Hypoxia has been widely implicated in numerous pathological conditions, including those associated with inflammation and tumorigenesis. A number of recent studies have implicated hypoxia in the control of microvascular damage, the basis for which is not fully understood. In the present study, it was identified that autophagy was induced in human umbilical vein endothelial cells (HUVECs) post treatment with hypoxia, and the induction of autophagy by hypoxia was enhanced by hypoxia‑inducible factor 1 (HIF‑1) gene overexpression and inhibited by HIF‑1 knockout. Furthermore, the autophagy induced by overexpression of HIF‑1 was associated with a reduction of HUVEC cell viability. Therefore, HIF‑1 reduced HUVEC cell viability by inducing autophagy. These findings provide evidence of an important link between hypoxia and microvascular damage associated with HIF‑1‑related autophagy.

Here, to elucidate the interaction mechanism and physicochemical properties of remimazolam and human serum albumin interactions, techniques such as fluorescence, circular dichroism (CD) spectroscopy, and isothermal titration calorimetry have been applied for study. The thermodynamic parameters at body temperature (ΔS = À207 JÁmol À1 ÁK À1 , ΔS = À9.76 Â 10 4 JÁmol À1 and ΔG = À3.34 Â 10 4 JÁmol À1 ; 310 K) manifests one strong binding site on the protein, which was modulated by van der Waals forces and hydrogen bonds. What is more, the results of CD, synchronous and three-dimensional fluorescence showed that remimazolam altered the microenvironment of the protein amino acid residues. A distance of 2.1 nm between the remimazolam and Trp shows the potential for resonance energy transfer. Furthermore, these results potentially provide information for illustrating the pharmacodynamics and toxicodynamics of remimazolam when it is applied clinically.

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