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Objective:To study the influernce of circadian genes hClock and hBmal1 on the chemosensitivity of SGC-7901 cells. Methods: SGC-7901 cells were cultivated under continuous darkness in vitro.The expression levels of the two main circadian genes hClock and hBmal1 at the different time were determined by real-time polymerase chain reaction(PCR). Docetaxel was administered at the peak and nadir time point respectively. The inhibition of SGC-7901 cell proliferation was measured using a CCK-8 kit. Result:The expression of circadian genes hClock and hBmal1 varied at different times, as shown by real-time PCR. The expression of circadian genes hClock and hBmal1 showed Phase oseillation. The maximum expression of hClock and hBmal1 mRNA was at 20:00. whereas their minimum expression was at 08:00. The inhibition ratio of docetaxel to SGC-7901 cells at the maximum expression of hClock and hBmal1 genes was lower than that at the minimum expression. Conclusion:Circadian Genes hClock and hBmal1 can reduce the drug sensitivity of SGC-7901 cell line to docetaxel in vitro.
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Purpose To examine the regulatory effect of recombinant human fibroblast growth factor-21 on the expression of liver X receptor α and glucose transporter protein 1 in the type 2 diabetes mellitus rats.Methods The rat models of type 2 diabetic mellitus were divided into four groups at random, ic. rhFGF-21 every day, after eight weeks of these treatment, Inspect the fasting blood glucose (FBG), fructosamine(FA), triglyceride(TG), T-cholesterol(TC), high density lipoprotein cholesterol(HDL-C) and low density lipoprotein cholesterol(LDL-C) of these rats, then detecting the mRNA expression of LXRα and GLUT1 by RT-PCR.Results (1) rhFGF-21 can reduce blood glucose steadily to near normal levels in diabetic rats. (2) The expression of LXRα and GLUT1 level was significantly higher in the rhFGF-21 treatment group than that in the model group. (3) rhFGF-21 megadoses and middle doses decreased FA, TG, TC,and LDL-C and elevated HDL-C.Conclusion rhFGF-21 could regulate the mRNA expression of LXRα and GLUT1 in diabetes rats, increase basal level glucose transport, then reduce blood glucose, improve lipid metabolize dysfunction.