The Mechanism of Crocetin Targeting Cardiovascular Disease Based on Network Pharmacology Constrained by Spectral Experiments.

The network pharmacology under conditions is a recent development trend. We use network pharmacology methods to analyze the mechanism of crocetin (CRO) that regulates cardiovascular diseases. In this work, the spectral experimental data of CRO-Protein interaction is first time combined with constraint conditions to solve the problems of targeting redundancy and lack of verification. CRO targets and cardiovascular disease targets were obtained by the target database. The STRING platform was used for PPI analysis. The GO and KEGG pathways of the target were analyzed using the Metascape platform; The core functional targets of CRO were screened by molecular docking techniques and the spectra of CRO and human serum albumin (HSA). Under the collaborative constraint conditions, the core targets of CRO that regulate cardiovascular diseases are ADRA1A, ADRA1B, CHRM1, CHRM2, GABRA1, and PTGS2; This study incorporates spectroscopy and molecular docking as constraints into the network pharmacological analysis, which significantly improves the credibility of network pharmacological analysis compared with unconstrained conditions. This method provides theoretical references for the in-depth study of the mechanism between active substances and protein targets for other medicines in network pharmacology.

Imaging human serum albumin behavior in process of PVOCs transportation in vivo: Spectroscopy analysis insight.

Pomelo volatile organic compounds (PVOCs) are used as food additives to provide unique flavors, thus, and the possible effects of VOC binding to albumin should be considered. Headspace solid-phase microextraction with gas chromatography-mass spectrometry was used to fingerprints adsorption of PVOCs on human serum albumin (HSA). Spectral data and molecular modeling were used to establish a binding model between PVOCs and HSA. Twenty-one common components were identified, and dipentene, linalylacetate, and nootkatone were identified as characteristic components. Thermodynamic calculations showed that dipentene and linalylacetate bound to HSA via van der Waals forces and hydrophobic interactions, whereas nootkatone bound to HSA via van der Waals forces alone. Molecular modeling showed that the volatile components were all bound to the hydrophobic pocket of HSA site I. Our results provide a useful basis for quality evaluation of pomelo and explain the mechanism of interaction between PVOCs and HSA.

[Neuroprotective effects of paeonol in a cell model of Parkinson disease].

OBJECTIVE: To investigate the effects of paeonol on neuron cell model of Parkinson disease (PD). METHODS: The cell model of Parkinson disease was induced by treatment of 1-Methyl-4-phenylpyridinium (MPP+) in PC12 cells, the PD model cells were treated with 1 µmol/L, 3 µmol/L or 9 µmol/L paeonol for 24h, respectively. Cell viability and LDH leakage were detected by MTT and lactate dehydrogenase (LDH) assay; the apoptosis of PC12 cells was assessed by Hoechst 33258 staining and flow cytometry; reactive oxygen species (ROS) production was detected by DCFH-DA method; and the ratio of Bax/Bcl-2 and activation of caspase-3 were determined by Western blotting. RESULTS: MPP+ treatment significantly reduced cell viability, increased LDH leakage, enhanced the proportion of apoptotic cells and ROS production. In addition, MPP+ treatment dramatically increased the Bax/Bcl-2 ratio, and the activation of caspase-3. Compared to PD model group, paeonol treatment significantly enhanced cell viability, decreased LDH leakage, inhibited the proportion of apoptotic cells and ROS production, reduced the Bax/Bcl-2 ratio and the activated caspase-3 protein. CONCLUSION: Paeonol can prevent PC12 cells from apoptosis induced by MPP+, and the mechanism may be associated with the down-regulation of ROS production, Bax/Bcl-2 ratio and Caspase-3 activation.