RESUMO
Objective To investigate the effect of Astragalus injection on iodine-131(131 I)induced thyroid radiation injury.Methods Two-stage SD male rats were randomly divided into three groups: control group, 131I irradiation group and Astragalus intervention 131I irradiation group.131I irradiation group and Astragalus intervention 131I irradiation group were treated with intragastric administration of 11.1MBq 131I, respectively.At the same time, the Astragalus intervention 131 I irradiation group was injected intraperitoneally 400 mg/(kg· d)Astragalus injection liquid.The levels of thyroid hormone were measured by solid-phase radioimmunoassay in the 2nd and 8th weeks of the experiment.The thyroid tissues from rats were HE stained into paraffin sections after 8 weeks.Administration of 0,25,50,100,200 MBq/ml into 131I irradiation of thyroid follicular carcinoma cells(WRO)lasted 24 hours, the proliferation and apoptosis of WRO in Astragalus membranaceus 0.5 g/L intervention and non-Astragalus intervention were detected by MTT assay and flow cytometry.Results Compared with the normal control group, FT3and FT4were significantly decreased in the 131 I irradiation group(P=0.021,0.017).The morphological changes of the follicular epithelial cells in the thyroid tissue were irregular and the hyaline degeneration was observed.However, compared with 131I irradiation group, FT3and FT4were significantly improved by Astragalus injection(P=0.033,0.045),and the degree of vitreous degeneration of thyroid tissue was alleviated.Cell experiments in vitro showed that the proliferation of thyroid cells was increased, but apoptosis was reduced.Conclusion Astragalus injection can improve the thyroid function and thyroid injury induced by 131 I in rats.
RESUMO
Objective: To investigate the role of EMT (epithelial-mesenchymal transition) and IGF- 1R (insulin-like growth factor I receptor) in acquired resistance to EGFR-TKIs (epidermal growth factor receptor-tyrosine kinase inhibitors) in NSCLC (non-small cell lung cancer). Methods: The EGFR mutant human lung adenocarcinoma PC-9 cell line and the EGFR wild-type H460 cell line were used to generate gefitinib-resistant PC-9 cells (named as PC-9/ZD cells) and erlotinib-resistant cells (named as H460/ER cells), respectively. MTT assay was used to measure the cell proliferation of PC9, PC-9/ZD, H460 and H460/ER cells. Wound-healing assay and Transwell assay were used to determine the migration and invasion capabilities of the cells. The protein and mRNA expressions of E-cadherin, vimentin, EGFR, ERK (extracellular signal-regulated kinase), AKT (protein kinase B) and IGF-1R were determined by Western blotting and RT-PCR (reverse transcription PCR), respectively. Results: Both PC-9/ZD and H460/ER cells acquired resistance to EGFR-TKIs which was to say that the sensitivities to gefitinib and erlotinib in PC-9/ ZD and H460/ER cells were significantly decreased, respectively (P < 0.05). Compared with PC-9 and H460 cells, the PC-9/ZD and H460/ER cells displayed mesenchymal phenotypes, and their capabilities of invasion and migration were enhanced (P < 0.05). The expression of mesenchymal cell marker vimentin was increased in both PC-9/ZD and H460/ER cells (P < 0.05), and the expression of E-cadherin was decreased in PC-9/ZD cells (P < 0.05). The expressions of IGF-1R and its phosphorylated form in both PC-9/ZD and H460/ER cells were significantly increased (P < 0.05) as compared with those in the PC-9 and H460 cells, accompanied by up-regulation of phosphorylation levels of AKT and ERK (P < 0.05). No significant difference was found in phosphorylation level of EGFR between PC-9 and PC-9/ZD cells (P < 0.05), while the phosphorylation level of EGFR was significantly decreased in H460/ER cells as compared with that in H460 cells (P < 0.05). Conclusion: The EMT in EGFR mutant gefitinib-resistant PC-9/ZD cells and the EGFR wild-type erlotinib-resistant H460/ER cells was accompanied by a increase in protein expression of IGF-1R, which suggests EMT and IGF-1R signal transduction may play an important role in acquired resistance to EGFR-TKIs in NSCLC cells. Copyright © 2013 by TUMOR.