The effect of Telmisartan on the expression of connexin43 and neointimal hyperplasia in a rabbit iliac artery restenosis model.

We established a rabbit iliac artery restenosis model to explore the impact of Telmisartan on the expression of Connexin43 (Cx43) and neointimal hyperplasia. Thirty New Zealand white rabbits were randomly divided into three groups: control group (n = 10), restenosis group (n = 10), and Telmisartan group (n = 10). The restenosis model was established by high-cholesterol diet combined with double-balloon injury of iliac arteries. In addition, Telmisartan at 5 mg/(kg day) was administered to the rabbits of Telmisartan group on the second day after the second balloon injury. All rabbits were killed at the end of the experiment followed by institution policy. Before sacrifice, blood samples were obtained to test serum angiotensinII (AngII). Iliac arteries were isolated for morphological analysis and determining the expression of Cx43 by HE staining, immunohistochemical analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western Blotting analysis. Then, the local AngII levels of arteries were measured by radioimmunoassay. As compared with controls, the expression of Cx43 mRNA (0.98 ± 0.08) vs. (1.27 ± 0.17), P < 0.01), and Cx43 protein [(0.75 ± 0.08) vs. (0.90 ± 0.08), P < 0.05] of restenosis group were increased, which were significantly higher than those of Telmisartan group [Cx43 mRNA: (1.27 ± 0.17) vs. (1.00 ± 0.20), P < 0.01; Cx43 protein: (0.90 ± 0.08) vs. (0.82 ± 0.05), P < 0.05]. Furthermore, The intima thickness [(266.12 ± 70.27) vs. (2.85 ± 0.19) µm, P < 0.01] and the local AngII [(115.6 ± 15.7) vs. (90.1 ± 7.7), P < 0.05] of restenosis group were raised when compared with controls. Telmisartan group exhibited thinner intima compared with restenosis group [(68.22 ± 24.37) vs. (266.12 ± 70.27), P < 0.01]. However, the local AngII levels between these two groups were approximate. In addition, the plasma concentration of AngII was not significantly different among three groups. In conclusion, Telmisartan can inhibit the expression of connexin43 and neointimal hyperplasia in iliac artery restenosis model.

Effect of a Co-Based Oxygen-Evolving Catalyst on TiO2-Photocatalyzed Organic Oxidation.

Cobalt phosphate (CoPi) is a promising cocatalyst for the (photo)electrochemical oxidation of water over semiconductor electrodes in phosphate solution, but the effect of CoPi on organic oxidation reactions has been little studied. Herein, we report a compound-sensitive effect of CoPi on the TiO2-photocatalyzed oxidation of phenol, 4-chlorophenol (CP), and 2,4-dichlorophenol (DCP) in a phosphate-containing suspension at pH 7.0. A photochemical method was used to deposit Pt onto TiO2 and then CoPi onto both Pt/TiO2 and TiO2. In all reactions, Pt/TiO2 and CoPi/TiO2 were always more active and less active, respectively, than TiO2. In comparison with Pt/TiO2, CoPi/Pt/TiO2 was less active for phenol oxidation but more active for CP and DCP oxidation. CoPi/Pt/TiO2 was also more active than Pt/TiO2 for the photocatalytic reduction of O2 into H2O2. For DCP oxidation in a phosphate-free suspension at pH 7, however, CoPi/Pt/TiO2 was much less active than either Pt/TiO2 or TiO2, which is ascribed to the dissolution of Co2+ ions that act as recombination centers. It is proposed that the CoIV species, formed by the hole oxidation of CoII/III in CoPi, are surface-bound and short-lived. They can react with a nearby adsorbed substrate (CP, DCP, and H2O2) but deactivate in the absence of either Pt (O2 reduction catalyst) or phosphate (CoPi repairer). Moreover, there is a synergism between the CoPi-mediated hole transfer and the Pt-mediated electron transfer, that improves the efficiency of the charge separation and, consequently, increases the rates of O2 reduction and organic oxidation.

Iodine-sensitized oxidation of ferrous ions under UV and visible light: the influencing factors and reaction mechanism.

The sensitized oxidation of Fe(2+) ions by I2 or I3(-) in acidic aqueous solution has been examined. The reactions could occur either under UV or visible light, with the stoichiometric formation of Fe(3+) and I(-). However, the I3(-)-sensitized reaction was fast and complete only in the presence of excess Fe(2+). Through a kinetics study, it becomes clear that I˙ and I2(-)˙ are the main reactive species for the I2 and I3(-)- sensitized oxidation of Fe(2+), respectively. Moreover, the quantum yields determined with the I2 and I3(-)-sensitized formation of Fe(3+) at 456 nm were 0.119 and 0.118, respectively. The I2-sensitized reaction was first order only in I2, and had an Arrhenius activation energy of 29.3 kJ mol(-1). It is proposed that the process of Fe(2+) oxidation by I˙ is fast, while the rate-determining step is the formation and self-recombination of I˙ radicals.

Rosuvastatin postconditioning protects isolated hearts against ischemia-reperfusion injury: The role of radical oxygen species, PI3K-Akt-GSK-3ß pathway, and mitochondrial permeability transition pore.

AIMS: Glycogen synthase kinase-3ß (GSK-3ß) and mitochondrial permeability transition pore (mPTP) play an important role in myocardial ischemia-reperfusion injury. The aim of this study was to investigate whether postconditioning with rosuvastatin is able to reduce myocardial ischemia-reperfusion injury and clarify the potential mechanisms. METHODS: Isolated rat hearts underwent 30 minutes of ischemia and 60 minutes of reperfusion in the presence or absence of rosuvastatin (1-50 nmol/L). The activity of signaling pathway was determined by Western blot analysis, and Ca2+ -induced mPTP opening was assessed by the use of a potentiometric method. RESULTS: Rosuvastatin significantly reduced myocardial infarct size and improved cardiac function at 5 and 10 nmol/L. Protection disappeared at higher concentration and reverted to increased damage at 50 nmol/L. At 5 nmol/L, rosuvastatin increased the phosphorylation of protein kinase B (Akt) and GSK-3ß, concomitant with a higher Ca2+ load required to open the mPTP. Rosuvastatin postconditioning also significantly increased superoxide dismutase activity and reduced malondialdehyde and radical oxygen species level. LY294002, phosphatidylinositol-3-kinase (PI3K) inhibitors, abolished these protective effects of rosuvastatin postconditioning. CONCLUSION: Rosuvastatin prevents myocardial ischemia-reperfusion injury by inducing phosphorylation of PI3K-Akt and GSK-3ß, preventing oxidative stress and subsequent inhibition of mPTP opening.

Different recycle behavior of Cu2+ and Fe3+ ions for phenol photodegradation over TiO2 and WO3.

Photocatalytic degradation of organic pollutants on TiO2 and WO3 have been widely studied, but the effects of Cu(2+) and Fe(3+) ions still remain unclear. In this work, we have found that the recycle behavior of Cu(2+) and Fe(3+) are greatly dependent on the photocatalytic activity of metal oxide used. With TiO2 (P25, anatase, and rutile), all the time profiles of phenol degradation in water under UV light well fitted to the apparent first-order rate equation. On the addition of Cu(2+), phenol degradation on anatase, rutile and WO3 also followed the first-order kinetics. On the addition of Fe(3+), the initial rate of phenol degradation on each oxide was increased, but only the reactions on three TiO2 became to follow the first order kinetics after half an hour. The relevant rate constants for phenol degradation in the presence of Cu(2+) or Fe(3+) were larger than those in the absence of metal ions. Under visible light, phenol degradation on WO3 was also accelerated on the addition of Fe(3+) or Cu(2+). Moreover, several influencing factors were examined, including the metal ion photolysis in solution. It becomes clear that as electron scavengers of TiO2 and WO3, Fe(3+) is better than Cu(2+), while they are better than O2. We propose that Fe(3+) recycle occurs through H2O2, photogenerated from TiO2, not from WO3, while Cu(2+) regeneration on a moderate photocatalyst is through the dissolved O2 in water.