Objective. Magnoliae officinalis cortex (MOC) is one of the most frequently used traditional Chinese medicine (TCM) for the treatment of acute pancreatitis (AP). Magnolia volatile oil (MVO) is considered to be one of the main active ingredients in MOC for AP treatment. However, the underlying mechanism of MVO in AP therapy is unknown. Methods. An integrated strategy of gas chromatography‐mass spectrum (GC‐MS), network pharmacology, and molecular docking simulation was employed to predict underlying mechanism of MVO in AP treatment. First, the compounds of MVO were identified by GC‐MS, and the targets of the identified characteristic compounds were collected from several databases, as well as AP‐related targets. Next, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were carried out to obtain the mechanism. Moreover, the binding activity between core therapeutic targets and their corresponding compounds was evaluated by molecular docking simulation. Results. GC‐MS results showed a total of 35 compounds that appeared in at least 18 out of 20 chromatograms were considered as characteristic compounds of MVO, and 33 compounds of those were identified. Network analysis demonstrated that 33 compounds regulated 142 AP‐related targets. Of those, 8 compounds (α‐eudesmol, γ‐eudesmol, (−)‐terpinen‐4‐ol, terpineol, hinesol, linalool, borneol, and β‐eudesmol) and 8 targets (TNF, IL‐1β, PPARγ, PPARα, PTGS2, NCOA1, CNR1, and ESR1) have a close relationship with AP treatment and were recognized as the key active compounds and the core therapeutic targets, respectively. The 142 targets were involved in both inflammation and calcium overload‐related biological pathways, such as neuroactive ligand‐receptor interaction, estrogen, MAPK, and calcium signaling pathway. Moreover, molecular docking simulation indicated that the 8 core therapeutic targets strongly interacted with their corresponding compounds. Conclusions. In summary, the present study elucidated that the efficacy of MVO in AP treatment might be attributed to anti‐inflammation and inhibition of calcium overload through multicomponents and multitargets.

Here, we have found for the first time that the catalytic activity of “naked” DNAzyme, a single-stranded G-quadruplex DNAzyme (S.DNAzyme), can be modulated by aflatoxin B1 (AFB1) and zearalenone (ZEN). In fact, S.DNAzyme can mimic the activity of horseradish peroxidase to perform oxidation of 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) to colored ABTS˙⁺ (dark green). This catalytic activity can be inhibited upon addition of AFB1, leading to color fade of the solution. But with ZEN, the solution color will change to a yellowish-brown or yellow color. Thus, we have exploited this finding to achieve label-free, naked-eye detection of AFB1 or ZEN, and have explored the possible detection mechanisms. This approach is able to detect AFB1 and ZEN concentrations as low as 0.18 μM and 0.29 μM, respectively. Even in real samples, the limit of detection values of these two analytes are lower than 3 μM. Notably, S.DNAzyme cross-reacted with three other tested aflatoxins, including aflatoxin B2, aflatoxin G1 and aflatoxin M1, revealing the potential for a broadly applicable method to identify the family of aflatoxins. The AFB1- or ZEN-triggered new catalytic reaction between “naked” DNAzyme and ABTS may offer new opportunities for on-site visual detection of mycotoxins.