4.5 Article

By regulating miR-182-5p/BCL10/CYCS, sufentanil reduces the apoptosis of umbilical cord mesenchymal stem cells caused by ropivacaine

期刊

BIOSCIENCE TRENDS
卷 13, 期 1, 页码 49-57

出版社

IRCA-BSSA
DOI: 10.5582/bst.2018.01291

关键词

Sufentanil; ropivacaine; umbilical cord mesenchymal stem cells; cell cycle arrest; apoptosis; miR-182-5p; BCL10; CYCS

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资金

  1. National Natural Science Foundation of China [31571196, 30801502]
  2. Shanghai Program for Support of Leading Disciplines-Integrated Chinese and Western Medicine [20180101, 20150407]
  3. Shanghai Municipal Science and Technology Commission [18401902200, 15401932200]
  4. Shanghai Pujiang Program [11PJ1401900]
  5. FY2008 JSPS Postdoctoral Fellowship for Foreign Researchers [P08471]
  6. Fund for Young Scientists of the Shanghai Municipal Health and Family Planning Commission [20184Y0218]

向作者/读者索取更多资源

Sufentanil is a type of opioid analgesic and is usually used to facilitate painless labor in combination with the local anesthetic ropivacaine. One aim of the current study was to investigate the effects of sufentanil and ropivacaine on umbilical cord mesenchymal stem cells (UCMSCs). A second aim of this study was to determine whether sufentanil attenuated the cytotoxicity of ropivacaine in vitro. UCMSCs were divided into 3 groups: one was treated with ropivacaine at a concentration of 50, 100, 200, or 400 mu g/mL, another was treated with sufentanil at a concentration of 0.5, 5, 50, or 500 nmol/L, and a third was treated with a combination of ropivacaine at a concentration of 200 mu g/mL and sufentanil at a concentration of 0.5, 5, 50, or 500 nmol/L. Results indicated that cell proliferation decreased in cells treated with ropivacaine while it increased in cells treated with sufentanil. In addition, sufentanil limited the inhibitory effect of ropivacaine on UCMSC growth in a dose- and time-dependent manner. Combined treatment with ropivacaine at a concentration of 200 mu g/mL and sufentanil at a concentration of 500 nmol/L decreased the proportion of dead and apoptotic UCMSCs, and fewer cells were arrested in the S phase compared to cells treated with ropivacaine. Sufentanil inhibited the apoptosis induced by ropivacaine by increasing miR-182-5p, which regulated the expression of mRNA of the pro-apoptotic genes B-cell lymphoma/leukemia 10 (BCL10) and cytochrome c, somatic (CYCS). Sufentanil also increased the expression of mRNA of anti-apoptotic genes. In short, ropivacaine inhibits the cell viability and induces the apoptosis of UCMSCs in vitro while sufentanil attenuates this apoptosis by regulating miR-182-5p/BCL10/CYCS.

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