Chicken Insulin-like growth factor 1 receptor

Background: The 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/Methods: Forty rats with ovarian cancer were divided into 4 groups: model group, and low dose (0.2 mu g/kg/hour DEX), medium dose (1.0 mu g/kg/hour DEX), and high dose (5.0 mu g/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. Results: Compared with the normal group, in the other groups the serum interleukin (IL)-2 and interferon gamma (INF-gamma) levels, CD4(+) and CD8(+) percentages, CD4(+)/CD8(+) ratio, and transformation rate of splenic lymphocytes were decreased, and the serum tumor necrosis factor alpha (TNF-alpha) 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). Conclusions: A 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.

Environmental factors and prenatal stress have long-term effects on offspring behavior, physical development, hypothalamic-pituitary-adrenal (HPA) axis regulation, immune activity, and disease susceptibility. To further understand the effects of prenatal cold stress on offspring, we investigated the behavior change; the expression of glucocorticoid receptor (GR), mineralocorticoid receptor (MR), brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 receptor (IGF1R), neuronal nuclei (NEUN), glial fibrillary acidic protein (GFAP), corticotropin-releasing hormone receptor 1 (CRHR1), Gamma-aminobutyric acid B receptor, 2 (GABAB2) proteins in hippocampus; the ratio of CD4/CD8 lymphocyte subsets and the level of norepinephrine (NE), dopamine (DA) in the peripheral blood of weaned offspring rats using behavioral tests and biology analysis methods. The results showed that prenatal cold stress affected offspring HPA axis activity, inhibited the expression of MR, BDNF and IGF1R in the hippocampus of male offspring, and lowered the expression of GR in female offspring. The expression levels of NEUN and GFAP in the hippocampus of male and female offspring were also reduced, which may have affected the growth and development of neurons. Moreover, prenatal cold stress inhibited the expression of CRHR1 and GABAB2 in the hippocampus of male offspring, leading to decreased anxiety-like behavior in offspring; a reduced ratio of CD4 and CD8 lymphocyte subsets in the peripheral blood of male offspring; and inhibition of offspring cell immunity. In summary, prenatal cold stress inhibits the growth and development of hippocampal neurons in weaned offspring rats, and induces offspring anxiety-like behavior reduced.