao؛ Wei Zhou؛ Jingen Lu* | ||
| Department of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R.China | ||
| چکیده | ||
| Objective(s): To reveal the detailed mechanism underlying the functions of salidroside on the inflammation of intestinal epithelial cells during IBD. Materials and Methods: Quantitative real-time PCR was employed to assess the expression of IL-6, IL-10, and α-defensins 5 and 6. ELISA assay was performed to measure the secretion of IL-6 and IL-10. MTT assay was used to determine the cell viability and proliferation. Western blot was used to assess the phosphorylation of NF-kB, Erk1/2, JNK, P38, JAK2, and STAT3. Results: Salidroside impaired the proliferation of intestinal epithelial cells at high concentrations (P< 0.05) and down-regulated interleukin-6 (IL-6) production induced by LPS (P<0.05). Western blot results showed that salidroside repressed the phosphorylation of NF-kB, Erk1/2, JNK, P38, JAK2 and STAT3 (P<0.05) and attenuated the activation of NF-κB, MAPK, and STAT3 pathways. Moreover, the expressions of α-defensin 5 and 6 were rescued by salidroside after LPS or SAC triggering (P<0.05). Conclusion: In summary, salidroside suppressed the expression of IL-6 and elevated the expression of defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways. The mechanism revealed here may be potentially useful for the treatment of IBD with salidroside. | ||
| کلیدواژهها | ||
| Defensin؛ IL-6؛ Intestinal epithelial cell؛ MAPK؛ NF-κB؛ Salidroside؛ STAT3 | ||
| مراجع | ||
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