Fluorescent Tb(III)-MOF for Fe(III) Ion Detection and Treatment Effect in Aortic Dissection by Reducing ß-receptor Expression and D-Dimer Production.

Iron is a class of essential elements involved in the metabolic process in all living organisms. However, excessive or deficient iron levels from normal ranges can lead to severe diseases. In this study, a fluorescent Tb(III)-based metal-organic framework with the chemical formula of [Tb(cptpy)3]n (1, Hcptpy = 4'-(4-carboxyphenyl)-2,2':6',2''-terpyridine) has been prepared under the hydrothermal condition successfully and its properties were determined by X-ray single-crystal diffraction, IR spectra, powder X-ray diffraction (PXRD) thermogravimetric analyses (TGA) and elemental analyses. Luminescent and sensing properties of complex 1 were examined closely, and it is shown that the Tb-MOF has the distinct ability to efficiently and selectively detect the Fe3+ ion and acetone. Furthermore, the RT-PCR was employed to determine the effect of compound on the ß-receptor and mmp-9 genes expression in cardiomyocytes. And the ELISA assay was used for the measurement of D-Dimer in the serum after compound treatment.

Cucurbitacins extracted from Cucumis melo L. (CuEC) exert a hypotensive effect via regulating vascular tone.

As an effective medicine for jaundice in traditional Chinese medicine, Cucumis melo L. has been widely used in China. However, its effect on vascular function is still unclear. In this study, we extracted the compounds of Cucumis melo L., and the major ingredients were identified as cucurbitacins (CuEC, cucurbitacins extracted from Cucumis melo L.), especially cucurbitacin B. We replicated the toxicity in mice by intraperitoneal injection of a high dose of CuEC (2 mg/kg) and demonstrated that the cause of death was CuEC-induced impairment of the endothelial barrier and, thus, increased vascular permeability via decreasing VE-cadherin conjunction. The administration of low doses of CuEC (1 mg/kg) led to a decline in systolic blood pressure (SBP) without causing toxicity in mice. More importantly, CuEC dramatically suppressed angiotensin II (Ang II)-induced SBP increase. Further studies demonstrated that CuEC facilitated acetylcholine-mediated vasodilation in mesenteric arteries of mice. In vitro studies showed that CuEC induced vasodilation in a dose-dependent manner in mesenteric arteries of both mice and rats. Pretreatment with CuEC inhibited phenylephrine-mediated vasoconstriction. In summary, a moderate dose of CuEC reduced SBP by improving blood vessel tension. Therefore, our study provides new experimental evidence for developing new antihypertensive drugs.