RESUMO
Polyoxometalates (POMs) have gained significant research attention because of their excellent properties in photocatalytic (PC) hydrogen production. Exploring POM-based compounds for heterogeneous photocatalysis is an ongoing task. Here, we obtain a water-insoluble inorganic-organic hybrid compound, (P2W18O62)3(C12N3H10)6(C12N3H11)6·9.5H2O (P-PW), formed by Dawson-type POM P2W18O626- (P2W18) anions and protonated 2-(pyridin-4-yl)-1H-benzo[d]imidazole (PHB) cations via noncovalent interactions. In the presence of the sacrificial agent triethanolamine, P-PW exhibits a PC H2 generation rate of 0.418 mmol/g/h, surpassing that of P2W18 and PHB by 15 and 17 times, respectively. This enhancement in PC performance of P-PW can be attributed to its band structure change from the precursor compounds, leading to increased light absorption and therefore more efficient PC hydrogen production.
RESUMO
BACKGROUND Diabetic nephropathy was one of the most serious and harmful diabetic complications, characterized by progressive loss of renal function and renal fibrosis. Aerobic exercise training is an important non-pharmacologic method to prevent and treat diabetes mellitus and diabetic complications. MATERIAL AND METHODS Intraperitoneal (i.p.) injection of streptozocin (STZ) was used to construct a type 1 diabetic mouse model. Renal function and mitochondrial function were measured by urinary protein level, Masson staining and ATP, superoxide production, and membrane potential, respectively. The purpose of the research was to explore the effect of aerobic exercise training on renal and renal mitochondrial function, as well as the expression of Sirt1and PGC1α in type-1 diabetic mice. RESULTS Sedentary diabetic mice exhibited increased urinary protein level, blood glucose, and collagen deposition in renal tissues compared with sedentary control mice, which were significantly mitigated by aerobic exercise training. Diabetic mice displayed renal tissue mitochondrial dysfunction (decreased mitochondrial ATP production and membrane potential), as well as increased mitochondrial superoxide production, which were reversed by aerobic exercise. By using Western blot analysis, we identified the decreased expression of Sirt1 and PGC1α in the renal tissue of diabetic mice, which were partly reversed by aerobic exercise training. Data showed that silencing of Sirt1 abrogated the beneficial effect of aerobic exercise training against diabetes-induced mitochondrial abnormalities and renal damage in mice. CONCLUSIONS Aerobic exercise training alleviates diabetes-induced renal injury by improving mitochondrial function.