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Natural Compounds: Impact on Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 179

Special Issue Editor


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Guest Editor
School of Pharmacy and Pharmaceutical Sciences, Ulster University, Coleraine BT52 1SA, UK
Interests: natural product pharmacology; psychopharmacology

Special Issue Information

Dear Colleagues,

The use of natural products serves as a principal therapeutic approach for a substantial proportion of the global population. Bioactive compounds derived from these sources fulfil a dual role: modulating physiological processes to produce therapeutic or toxic effects and providing a foundational scaffold for the development of novel pharmacological agents. Recent advancements have significantly enhanced our ability to identify, characterize, and mechanistically understand the active constituents within natural products. These innovations have also facilitated the exploration of novel chemical pharmacophores with potential therapeutic applications.

This Special Issue aims to showcase recent research and methodological innovations that highlight the role of naturally derived compounds in both pathological and physiological contexts. We welcome original research articles and reviews that examine the therapeutic efficacy, safety profiles, and mechanistic pathways of natural products in the management of specific health conditions. Submissions addressing efficacy, toxicity, and their underlying mechanisms are especially encouraged.

Dr. Charles Benneh
Guest Editor

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Keywords

  • natural compounds
  • bioactive compounds
  • efficacy
  • toxicity
  • mechanism
  • compound isolation
  • chemical characterisation

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Published Papers (1 paper)

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Research

22 pages, 4261 KB  
Article
Nephrotoxicity of Evodiamine in Mice: Mechanistic Insights from Integrated Network Toxicology and Transcriptomic Profiling
by Xuehua Zhang, Yue Pan, Yuanyuan Xiao, Ziyan Wu, Huilan Yang, Yanjun Liu, Yan Wang, Tianqi Chen and Wenchao Tang
Int. J. Mol. Sci. 2026, 27(9), 3793; https://doi.org/10.3390/ijms27093793 - 24 Apr 2026
Abstract
The aim of this study was to evaluate the nephrotoxicity and molecular mechanism of Evodiamine (EVO). We combined RNA sequencing (RNA-seq) and network toxicology (NT) screening of potential target genes and signaling pathways, used molecular docking to validate core targets, and detected the [...] Read more.
The aim of this study was to evaluate the nephrotoxicity and molecular mechanism of Evodiamine (EVO). We combined RNA sequencing (RNA-seq) and network toxicology (NT) screening of potential target genes and signaling pathways, used molecular docking to validate core targets, and detected the mRNA expression of the key genes through quantitative real-time polymerase chain reaction (qRT-PCR). After exposure to EVO, body weight of mice decreased significantly, and the levels of renal index, Blood Urea Nitrogen (BUN) and Creatinine (Cr) were significantly increased, with varying degrees of pathological damage to the kidneys. NT identified 125 intersecting targets of EVO exposure related to kidney injury, including AKT1, TNF, TP53, etc. Among the 2888 differentially expressed genes obtained from RNA-seq, 504 genes were up-regulated and 2384 genes were down-regulated. By integrating NT and RNA-seq, 24 intersecting targets were identified. Among them, TRPV1, NOS3, HSP90AA1, and PPARG were selected for molecular docking validation. The results indicated that EVO had the highest affinity for PPARG (−8.07 kcal/mol). The qRT-PCR results indicated that the expression of the Pparg and Hsp90aa1 genes was significantly down-regulated, and the expression of the Nos3 and Trpv1 genes was significantly up-regulated. Immunohistochemistry further confirmed that EVO inhibited the expression of HSP90AA1 and PPARG, while enhancing that of TRPV1 and NOS3. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis suggested that EVO-induced nephrotoxicity is related to signaling pathways such as inflammatory mediator regulation of TRP channels, the PPAR signaling pathway, and the Apelin signaling pathway. In summary, the nephrotoxic effect of EVO may be related to the inhibition of the PPARG signaling pathway, the activation of the TRPV1 channel, the reduction in HSP90AA1 expression, and the imbalance of the Apelin-NOS3 pathway. This study provides a theoretical reference for clarifying the potential mechanism of renal injury caused by EVO and guiding its safe use. Full article
(This article belongs to the Special Issue Natural Compounds: Impact on Health and Diseases)
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