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I. Yu. Lebedeva V. A. Lebedev T. I. Kuz'mina 《Journal of Evolutionary Biochemistry and Physiology》2004,40(2):144-152
A comparative study of effects of Mg2+ ions on specific and competitive binding of the bovine somatotropic hormone (STH) and bovine prolactin (PL) with cells of cow granulosum is carried out. It is found that Mg2+ increases the level of specific binding of 125I-PL with the cells at concentrations from 1 to 70 mM and decreases the level of specific binding of 125I-STH at a concentration of 70 mM. Analysis of the data by Scatchard's method has shown that the decrease of the level of specific binding of 125I-PL in the absence of MgCl2 and 125I-STH at a MgCl2 concentration of 70 mM is caused mainly by a decrease of the number of active binding sites on the cells. Oppositely directed effects of the studied divalent cations on the capability of unlabelled STH (25 µg/ml) and PL (25 µg/ml) for cross-suppression of specific binding of 125I-PL and 125I-STH, respectively, with the granulosum cells have been revealed. At the same time, with increase of Mg2+ ion concentration, the degree of replacement of 125I-STH and 125I-PL with unlabelled STH and PL, respectively, did not change. The obtained results are considered in connection with electrostatic model of participation of the divalent cations in interaction of PL and STH with receptors on cells. 相似文献
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Jung-Sheng Yu Wei-Chun Chen Chin-Kai Tseng Chun-Kuang Lin Yao-Chin Hsu Yen-Hsu Chen Jin-Ching Lee 《PloS one》2016,11(3)
Hepatitis C virus (HCV) infection-induced oxidative stress is a major risk factor for the development of HCV-associated liver disease. Sulforaphane (SFN) is an antioxidant phytocompound that acts against cellular oxidative stress and tumorigenesis. However, there is little known about its anti-viral activity. In this study, we demonstrated that SFN significantly suppressed HCV protein and RNA levels in HCV replicon cells and infectious system, with an IC50 value of 5.7 ± 0.2 μM. Moreover, combination of SFN with anti-viral drugs displayed synergistic effects in the suppression of HCV replication. In addition, we found nuclear factor erythroid 2-related factor 2 (Nrf2)/HO-1 induction in response to SFN and determined the signaling pathways involved in this process, including inhibition of NS3 protease activity and induction of IFN response. In contrast, the anti-viral activities were attenuated by knockdown of HO-1 with specific inhibitor (SnPP) and shRNA, suggesting that anti-HCV activity of SFN is dependent on HO-1 expression. Otherwise, SFN stimulated the phosphorylation of phosphoinositide 3-kinase (PI3K) leading Nrf2-mediated HO-1 expression against HCV replication. Overall, our results indicated that HO-1 is essential in SFN-mediated anti-HCV activity and provide new insights in the molecular mechanism of SFN in HCV replication. 相似文献
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