Psychoactive Plant Database - Neuroactive Phytochemical Collection

1. Biomed Chromatogr. 2024 Sep 24:e5973. doi: 10.1002/bmc.5973. Online ahead of 
print.

Anti-LSSDS pharmacological components identification of YuHuangLian based on the 
combination of spectrum-effect analysis and network pharmacology as well as 
molecular docking.

Xu B(1)(2)(3)(4), Chen S(1), Liu J(5), Wu D(1), Sun W(1), Liu S(1), Hu 
Y(1)(2)(3), Wang H(1)(2)(3), Wang J(1)(2)(3), Yang B(1)(2)(3), Li W(1)(2)(3), Ma 
S(5).

Author information:
(1)School of Pharmacy, Harbin University of Commerce, Harbin, China.
(2)Engineering Research Center of Natural Anti-cancer Drugs, Ministry of 
Education, Harbin, China.
(3)Heilongjiang Key Laboratory of Preventive and Therapeutic Drug Research of 
Senile Diseases, Harbin, China.
(4)Engineering Research Center of Chinese Medicine Production and New Drug 
Development, Beijing University of TCM, Beijing, China.
(5)National Institutes for Food and Drug Control, Beijing, China.

This research aimed to investigate the pharmacological components for liver 
stagnation and spleen deficiency syndrome (LSSDS) of Evodia rutaecarpa (also 
called Yu HuangLian [YHL]) by exploring the spectrum-effect relationship between 
fingerprints and pharmacological actions. The fingerprints of 17 batches of YHL 
with different preparation conditions according to Box-Behnken Design were 
generated and analyzed to identify the common peaks by HPLC and FT-IR. 
Vasoactive intestinal peptide (vip), substance P, and 5-HT levels in colon 
sample were measured by ELISA. Gray degree correlation and orthogonal partial 
least squares were employed to explore the correlation degree between components 
and pharmacologic activity. The presumed pharmacological components were further 
confirmed by network pharmacology, molecular docking, and qRT-PCR. The 
columbamine, jatrorrhizine, coptisine, berberine, rutecarpine, and evodiamine of 
the 14 common peaks in HPLC fingerprints were significantly correlated with the 
pharmacological indexes. Similarly, there was a strong correlation with -OH, 
δNC-H, and νC-O-C of the 10 common peaks in FT-IR fingerprints. PTGS2 and CHRM3 
were the main targets intervening LSSDS, and the presumed pharmacological 
components could markedly increase the expression of CHRM3 and obviously reduce 
the expression of PTGS2 compared with the model group.

© 2024 John Wiley & Sons, Ltd.

DOI: 10.1002/bmc.5973
PMID: 39318149


2. Phytomedicine. 2024 Nov;134:155954. doi: 10.1016/j.phymed.2024.155954. Epub
2024  Aug 13.

Jiao-tai-wan and its effective component-coptisine alleviate cognitive 
impairment in db/db mice through the JAK2/STAT3 signaling pathway.

Nie K(1), Gao Y(1), Wang H(1), Su H(2), Chen S(1), Jiang X(1), Dong H(3), Tang 
Y(4).

Author information:
(1)Institute of Integrated Traditional Chinese and Western Medicine, Tongji 
Hospital, Tongji Medical College, Huazhong University of Science and Technology, 
Wuhan, Hubei 430030, China.
(2)Department of Integrated Traditional Chinese and Western Medicine, Tongji 
Hospital, Tongji Medical College, Huazhong University of Science and Technology, 
Wuhan, Hubei 430030, China.
(3)Institute of Integrated Traditional Chinese and Western Medicine, Tongji 
Hospital, Tongji Medical College, Huazhong University of Science and Technology, 
Wuhan, Hubei 430030, China. Electronic address: tjhdonghui@163.com.
(4)Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical 
College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, 
China. Electronic address: 5975008414@qq.com.

BACKGROUND: Cognitive impairment (CI) is now well-accepted as a complication and 
comorbidity of diabetes mellitus (DM), becoming a serious medical and social 
problem. Jiao-tai-wan (JTW), one of noted traditional Chinese medicine (TCM), 
showed dual therapeutic effects on DM and CI. Nevertheless, the potential 
mechanism is unclear.
PURPOSE: This study sought to investigate the mechanism how JTW protected 
against DM and CI and screen the active component in JTW.
METHODS: Db/db mice were used as mouse models. Mice were treated by gavage with 
0.9 % saline (0.1 mL/10g/d), low dose of JTW (2.4 g/kg/d) or high dose of JTW 
(4.8 g/kg/d) for 8 weeks separately. To access the effects of JTW, the levels of 
OGTT, HOMA-IR, blood lipids, inflammatory cytokines in serum and hippocampus 
were measured, behavioral tests were conducted, and histopathological changes 
were observed. The mechanism exploration was performed via network pharmacology, 
RT-qPCR, western blot, and immunofluorescence staining (IF). The impact and 
mechanism of coptisine in vitro were investigated using BV2 cells induced by LPS 
as cellular models. In vitro experiments were conducted in two parts. The first 
part comprised four groups: Control group, LPS group, LPS+LCOP group and 
LPS+HCOP group. The second part consisted of four groups: Control group, LPS 
group, LPS+HCOP group, and LPS+ Fed group. The western blot and RT-qPCR methods 
were used to examine the changes in biomarkers of the JAK2/STAT3 signaling 
pathways in BV2 cells.
RESULTS: The results demonstrated that JTW could improve OGTT and HOMA-IR, 
reduce the serum levels of LDL-C, HDL-C, TG, and TC, restore neuronal 
dysfunction and synaptic plasticity, and decrease the deposition of Aβ in the 
hippocampus. The findings from ELISA, IF, and RT-qPCR revealed that JTW could 
alleviate microglial activation and inflammatory status in vivo and coptisine 
could play the same role in vitro. Moreover, the changes of the JAK2/STAT3 
signaling pathway in LPS-induced BV2 cells or hippocampus of db/db mice were 
distinctly reversed by coptisine or JTW, respectively.
CONCLUSION: Our study suggested that JTW and its effective component coptisine 
could alleviate diabetes mellitus-related cognitive impairment, closely linked 
to the JAK2/STAT3 signaling pathway.

Copyright © 2024 The Author(s). Published by Elsevier GmbH.. All rights 
reserved.

DOI: 10.1016/j.phymed.2024.155954
PMID: 39178683 [Indexed for MEDLINE]

Conflict of interest statement: Declaration of competing interest All authors 
declare that there are no conflicts of interest.


3. Curr Top Med Chem. 2024;24(23):2013-2032. doi: 
10.2174/0115680266305274240723120426.

Coptis Chinensis Franch: Substance Basis, Mechanism of Action and Quality 
Control Standard Revealed Based on the Q-marker Concept and New Strategy of 
Systemic Pharmacology and Biosynthesis Research.

Zheng Y(1), Zhang M(1), Wu X(1), Tan R(1), Jiang H(1).

Author information:
(1)School of Life Science and Engineering, Southwest Jiaotong University, 
Chengdu, 613100, P.R. China.

Coptis chinensis Franch. (Ranunculaceae, Coptis), a traditional Chinese medicine 
(TCM) with thousands of years of clinical use history, also a natural medicine 
available in many countries, has wide pharmacological mechanisms and significant 
bioactivity according to its traditional efficacy combined with modern 
scientific research. The quality marker (Q-marker) of C. chinensis Franch. is 
predicted in this paper based on the chemical composition and pharmacological 
effects of the plant, as well as the current system pharmacology, plant 
relatedness, biosynthetic pathways and quantitative analysis of multi-components 
(QAMS). Natural medicine has the advantage of being multi-component, 
multi-pathway and multi-target. However, there are few reports on safety 
evaluation. This review predicts the Q-marker of C. chinensis, the safety and 
efficacy of C. chinensis is provided. Studies from 1975 to 2023 were reviewed 
from PubMed, Elsevier, ScienceDirect, Web of Science, SpringerLink, and Google 
Scholar. Alkaloids and organic acids are the two main component categories of 
Q-Markers. The specific alkaloids identified through predictive results include 
berberine, coptisine, palmatine, epiberberine, jatrorrhizine, columbamine, and 
berberrubine. Quinic acid and malic acid, due to their influence on the content 
of alkaloids and their ability to aid in identifying the active components of C. 
chinensis, are also considered Q-markers. The research strategy of "exploring 
chemical components, exploring pharmacological activities, constructing 
pharmacological mechanism network and locating biosynthetic pathways" was used 
to accurately screen the quality markers of C. chinensis in this review and 
summarise the quality evaluation methods and criteria. In addition, we updated 
the biosynthetic pathway of C. chinensis and refined the specific synthetic 
pathways of jatrorrhizine (quality markers) and epiberberine (quality markers). 
Finally, we summarised the quality evaluation methods of C. chinensis, which 
provide an important reference for resource evaluation and provide a key 
reference for the discovery of new functional chemical entities for natural 
medicines.

Copyright© Bentham Science Publishers; For any queries, please email at 
epub@benthamscience.net.

DOI: 10.2174/0115680266305274240723120426
PMID: 39136504 [Indexed for MEDLINE]


4. J Ethnopharmacol. 2024 Dec 5;335:118680. doi: 10.1016/j.jep.2024.118680. Epub 
2024 Aug 8.

Coptisine alleviates colitis through modulating gut microbiota and inhibiting 
TXNIP/NLRP3 inflammasome.

Li C(1), Deng L(2), Pu M(2), Ye X(3), Lu Q(4).

Author information:
(1)Department of Pharmacology, Zunyi Medical University, Zhuhai Campus, Zhuhai 
519041, PR China; Key Laboratory of Basic Pharmacology of Ministry of Education 
and Joint International Research Laboratory of Ethnomedicine of Ministry of 
Education, Zunyi Medical University, Zunyi 563000, PR China; Key Laboratory of 
Basic Pharmacology of Guizhou Province and School of Pharmacy, Zunyi Medical 
University, Zunyi 563000, PR China.
(2)Department of Pharmacology, Zunyi Medical University, Zhuhai Campus, Zhuhai 
519041, PR China.
(3)Department of Pharmaceutical Sciences, Zunyi Medical University, Zhuhai 
Campus, Zhuhai 519041, PR China.
(4)Department of Pharmaceutical Sciences, Zunyi Medical University, Zhuhai 
Campus, Zhuhai 519041, PR China. Electronic address: luqiang@zmu.edu.cn.

ETHNOPHARMACOLOGICAL RELEVANCE: Ulcerative colitis (UC) is a disease involving 
the enteric canal which is characterised by chronisch inflammatory reaction. 
Coptisine (COP), the distinctive component of Coptis chinensis Franch., is 
famous for its anti-inflammation, antioxidation, anti-bacteria, and anti-cancer. 
Earlier researches certified that COP is a prospective remedy for colitis, but 
the mechanism of colitis and the therapeutical target of COP are deficiently 
elucidated.
AIM OF THIS STUDY: In this follow-up study, we adopted dextran sulfate sodium 
(DSS)-elicited UC model to further elucidate the possible mechanism of COP on UC 
in mice.
MATERIALS AND METHODS: COP and the positive drug sulfasalazine (SASP) were 
administered by oral gavage in DSS-induced colitis mouse model. Oxidative 
stress, inflammatory cytokines, intestinal barrier permeability, protein 
expression of the TXNIP/NLRP3 inflammasome pathway and intestinal microbiome 
structure were assessed.
RESULTS: Among this investigation, our team discovered that COP could mitigate 
DSS-elicited UC in murines, with prominent amelioration in weight loss, disease 
activity index, intestinal permeability (serum diamine oxidase and D-lactate), 
contracted colonal length and histologic alterations. Furthermore, COP greatly 
lowered the generation of pro-inflammatory factors, malondialdehyde (MDA) 
activity and reactive oxygen species (ROS) level, while increased superoxide 
dismutase (SOD) activity in colonal tissues. Additionally, COP downmodulated the 
proteic expressions of thioredoxin-interacting protein (TXNIP), NOD-like 
receptor protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), 
caspase-1, IL-1β and IL-18. Enteric microbiome sequencing displayed that DSS and 
COP tremendously influenced the constitution and diversity of enteric microbes 
in DSS-elicited UC murines. Besides, COP elevated the abundance of probiotic 
bacteria Bacteroidota, Akkermansia_muciniphila and Bacteroides_acidifaciens, 
lowered the proportions of potential pathogenic bacteria, such as 
Lachnospiraceae, Acetatifactor_muris, Clostridium_XlVa, Alistipes and 
Oscillibacter, and reduced the ratio of Bacillota/Bacteroidota, which vastly 
helped to reverse the enteric microbiome to a balanceable condition. Alterations 
in these bacteria were strongly correlated with the colitis relative index.
CONCLUSION: The mechanism of COP against UC is connected with the suppression of 
TXNIP/NLRP3 inflammasome signalling pathway and the adjustment of the enteric 
microbiome profiles. The proofs offer new understandings upon the anti-UC 
function of COP, which might be a prospective candidate against UC.

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

DOI: 10.1016/j.jep.2024.118680
PMID: 39117021 [Indexed for MEDLINE]

Conflict of interest statement: Declaration of competing interest The authors 
declared that there was no conflict of interest.


5. Adv Sci (Weinh). 2024 Sep;11(35):e2401748. doi: 10.1002/advs.202401748. Epub 
2024 Jul 12.

Overcoming Cancer Persister Cells by Stabilizing the ATF4 Promoter G-quadruplex.

Xiao C(1), Li Y(1), Liu Y(1), Dong R(1), He X(1), Lin Q(1), Zang X(1), Wang 
K(1), Xia Y(1)(2), Kong L(1).

Author information:
(1)State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of 
Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, 
China Pharmaceutical University, Nanjing, 210009, China.
(2)Shenzhen Research Institute of China Pharmaceutical University, Shenzhen, 
518057, China.

Persister cells (PS) selected for anticancer therapy have been recognized as a 
significant contributor to the development of treatment-resistant malignancies. 
It is found that imposing glutamine restriction induces the generation of PS, 
which paradoxically bestows heightened resistance to glutamine restriction 
treatment by activating the integrated stress response and initiating 
the general control nonderepressible 2-activating transcription factor 
4-alanine, serine, cysteine-preferring transporter 2 (GCN2-ATF4-ASCT2) axis. 
Central to this phenomenon is the stress-induced ATF4 translational 
reprogramming. Unfortunately, directly targeting ATF4 protein has proven to be a 
formidable challenge because of its flat surface. Nonetheless, a G-quadruplex 
structure located within the promoter region of ATF4 (ATF4-G4) is uncovered and 
resolved, which functions as a transcriptional regulator and can be targeted by 
small molecules. The investigation identifies the natural compound coptisine 
(COP) as a potent binder that interacts with and stabilizes ATF4-G4. For the 
first time, the high-resolution structure of the COP-ATF4-G4 complex is 
determined. The formation of this stable complex disrupts the interaction 
between transcription factor AP-2 alpha (TFAP2A) and ATF4-G4, resulting in a 
substantial reduction in intracellular ATF4 levels and the eventual death of 
cancer cells. These seminal findings underscore the potential of targeting the 
ATF4-G4 structure to yield significant therapeutic advantages within the realm 
of persister cancer cells induced by glutamine-restricted therapy.

© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.

DOI: 10.1002/advs.202401748
PMCID: PMC11425212
PMID: 38994891 [Indexed for MEDLINE]

Conflict of interest statement: The authors declare no conflict of interest.