Abstract
BackgroundThe aim of this study was to explore the effect of dexmedetomidine (DEX)-mediated insulin-like growth factor 2 (IGF2) signal pathway on immune function and cancer cell invasion and migration in rats with ovarian cancer.Material/MethodsForty rats with ovarian cancer were divided into 4 groups: model group, and low dose (0.2 μg/kg/hour DEX), medium dose (1.0 μg/kg/hour DEX), and high dose (5.0 μg/kg/hour DEX) DEX groups. In addition, 10 Fischer344 rats were selected as a normal group. Human NUTU-19 poorly differentiated epithelial ovarian cancer cell line cells were divided into 4 groups: a blank group and low dose, medium dose, and high dose DEX NUTU-19 groups.ResultsCompared with the normal group, in the other groups the serum interleukin (IL)-2 and interferon gamma (INF-γ) levels, CD4+ and CD8+ percentages, CD4+/CD8+ ratio, and transformation rate of splenic lymphocytes were decreased, and the serum tumor necrosis factor alpha (TNF-α) level, IGF2, insulin-like growth factor 1 receptor (IGF1R), insulin receptor substrate 1 (IRS1) mRNA, and protein expressions in ovarian tissue were increased (all P<0.05). Results in the DEX groups compared with model group were the opposite of those in the other groups compared with normal group (all P<0.05). Compared with the blank group, in the other groups the proliferation, invasion, and migration of ovarian cancer cells were reduced significantly (all P<0.05). Compared with the low dose DEX NUTU-19 group, in the high dose DEX NUTU-19 group the invasion and migration of ovarian cancer cells weakened significantly (both P<0.05).ConclusionsA certain dose of DEX can effectively inhibit IGF2 signal pathway activation to improve the immune function of rats with ovarian cancer, inhibiting the invasion and migration of ovarian cancer cells.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Medical science monitor : international medical journal of experimental and clinical research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.