Plantamajoside attenuates isoproterenol-induced cardiac hypertrophy associated with the HDAC2 and AKT/ GSK-3ß signaling pathway.

As a compensatory response to cardiac overload, cardiac hypertrophy is closely associated with the occurrence and development of a variety of cardiovascular diseases, in which histone deacetylase 2 (HDAC2) has been reported to play an important role. Plantamajoside (PMS) is an active component extracted from Herba Plantaginis, which is a traditional Chinese medicine, and many biological activities of PMS have been reported. Here, we investigated the effects and mechanism of PMS on isoproterenol (ISO)-induced cardiac hypertrophy. ISO at 10 µmol/L was used in vitro to induce H9c2 cardiomyocyte hypertrophy. Cell viability and cell surface area were determined by MTT assay and immunocytochemistry, respectively. Furthermore, an in vivo, cardiac hypertrophy model was established by subcutaneous injection of ISO. Pathological alterations and fibrosis in the myocardium were studied by H&E and Masson's trichrome staining, respectively. Myocardial injury-related genes and proteins were detected by real-time PCR and western blotting. HDAC2 and its downstream proteins, AKT and GSK3ß, were analyzed by western blotting. Our results showed that, in vitro, PMS inhibited the ISO-induced increase in H9c2 cell surface area and the mRNA expression of ANP, BNP and Myh7. In vivo, PMS improved the ISO-induced decrease in cardiac function, inhibited the increase in cardiac anatomical parameters and alleviated the histopathological changes in cardiac tissues. Moreover, PMS inhibited the mRNA and protein expression of ANP, BNP, Myh7, COL1 and COL3. Furthermore, PMS suppressed the activity of HDAC2 and down-regulated the expression of the downstream proteins p-AKT and p-GSK3ß both in vitro and in vivo. Overall, our results indicated that PMS exerts significant cardioprotective effects against ISO-induced cardiac hypertrophy, and this protective effect may be mediated by inhibition of the HDAC2 and AKT/GSK-3ß signaling pathway.

Hg2+ reduction and re-emission from simulated wet flue gas desulfurization liquors.

In this study, considering that Hg(2+) in wet flue gas desulfurization (FGD) systems can easily be reduced and then released into atmosphere, causing secondary pollution, the researches about Hg(2+) reduction and Hg(0) re-emission mechanism were carried out. The effects of several experimental parameters on the reduction were studied, including initial pH, temperature, and concentrations of Cl(-) and S(IV). Our experimental results indicated that Cl(-) had a restraining effect on the Hg(2+) reduction and Hg(0) re-emission, after 24h reaction, only 20.5% of Hg(2+) was reduced with 100mM Cl(-) in simulated desulfurization solution. Cl(-) can slow Hg(2+) reduction and Hg(0) re-emissions dramatically through changing reaction mechanism, with formation of new intermediate: ClHgSO(3)(-), which can decompose to Hg(0), but much more slowly than Hg(SO(3))(2)(2-) or HgSO(3). Simulating the conditions of the practical application (initial pH 5, T=50 degrees C, S(IV)=5 mM, Cl(-)=100 mM), we also found that Ca(2+), NO(3)(-), F(-), etc. all had obvious effects on reduction rates. Based on the material balance and characteristic of the reactants, the reduction emission mechanism of Hg(2+) has been established, providing theoretical basis for industrial application of mercury control in wet FGD systems.