Psychoactive Plant Database - Neuroactive Phytochemical Collection

1. Hereditas. 2024 Sep 6;161(1):31. doi: 10.1186/s41065-024-00334-y.

Exploring the molecular mechanism of ginseng against anthracycline-induced 
cardiotoxicity based on network pharmacology, molecular docking and molecular 
dynamics simulation.

Xie L(#)(1), Liu H(#)(2), Zhang K(#)(2), Pan Y(2), Chen M(1), Xue X(1), Wan 
G(3).

Author information:
(1)Department of Oncology, Institute of Medicine and Nursing, Renmin Hospital, 
Hubei University of Medicine, Shiyan, Hubei, 442000, China.
(2)Department of Oncology, Renmin Hospital, Hubei University of Medicine, 39 
Chaoyang Road, Shiyan, Hubei, 442000, China.
(3)Department of Oncology, Renmin Hospital, Hubei University of Medicine, 39 
Chaoyang Road, Shiyan, Hubei, 442000, China. 15gxwan@stu.edu.cn.
(#)Contributed equally

BACKGROUND: Previous clinical and basic studies have revealed that ginseng might 
have cardioprotective properties against anthracycline-induced cardiotoxicity 
(AIC). However, the underlying mechanism of ginseng action against AIC remains 
insufficiently understood. The aim of this study was to explore the related 
targets and pathways of ginseng against AIC using network pharmacology, 
molecular docking, cellular thermal shift assay (CETSA) and molecular dynamics 
(MD) simulations.
RESULTS: Fourteen drug-disease common targets were identified. Enrichment 
analysis showed that the AGE-RAGE in diabetic complications, fluid shear stress 
and atherosclerosis, and TNF signaling pathway were potentially involved in the 
action of ginseng against AIC. Molecular docking demonstrated that the core 
components including Kaempferol, beta-Sitosterol, and Fumarine had notable 
binding activity with the three core targets CCNA2, STAT1, and ICAM1. 
Furthermore, the stable complex of STAT1 and Kaempferol with favorable affinity 
was further confirmed by CETSA and MD simulation.
CONCLUSIONS: This study suggested that ginseng might exert their protective 
effects against AIC through the derived effector compounds beta-Sitosterol, 
Kaempferol and Fumarine by targeting CCNA2, STAT1, and ICAM1, and modulating 
AGE-RAGE in diabetic complications, fluid shear stress and atherosclerosis, and 
TNF signaling pathways.

© 2024. The Author(s).

DOI: 10.1186/s41065-024-00334-y
PMCID: PMC11378563
PMID: 39243097 [Indexed for MEDLINE]

Conflict of interest statement: The authors declare no competing interests.


2. Medicine (Baltimore). 2024 Aug 23;103(34):e39384. doi: 
10.1097/MD.0000000000039384.

Network pharmacology and molecular docking reveal potential mechanisms of 
ginseng in the treatment of diabetes mellitus-induced erectile dysfunction and 
asthenospermia.

Liu L(1)(2), Zhang Y(3)(4), Yang J(2), Chen W(5), Lan K(4), Shi Y(3), Zhang 
X(6), Xing X(7).

Author information:
(1)Department of Andrology, Xi'an Hospital of Traditional Chinese 
Medicine,Xi'an, P. R. China.
(2)School of Integrated Chinese and Western Medicine, Gansu University of 
Chinese Medicine, Lanzhou, P. R. China.
(3)Department of Urology, Key Laboratory of Urological Disease of Gansu 
Province, Clinical Center of Gansu Province for Nephron-Urology, Lanzhou 
University Second Hospital, Lanzhou, P. R. China.
(4)Department of Urology, Shantou Central Hospital, Shantou, P. R. China.
(5)The Second Clinical Medical College, Lanzhou University, Lanzhou, P. R. 
China.
(6)Department of Cardiology, Affiliated Hospital of Gansu Medical College, 
Pingliang, P. R. China.
(7)Department of Urology and Andrology, Affiliated Hospital of Gansu University 
of Chinese Medicine, Lanzhou, P. R. China.

Diabetes mellitus (DM) is a chronic metabolic disease that predisposes to 
chronic damage and dysfunction of various organs, including leading to erectile 
dysfunction (ED) and asthenospermia. Literature suggests that ginseng plays an 
important role in the treatment and management of DM. Ginseng may have a 
therapeutic effect on the complications of DM-induced ED and asthenospermia. The 
study aimed to explore the mechanisms of ginseng in the treatment of DM-induced 
ED and asthenospermia following the Traditional Chinese Medicine (TCM) theory of 
"treating different diseases with the same treatment." This study used network 
pharmacology and molecular docking to examine the potential targets and 
pharmacological mechanism of Ginseng for the treatment of DM-induced ED and 
asthenospermia. The chemical ingredients and targets of ginseng were acquired 
using the Traditional Chinese Medicine Systems Pharmacology database and 
analysis platform. The targets of DM, ED, and asthenospermia were extracted with 
the GeneCards and Online Mendelian Inheritance in Man databases. A 
protein-protein interaction network analysis was constructed. The Metascape 
platform was applied for analyzing the gene ontology and Kyoto Encyclopedia of 
Genes and Genomes pathways. AutoDock Vina was used to perform molecular docking. 
Network pharmacology revealed that the main active components of the target of 
action were kaempferol, beta-sitosterol, ginsenoside rh2, stigmasterol, and 
fumarine. Core targets of the protein-protein interaction network included TNF, 
IL-1β, AKT1, PTGS2, BCL2, and JUN. Kyoto Encyclopedia of Genes and Genomes 
enrichment analysis showed that they were mainly involved in AGE-RAGE signaling 
pathway in diabetic complications, TNF signaling pathway, Lipid and 
atherosclerosis. The interactions of core active components and targets were 
analyzed by molecular docking. Ginseng may play a comprehensive therapeutic role 
in the treatment of DM-induced ED and asthenospermia through "multicomponent, 
multi-target, and multi-pathway" biological mechanisms such as inflammation and 
oxidative stress.

Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

DOI: 10.1097/MD.0000000000039384
PMCID: PMC11346898
PMID: 39183406 [Indexed for MEDLINE]

Conflict of interest statement: The authors have no conflicts of interest to 
disclose.


3. Naunyn Schmiedebergs Arch Pharmacol. 2024 Jul 25. doi: 
10.1007/s00210-024-03278-2. Online ahead of print.

Revealing the active ingredients and mechanisms of Xiatianwu against 
hepatocellular carcinoma: a study based on network pharmacology and 
bioinformatics.

Wang H(1), Zhang W(1), Li L(1), Wang H(2), Jiang H(1), Li W(1), Huang J(3), Wan 
Y(4).

Author information:
(1)Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 
100029, China.
(2)Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, 
China.
(3)Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 
100029, China. zryhhuang@163.com.
(4)Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 
100029, China. wanyuxiang@bucm.edu.cn.

Xiatianwu is a traditional Chinese medicine. This study investigates the 
function of Xiatianwu in treating HCC through database analyses and in vitro 
experiments. The active ingredients of Xiatianwu were identified from TCMSP and 
HERB databases and their targets were predicted by Swiss TargetPrediction. The 
HCC dataset was screened using the GEO database, and the differentially 
expressed genes between HCC and non-tumor liver tissues were analyzed to 
identify overlapping targets with Xiatianwu. The intersecting targets underwent 
enrichment analysis using R software to elucidate the molecular mechanisms of 
Xiatianwu against HCC. Core targets were identified using the PPI network and 
MCODE algorithm. Clinical relevance and disease prognosis in HCC were verified 
using the TCGA database. Meanwhile, binding affinities among components and 
targets were validated with molecular docking. Finally, the anti-HCC efficacy of 
the active ingredient was validated in vitro. Our findings revealed that eight 
active ingredients of Xiatianwu interacted with 11 key targets, providing 
anti-HCC efficacy. Molecular docking indicated that bicuculline and fumarine 
exhibited superior binding abilities. Bicuculline, a representative ingredient 
of Xiatianwu, was chosen for in vitro validation. Results demonstrated that 
bicuculline, in a dose-dependent manner inhibited HCC cell viability, reduced 
migration, suppressed the G0/M cell cycle, and decreased core protein 
expression. Xiatianwu demonstrates significant potential for clinical 
application in treating HCC. Bicuculline, a key active ingredient of Xiatianwu, 
exerts anti-HCC effects by inhibiting the cell cycle.

© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
part of Springer Nature.

DOI: 10.1007/s00210-024-03278-2
PMID: 39052060


4. J Ethnopharmacol. 2024 Apr 6;323:117713. doi: 10.1016/j.jep.2024.117713. Epub 
2024 Jan 3.

Exploring the effect of Anshen Dingzhi prescription on hippocampal mitochondrial 
signals in single prolonged stress mouse model.

Wang J(1), Zhao P(1), Cheng P(1), Zhang Z(1), Yang S(2), Wang J(2), Wang X(3), 
Zhu G(4).

Author information:
(1)Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine 
of IHM, and Key Laboratory of Molecular Biology (Brain Diseases), Anhui 
University of Chinese Medicine, Hefei, 230012, China.
(2)Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine 
of IHM, and Key Laboratory of Molecular Biology (Brain Diseases), Anhui 
University of Chinese Medicine, Hefei, 230012, China; Acupuncture and 
Moxibustion Clinical Medical Research Center of Anhui Province, The Second 
Affiliation Hospital of Anhui University of Chinese Medicine, Hefei, 230061, 
China.
(3)Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine 
of IHM, and Key Laboratory of Molecular Biology (Brain Diseases), Anhui 
University of Chinese Medicine, Hefei, 230012, China. Electronic address: 
wangxuncui@163.com.
(4)Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine 
of IHM, and Key Laboratory of Molecular Biology (Brain Diseases), Anhui 
University of Chinese Medicine, Hefei, 230012, China. Electronic address: 
guoqizhu@gmail.com.

HEADINGS ETHNOPHARMACOLOGICAL RELEVANCE: Anshen Dingzhi prescription (ADP), 
which was first published in the masterpiece of traditional Chinese Medicine in 
the Qing Dynasty, "Yi Xue Xin Wu" (1732 CE), is documented to interrupt 
panic-related disorders. However, the mechanism of its action is still not 
clear.
AIM OF THE STUDY: This study aims to investigate the effects of ADP on 
post-traumatic stress disorder (PTSD)-like behaviors and explore the mechanism 
from perspective of sirtuin1 (SIRT1)-peroxisome proliferator-activated receptor 
gamma co-activator 1 alpha (PGC-1α)-dependent mitochondrial function.
MATERIALS AND METHODS: The changes of SIRT1-PGC-1α signal and mitochondrial 
function were evaluated in the hippocampus of mice receiving single prolonged 
stress (SPS). Later, the roles of this signaling pathway played in fear memory 
generalization and anxiety-like behavior in SPS mice was investigated using two 
agonists of this signaling pathway. On this basis, the effects of ADP 
(36.8 mg/kg) with definite therapeutic effects, on mitochondrial function were 
investigated and further confirmed by a SIRT1 inhibitor. Finally, the possible 
components of ADP targeting PGC-1α were monitored through bioinformatics.
RESULTS: Compared with control mice, SIRT1-PGC-1α signal in the hippocampus was 
impaired in SPS mice, accompanied with dysfunction of mitochondria and abnormal 
expression of synaptic proteins. The agonists of SIRT1-PGC-1α signal, ZLN005, as 
well as resveratrol improved the behavioral changes of mice caused by SPS, 
reversed the decline of proteins in SIRT1-PGC-1α signal, mitochondrial 
dysfunction, and the abnormal expression of synaptic proteins. The fingerprint 
was established for the quality control of ADP. At a dose of 36.8 mg/kg, ADP 
could prevent fear memory generalization and anxiety-like behavior in SPS mice. 
Mechanically, ADP promoted SIRT1-PGC-1α signal and repaired mitochondrial 
function. Importantly, SIRT1 inhibitor, selisistat eliminated the ameliorative 
effects of ADP on behavioral and mitochondrial function. Through molecular 
docking simulation, the brain-entering components of ADP, including malkangunin, 
Rg5, fumarine, frutinone A, celabenzine, and inermin had high binding energy 
with PGC-1α.
CONCLUSION: Dysfunction of SIRT1-PGC-1α-dependent mitochondrial function is 
attributed to SPS-triggered fear generalization and anxiety-like behavior, and 
ADP could improve PTSD-like behaviors likely through activating this signaling 
pathway.

Copyright © 2024 Elsevier B.V. All rights reserved.

DOI: 10.1016/j.jep.2024.117713
PMID: 38181935 [Indexed for MEDLINE]

Conflict of interest statement: Declaration of competing interest The authors 
declare that they have no known competing financial interests or personal 
relationships that could have appeared to influence the work reported in this 
paper.


5. Front Pharmacol. 2023 Oct 18;14:1258138. doi: 10.3389/fphar.2023.1258138. 
eCollection 2023.

Integration of metabolomics and network pharmacology to reveal the protective 
mechanism underlying Qibai Pingfei capsule on chronic obstructive pulmonary 
disease.

Xie J(1), Liu M(1), Gao Y(2)(3), Liu C(1), Wu F(4), Tong J(2)(3)(4), Li Z(2)(3), 
Zhu J(1)(2)(5).

Author information:
(1)College of Integrated Chinese and Western Medicine, Anhui University of 
Chinese Medicine, Hefei, Anhui, China.
(2)Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine, 
Institute of Health and Medicine, Anhui University of Chinese Medicine, Hefei, 
China.
(3)The First Affiliated Hospital of Anhui University of Traditional Chinese 
Medicine, Hefei, Anhui, China.
(4)College of Traditional Chinese Medicine, Anhui University of Chinese 
Medicine, Hefei, Anhui, China.
(5)Institutes of Integrative Medicine, Fudan University, Shanghai, China.

In this study, we have employed metabolomics technology in combination with 
network pharmacology to ascertain the key metabolites and hub genes. The 
objective was to explore the pathway of Qibai Pingfei Capsule (QBPF) in treating 
COPD through metabolomics. We identified 96 differential metabolites in the lung 
tissues of rats belonging to control and model groups, out of which 47 were 
observed to be critical (VIP >2, p < 0.05). Furthermore, 16 important 
differential metabolites were reversed after QBPF treatment. Using network 
pharmacology, we identified 176 core targets of 81 drug-active ingredients. Our 
comprehensive analysis of network pharmacology and metabolomics enabled us to 
identify a core target, prostaglandin-endoperoxide synthase 2 (PTGS2), and a 
core metabolic pathway for glutathione metabolism. Finally, the result of 
molecular docking showed that PTGS2 had strong binding activity to 18 compounds 
including Fumarine and Kaempferol, etc.. PTGS2 is a marker of ferroptosis, so we 
wanted to explore whether QBPF could inhibit ferroptosis in COPD. The results 
showed that ferroptosis was involved in the pathogenesis of COPD, and QBPF could 
inhibit the occurrence of ferroptosis. In conclusion, the mechanism of QBPF for 
treating COPD may be related to PTGS2 expression, glutathione metabolism and 
ferroptosis.

Copyright © 2023 Xie, Liu, Gao, Liu, Wu, Tong, Li and Zhu.

DOI: 10.3389/fphar.2023.1258138
PMCID: PMC10618342
PMID: 37920214

Conflict of interest statement: The authors declare that the research was 
conducted in the absence of any commercial or financial relationships that could 
be construed as a potential conflict of interest.