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ObjectiveTo investigate the effects of vascular endothelial growth factor (VEGF) and dexamethasone on mRNA expressions of surfactant protein B (SP-B) and transforming growth factor-β1 (TGF-β1) of type Ⅱ alveolar epithelial cell (AECⅡ). MethodsAECⅡ were isolated and purified from fetal rat lung tissues,then cultured with different dose of VEGF (25,50 and 100 ng/ml) and dexamethasone (25,50,100 and 200 nmol/ml).The mRNA levels of SP-B and TGF-β1 were detected by real-time quantitative polymerase chain reaction (RT-PCR) and expression of TGF-β1 protein was detected by immunocytochemistry.ANOVAor q-test wasappliedtocompare the difference among groups.ResultsCompared with control group,SP-B mRNA levels in 25 ng/ml VEGF group and 25,50,100 and 200 nmol/ml dexamethasone groups were higher (13.500±3.172,3.547±0.690,5.219±0.782,3.493±0.335,and 3.981 ± 1.133 vs 1.001 ± 0.059,q=-5.286,-4.943,- 7.228,- 9.906 and - 3.525 respectively,P＜0.05) ; TGF-β1 mRNA expression of 25 ng/ml VEGF group,50,100 and 200 nmol/ml dexamethasone group was lower (0.451 ± 0.078,0.579±0.019,0.422 ± 0.020 and 0.769 ± 0.025 vs 1.019±0.226,q=4.110,3.356,4.551 and 1.901 respectively,P＜0.05) ; other groups had no significant differences compared with control group (P＞0.05).Immunocytochemistry showed that the positive rate of TGF-β1 expression in 25 ng/ml VEGF,50,100 and 200 nmol/ml dexamethasone group was 23％,26％,22％ and 29％,respectively,while in the control group,the expression of TGF-β1 was positive in most of the AECⅡ (80％).ConclusionsBoth VEGF and dexamethasone could increase the expression of SP-B at mRNA level at appropriate concentrations.At the same time,the expression of TGF-β1 is inhibited.It is suggested that both VEGF and dexamethasone might increase the mRNA expression of SP-B by inhibiting the expression of TGF-β1.
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Objectives To study the radiation-protective effects produced by the estrogenic activities of genistein(Gen) .Method After blocking estrogen receptor activities by Tamoxifen and Faslodex,the effects of Gen on 30d survival rate and average life span of the mice were monitored after exposure to lethal dose ? radiation(7.5Gy),and the effects of Gen on innate(nonspecific) immune response as well as humoral(B-cell mediated)immune response of the mice were examined after exposure to 4.0Gy ? radiation.Results Gen can enhance the survival rate,average life span,and immune response of the ?-radiation exposed mice.While Tamoxifen had no significant effects on survival rate and immune response of the exposed mice,Faslodex caused a decrease in survival rate and average life span and also inhibited the immune response in those exposed mice.Conclusion Genistein can enhance the radiation tolerance in mice through activation of estrogen receptor ? pathway.
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Objective To study the radiation-protective effects produced by the estrogenic activities of genistein(Gen) for providing experimental basis to develop the food for radiation protection. Method After blocking estrogen receptor (ER) activities by Tamoxifen and Faslodex,the effects of Gen on peripheral leucocytes and lymphocyte counts,serum haemolysin and delayed type of hypersensitivity of the mice were examined after exposure to 4 Gy ? radiation. Results Gen was shown to inhibit the decrease of peripheral leucocytes and lymphocyte counts and the decreased immune response of the ?-irradiated mice. Faslodex (ER? blocker) + Gen eliminated the protective effect of Gen and still caused the similar effects in hematological response and immune response after irradiation. Tamoxifen (ER? blocker) did not have these effects. Conclusion Gen can enhance the immune function in irradiated mice through activation of estrogen receptor ? pathway.