CYP3A4-mediated Phase I biotransformation is the rate-limiting step of elimination for many commonly used clinically agents. The modulatory effects of herbal medicines on CYP3A4 activity are one of the risk factors affecting the safe use of drug and herbal medicine. In the present study, the inhibitory effects of nearly hundred kinds of herbal medicines against CYP3A4 were evaluated based on a visual high-throughput screening method. Furthermore, biflavone components including bilobetin (7-demethylginkgetin, DGK), ginkgetin (GK), isoginkgetin (IGK), and amentoflavone (AMF) were identified as the main inhibitory components of Ginkgo biloba L. (GB) and Selaginella tamariscina (P. Beauv.) Spring (ST), which displayed very strong inhibitory effects toward CYP3A4. The inhibitory effects of these biflavones on clinical drugs that mainly undergo CYP3A4-dependent metabolism were evaluated. The IC₅₀ of GK toward tamoxifen, gefitinib and ticagrelor were found to be of 0.478 ± 0.003, 0.869 ± 0.001, and 1.61 ± 0.039 μM, respectively. These results suggest the potential pharmacokinetic interactions between the identified biflavones and clinical drugs undergoing CYP3A4-mediated biotransformation. The obtained information is important for guiding the rational use of herbal medicine in combination with synthetic pharmaceuticals.

Phyllodium pulchellum(P. pulchellum) is a folk medicine with a significant number of bioactivities. The aim of this study was to investigate the effects displayed by alkaloids fractions, isolated from the roots ofP. pulchellum, on neurotransmitters monoamine levels and on monoamine oxidase (MAO) activity. Six alkaloids, which had indolealkylamine orβ‐carboline skeleton, were obtained by chromatographic technologies and identified by spectroscopic methods such as NMR and MS. After treatment with alkaloids ofP. pulchellum, the reduction of DA levels (54.55%) and 5‐HT levels (35.01%) in rat brain was observed by HPLC‐FLD. The effect of alkaloids on the monoamines metabolism was mainly related to MAO inhibition, characterized by IC₅₀values of 37.35 ± 6.41 and 126.53 ± 5.39 μg/mL for MAO‐A and MAO‐B, respectively. The acute toxicity indicated thatP. pulchellumextract was nontoxic.

The dried root of Inula helenium L., known as Inulae Radix in Mongolian medicine, is a widely used heat-clearing plant drug within the Asteraceae family. Alantolactone (ATL), a compound derived from Inulae Radix, is a sesquiterpene lactone with a range of biological activities. However, there is a lack of studies investigating its effectiveness in the treatment of hypertension. The aim of this study is to explore the regulatory effect of alantolactone on blood pressure and its underlying mechanism. Network pharmacology analysis suggested that ATL had a potential therapeutic effect on hypertension induced by angiotensin II (Ang II). Subsequently, the results of animal experiments demonstrated that ATL could suppress the increase in blood pressure caused by Ang II. Vascular ring experiments indicated that ATL could inhibit the vascular contractions induced by Ang II, Phenylephrine, and Ca2⁺. Further experiments demonstrated that ATL could inhibit the calcium influx induced by Ang II and increase the expression of pMLC2. Molecular docking experiments showed that ATL had a high binding affinity with L-type Voltage-gated Calcium Channels (VGCC), and vascular ring experiments indicated that ATL could significantly inhibit the vascular contractions caused by the agonists of L-type VGCC. In addition, we also observed that ATL had an ameliorative effect on the vascular remodeling induced by Ang II. ATL exerted an antihypertensive effect by inhibiting the activation of L-type VGCC and reducing calcium influx.

NAD(P)H quinone oxidoreductase 1 (NQO1) plays a critical role in catalyzing the reduction of quinones, thereby exerting both chemical protection and biological activation. The expression level of NQO1 in various tumor cells, especially glioma, lung cancer, colon cancer and breast cancer cells, is higher than that in normal tissues, the detection of NQO1 activity is important to understand tumor development mechanisms. Herein, a near-infrared (NIR) fluorescent probe DDANQ was rationally designed and synthesized through a systematic approach. The optical properties and enzyme selectivity of DDANQ were also elucidated by chemical calculation and molecular docking methods. The results showed that DDANQ showed excellent stability, and displayed good selectivity and sensitivity toward NQO1. DDANQ could be used as a molecular tool to elucidate the activity and function of NQO1 in physiological and pathological processes, which could provide valuable insights for tumor diagnosis and treatment.