Metabolic dysfunction-associated steatotic liver disease (MASLD), as a liver phenotype of metabolic syndrome, has a global prevalence of up to 32.4%. Its pathogenesis involves complex pathological networks, including lipid metabolism disorders, oxidative stress, inflammation, and insulin resistance. Faced with the limitations of existing single-target drugs, curcumin, a natural polyphenolic compound, has demonstrated significant potential for the prevention and treatment of MASLD due to its multidimensional pharmacological activities, such as antioxidant, anti-inflammatory, metabolic regulation, and mitochondrial function repair. This article provides a systematic review of recent research on curcumin therapeutic mechanisms and clinical evidence in MASLD, with a focus on its antioxidant effect, improvement of mitochondrial function, anti-inflammatory effect, reduction of insulin resistance, and regulation of gut microbiota. It also examines the current efficacy and limitations of curcumin-based combination therapies and their derivatives in the treatment of MASLD. As research on MASLD progresses, curcumin shows great potential for therapeutic applications. Future studies should target long-term impacts, such as subclinical oxidative stress and epigenetic modifications. Furthermore, this article addresses persistent challenges such as curcumin's inherently low bioavailability and the lack of standardized dosing protocols, which should guide future clinical research efforts.

This study aims to investigate the phototoxic effects of imperatorin(IMO) and its potential mechanisms of inducing skin photodamage and cellular senescence. A phototoxicity model was established on the dorsal skin of SD rats, which were randomly divided into a control group, an IMO group(0.8 mg·cm~(-2)), a long-wave ultraviolet A(UVA) group(10 J·cm~(-2)), and an IMO + UVA group. The rats were continuously observed for 72 h, and Draize skin scores were assessed. Hematoxylin-eosin(HE) staining was used to observe histopathological changes, and Verhoeff-Van Gieson(VVG) staining was utilized to evaluate changes in dermal elastic and collagen fibers. Human dermal fibroblasts(HDF) were cultured in vitro and divided into control, IMO, UVA(1 J·cm~(-2)), and groups of IMO with low, medium, and high doses(1, 2.5, and 5 μg·mL~(-1)) + UVA. The CCK-8 assay was used to assess the cell viability. Transcriptomics by RNA-seq was used to analyze the changes in gene expression. Real-time quantitative PCR(RT-qPCR) was used to detect the mRNA expressions of the top 10 senescence-associated genes. Enzyme-linked immunosorbent assay(ELISA) was used to detect the levels of senescence-associated secretory phenotype(SASP) factors like matrix metalloproteinase-3(MMP-3), interleukin(IL)-6, and IL-8. Immunofluorescence was used to evaluate the senescence-associated heterochromatin foci(SAHF) markers like heterochromatin protein 1γ(HP1γ) and trimethylation of histone H3 at lysine 9(H3K9me3). Senescence-associated β-galactosidase(SA-β-gal) staining was performed to detect the senescent cells, and Western blot was used to detect the expression and localization of growth arrest and DNA damage-inducible alpha(GADD45A), G_2/M phase-specific cyclin B1(Cyclin B1), and cyclin-dependent kinase 1(CDK1) proteins. Flow cytometry was used to analyze the cell cycle. The siRNA was used to silence GADD45A gene to verify its function. In vivo results show that, compared to the control group, the IMO + UVA group has significantly higher skin damage scores, with stratum corneum loss, inflammatory cell infiltration, reduced collagen fiber density, and abnormal deposition of elastic fibers. In vitro results demonstrate that IMO + UVA significantly inhibits the cell viability of HDF(P<0.05). RNA-seq and RT-qPCR verifications indicate that IMO + UVA significantly upregulate the expressions of senescence-associated genes, with GADD45A gene showing the most significant change. The IMO + UVA group also shows significant increases in SASP factor secretion, SA-β-gal activity, SAHF formation, and the proportion of cells in the G_2/M phase(P<0.05). Western blot results demonstrate that IMO + UVA promote the expression of GADD45A protein and inhibit nuclear translocation of Cyclin B1, thereby reducing the kinase activity of the Cyclin B1-CDK1 complex. Silencing GADD45A gene effectively alleviates G_2/M phase arrest and cellular senescence phenotype. In summary, IMO in combination with UVA can induce photodamage to the skin and accelerate cellular senescence, and the mechanism may involve G_2/M phase arrest mediated by the activation of the GADD45A/Cyclin B1/CDK1 axis.

Medicinal plants with storage root expansion play essential roles in food supply, disease prevention, and therapeutic applications. Storage-root enlargement is a highly coordinated developmental process involving primary root specialization, secondary growth, and organ-specific differentiation. Recent studies have revealed that endogenous phytohormones, including auxin, cytokinin, gibberellin, abscisic acid, and jasmonic acid, regulate this process through interconnected signaling pathways that control cell division, cambial activity, and radial growth. Transcription factors such as the ARF, AUX/IAA, NAC, and PLT families function as central regulatory nodes that integrate hormonal and environmental signals. These regulatory networks modulate lignin deposition, carbohydrate metabolism, and secondary meristem activity. These coordinated processes ultimately drive structural remodeling and functional differentiation during root enlargement. Environmental factors, including temperature, CO2 concentration, nutrient availability, water status, and rhizosphere1830107 microbial communities, further influence these molecular pathways by reshaping hormone balance, assimilate allocation, and root developmental programs. Despite recent progress, the core regulatory modules and species-specific mechanisms underlying storage-root enlargement in medicinal plants remain poorly understood. This review synthesizes current knowledge on the hormonal, transcriptional, and environmental regulation of storage-root enlargement in medicinal plants and highlights future research directions to improve root yield, medicinal quality, and bioactive compound accumulation.

Although Zanthoxylum bungeanum essential oil is rich in bioactive compounds, its broader application is restricted by inherent volatility and oxidative instability. This study aimed to investigate how the degree of deacetylation (DD) modulates the interfacial interactions between deacetylated konjac glucomannan and soy protein isolate composite wall materials. The microcapsules exhibited the optimal performance at a DD of 27.44%, with the highest encapsulation efficiency of 79.75% ± 1.70%, the smallest emulsion droplet size of 0.99 ± 0.01 μm, and the highest storage modulus value. Structural characterization and molecular docking (binding energy of -7.0 for the optimal formation) indicated that deacetylation to this degree reduced steric hindrance, thus promoting the formation of a physical network driven by hydrogen bonding and hydrophobic interactions. The optimized matrix significantly improved sanshool stability over a 33-day storage period and enabled targeted intestinal release, with a release rate 42% higher than that of single-protein microcapsules. This study establishes a structural basis for designing polysaccharide-protein composite wall materials to encapsulate and deliver volatile bioactive oils.

Hydroxy-alpha-sanshool (HAS) constitutes the foundation for Zanthoxylum armatum DC. (ZADC)'s pungency, pharmacological activity, and toxicity. Recent studies have suggested that HAS may have toxic effects on multiple organs. In earlier research, we also found that HAS may have renal toxicity, but the site of its toxic effect and the active mechanism remain unclear. In our study, we used C57BL/6 J mice and HK-2 cells to prove that HAS activated the IKK beta-mediated NF-kappa B signaling pathway, induced an increase in NGAL protein expression, and the excessive secretion of NGAL further induced an increase in intracellular Fe ion levels. This abnormal increase in intracellular Fe ions elevated ROS and MDA while reducing GSH and SOD levels, and contributed to ferroptosis in renal tubular epithelial cells, resulting in kidney damage. Further treatment with the IKK beta inhibitor IMD 0354 and lentiviral transfection of HK-2 cells confirmed our findings. This research offers new perspectives on the mechanism of HAS-caused kidney damage and strengthens the theoretical basis for HAS application in food and drug industries.

AIM OF THE STUDY:To comprehensively explore the impact of Zanthoxylum armatum DC. (ZADC) on liver injury and disclose its mechanistic underpinnings, thereby laying a scientific foundation for the secure application of ZADC. MATERIALS AND METHODS:The ethyl acetate extract of ZADC (ZADC-EA) was subjected to analysis via Q-Orbitrap LC-MS/MS. The damage effect of ZADC-EA was appraised by determining cell viability, liver function index, and inflammation levels. Western blot, RT-qPCR, flow cytometry, and immunofluorescence were employed to detect DNA double-strand breaks (DSBs) and cellular senescence, with the aim of unraveling the mechanism of liver injury instigated by ZADC-EA. RESULTS:Chemical composition analysis unveiled the presence of flavonoids, organic acids, and coumarins in ZADC-EA. Exposure to ZADC-EA caused a decrease in the viability of HepG2 cells and an elevation in the levels of liver injury markers and inflammatory factors. Moreover, treatment with ZADC-EA triggered DSBs and activated the p53-p21 pathway, culminating in the induction of cellular senescence. CONCLUSIONS:The research provides a novel perspective for the safety assessment of ZADC. It has been demonstrated that ZADC-EA can precipitate DSBs and induce cellular senescence by activating the p53-p21 signaling pathway, thereby giving rise to liver damage.

BackgroundAs a resource with a variety of medicinal and edible values, Zanthoxylum bungeanum Maxim has been found to improve high-fat diet-induced metabolic-associated fatty liver disease (MAFLD).Aim of the studyThe aim of this study was to predict the main active metabolites in Z. bungeanum Maxim. Based on network analysis, and to explore and validate their potential mechanisms of action through lipidomics and transcriptomic techniques.Materials and MethodsMAFLD mouse model and cell model were established to evaluate the effect of active components in Z. bungeanum Maxim. on MAFLD. Serum biochemical indexes, pathological staining observation, lipid group and transcriptome were used to verify the mechanism of action of active components in Z. bungeanum Maxim. on MAFLD.ResultsQuercetin can regulate the liver lipid metabolites of MAFLD mice through the Glycerophospholipid metabolic pathway, thereby improving liver lipid accumulation and liver injury. At the same time, quercetin can also improve MAFLD by reducing oleic acid-induced lipid accumulation in HepG2 cells, and inhibit ferroptosis through the p38 MAPK/ERK signaling pathway, thereby alleviating the progression of MAFLD.ConclusionQuercetin isolated from Z. bungeanum Maxim. has ameliorative effects on MAFLD, probably mainly by affecting lipid metabolic pathways and MAPK signaling pathways.

Drug-induced liver injury (DILI) poses critical challenges in preclinical drug development and is a primary reason for candidate drug attrition. The incidence of DILI has risen in recent years. While immune-related genes (IRGs) are crucial in immune infiltration, their expression and regulatory mechanisms in tolvaptan-induced DILI remain largely uncharacterized. RNA sequencing data related to DILI and associated clinical data were sourced from the Gene Expression Omnibus (GEO), and IRGs were obtained from the ImmPort database. Differentially expressed genes (DEGs) from DILI and IRGs were intersected to identify differentially expressed immune-related genes (DEIRGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to elucidate the biological functions of DEIRGs. In addition, a protein-protein interaction (PPI) network of DEIRGs was constructed. Immunocytes and immune regulation analyses were conducted using the CIBERSORT tool. Receiver operating characteristic (ROC) curves were constructed to assess the diagnostic accuracy of individual DEIRGs. Networks of transcription factor and microRNA co-regulation were constructed using the NetworkAnalyst database. The expression of DEIRGs in DILI samples was quantified with RT-qPCR. From GSE99878, 204 DEGs were identified, with 23 matching IRGs exhibiting significant expression differences in 17 DEIRGs. The ROC curve analysis suggested satisfactory diagnostic values for six DEIRGs. The potential gene regulatory network comprised 214 microRNAs, 257 transcription factors, and 23 DEIRGs. Finally, RT-qPCR confirmed the expression levels of nine DEIRGs, aligning with public database results. The study revealed numerous immune-related biomarkers, verifying expression in five pivotal genes (ICAM1, CXCL10, IGF1, CX3CL1, and EGFR) and highlighting four genes with notable diagnostic potential (TNFAIP3, BDNF, NR1D2, and PPARA). Additionally, it explored the roles of key biomarkers in inflammatory responses, relevant signaling pathways, and interaction networks, offering new insights into DILI diagnosis, mechanistic understanding, and treatment strategies.

Globally, liver disease has emerged as a significant contributor to morbidity and mortality. The onset and progression of liver diseases are intricately linked to the modulation of autophagy, a highly conserved cellular process. Autophagy involves the systematic degradation and recycling of intracellular components, thereby maintaining cellular homeostasis. As a dynamic regulatory mechanism, autophagy plays a crucial bidirectional role in the pathogenesis of liver diseases. Natural products derived from Traditional Chinese Medicine (TCM) are abundant in nature and possess unique chemical structures and biological properties, which confer a diverse range of pharmacological activities, as demonstrated by extensive research. In recent years, pharmacological studies have revealed an additional potential function of these natural products: the regulation of autophagy. Investigating the relationship between liver diseases and autophagy can enhance our understanding of the molecular mechanisms underlying liver disease pathogenesis, providing a theoretical foundation for the development of novel therapeutic strategies targeting autophagy. This review comprehensively synthesizes current knowledge on the roles of TCM-derived natural products in liver diseases and autophagy. It further explores the mechanisms by which these natural products modulate autophagy in the context of liver diseases, including key signaling pathways such as AMPK, PI3K/Akt/mTOR, and ROS, as well as critical molecular targets like p62 and Beclin-1. By summarizing and analyzing the regulatory effects of natural products on liver diseases through autophagy, this review aims to inspire innovative approaches for the development of autophagy-based therapeutics for liver diseases.

The endoplasmic reticulum (ER) is a crucial cellular organelle involved in protein synthesis, folding, modification, and transport. Exposure to internal and external stressors can induce endoplasmic reticulum stress (ERS), leading to abnormal protein folding and ER malfunction. This stress can disrupt lipid synthesis, metabolism, and transport processes. Fatty acid oxidation is the primary energy source for the renal system. When energy intake exceeds the storage capacity of adipose tissue, lipids accumulate abnormally in non-adipose tissues, including kidneys, liver, and pancreas. Lipids accumulate in the kidneys of nearly all cell types, including thylakoid membranous, pedunculated, and proximal renal tubular epithelial cells. Intracellular free fatty acids can significantly disrupt renal lipid metabolism, contributing to ischemia-reperfusion acute kidney injury, diabetic nephropathy, renal fibrosis, and lupus nephritis. Consequently, this study delineated the primary signaling pathways and mechanisms of the ERS-induced unfolded protein response, explored the mechanistic link between ERS and lipid metabolism, and elucidated its role in renal lipid metabolism. This study aimed to offer new perspectives on managing and treating renal disorders.

Introduction:Growing evidence suggests that gut microbiota may influence renal function via the gut-kidney axis. This study assessed gut microbial composition, metabolic indicators, and inflammatory markers in elderly individuals with varying degrees of hypertensive kidney involvement. Methods:Seventy participants were stratified into three groups: healthy controls, hypertensive without renal impairment, and hypertensive with chronic kidney disease. Results:The chronic kidney disease group exhibited elevated serum urea and creatinine and reduced eGFR, along with increased levels of KIM-1, NGAL, IL-18, TNF-α, IL-6, NF-κB, and FMO3. Urinary TMAO was significantly decreased in both hypertensive groups, while serum TMAO remained unchanged. Although α- and β-diversity indices were comparable across groups, compositional shifts were noted, including higher relative abundance of Escherichia-Shigella and Haemophilus and lower levels of Faecalibacterium. Correlation analyses revealed associations between specific genera and host metabolic or inflammatory markers, such as a positive correlation between Enterobacter and urinary TMAO, and inverse correlations between Veillonella and both eGFR and urinary TMAO. Functional prediction indicated increased amino acid metabolism in the chronic kidney disease group. Discussion:These findings suggest interrelated patterns involving gut microbial composition, toxin handling, and inflammatory status in elderly hypertensive individuals, supporting further investigation into microbiota-associated biomarkers within the framework of the gut-kidney axis.

High-sugar foods may form an aldehyde compound called 5-hydroxymethylfurfural (5-HMF) during heating or preservation. This kind of material has been shown to be nephrotoxic, the exact mechanism causing this toxic impact is yet unknown. This study determined that lipotoxicity may be the key to the renal injury caused by 5HMF, and its mechanistic mechanism of action may be related to endoplasmic reticulum stress (ERS). The results of in vivo experiments showed that mice given 5-HMF treatment included renal tubular luminal cell necrosis and glomerular atrophy, a large number of tubular degeneration. In vivo and in vitro experiments showed that total cholesterol (TC), triglyceride (TG), and low density lipoprotein cholesterol (LDL-C) levels were significantly elevated in the 5-HMF group, while high density lipoprotein cholesterol (HDL-C) levels were decreased. Inspired by this result, further studies revealed that the endoplasmic reticulum lumen in the 5-HMF-treated group showed different degrees of dilatation, and the levels of ERS-related genes GRP78, PERK, p-eIF2 alpha/eIF2 alpha, and CHOP, as well as the lipid synthesis-related genes SREBP1-c, ACC, and FASN, were elevated, and the level of the lipolytic gene CPT1C was decreased. Stimulation of PERK using GSK2606414 inhibitor resulted in decreased expression of both ERS and lipid synthesis-related genes and increased expression of lipolytic genes. This provides a theoretical reference for the safety evaluation of 5-HMF and suggests that targeting and regulating the ERS pathway is a new strategy to combat thermally processed food-related nephrotoxicity.

The identification of functional brown adipose tissue (BAT) and beige adipose tissue with significant thermogenic capabilities in adults has opened new avenues in the battle against obesity and its associated comorbidities.However, although obesity can be alleviated through strategies such as increasing physical activity, improving diet, and drug intervention, these methods all have inherent limitations, such as low compliance and obvious side effects. Consequently, there is an urgent need to investigate novel and effective methods for combating obesity. With ongoing advancements in stem cell technology, stem cell therapy has emerged as a promising strategy. Recent studies have demonstrated that certain pluripotent stem cells can differentiate into BAT under specific conditions and, when transplanted into mice, can elevate the animals’ body temperature and metabolic rate. This suggests that pluripotent stem cells may represent a viable therapeutic option for addressing metabolic disorders such as obesity and diabetes. Owing to their distinct advantages, pluripotent stem cells have become the preferred choice for stem cell therapy in the treatment of obesity. This article will mainly focus on the differentiation process of pluripotent stem cells into brown adipocytes, as well as the application of gene editing technology in this field.

Astaxanthin (AST), a ketocarotenoid, is prevalent in aquatic life forms. AST has a variety of health-promoting effects, such as anti-oxidation, anti-cancer, eye protection, anti-inflammatory, immune regulation, skin care, anti-diabetes, neuroprotection, etc. It holds significant potential for applications in healthcare products, food additives, pharmaceuticals, cosmetics, and aquaculture. The production capacity of AST limits its wide application to a certain extent. The instability and safety risks associated with the chemical synthesis of AST have led to increased interest in its biosynthetic pathway. In this paper, the synthesis pathway, biological activity, and application prospects of AST were reviewed. To enhance the market accessibility of AST, investigating innovative synthesis techniques and its emergent biological effects is crucial.

Safflower (Carthamus tinctorius L.), also known as Honghua, blueflower, or prickly safflower, is a medicinal herb effective in promoting blood circulation, dredging meridians, eliminating blood stasis, and relieving pain. Safflower contains complex chemical components, including flavonoids, alkaloids, organic acids, pigments, etc. Among them, flavonoids such as chalcone compounds, quercetin, rutin, and kaempferol serve as the material basis for the pharmacological effects of safflower. Flavonoids in safflower exhibit diverse biological activities, including cardiovascular and cerebrovascular protection, antioxidant, neuroprotective, antitumor, anti-inflammatory, and immunomodulatory effects. Additionally, they show great potential in gynecological diseases, food production, and other fields. With extensive research by scholars on the active mechanisms and targets of safflower flavonoids, their application prospects in the medical field have been found to be extremely broad. This review used keywords such as “Carthamus tinctorius L.,” “safflower,” “flavonoids,” “therapeutic effect,” “mechanism,” “application,” etc., to search relevant studies up to January 2025 in multiple internationally recognized databases (including PubMed, Web of Science, CNKI, Wan fang, Sci Finder, Elsevier, cnipa), finally including 143 high-quality studies. Representative images were drawn using BioRender and ChemDraw software to focus on presenting the action mechanisms and targets of safflower flavonoids. This article systematically reviews the pharmacological effects of safflower flavonoids and their applications in various fields in recent years, aiming to provide theoretical guidance and scientific basis for the comprehensive utilization of safflower resources and further research.

Background Zanthoxylum armatum DC. (ZADC) is a novel food raw material resource, offering both edible and medicinal properties. Recent research has unveiled the toxic nature of ZADC, particularly its close association with the nervous system. In a prior study, we observed that administering methanol extract of Zanthoxylum armatum DC. (MZADC) to rats via gavage at a dose of 1.038 g/kg resulted in various neurotoxicity symptoms, including excessive salivation, reduced mobility, unsteady gait, muscle twitching, and altered respiratory rates. Materials and methods We conducted cell-based research to assess the safety of ZADC and elucidate its potential toxic mechanism. In addition, we used experimental methods such as Cell Counting Kit-8, Western blot, and Flow cytometry to detect cytotoxicity in SH-SY5Y cells after intervention with MZADC. Results Following exposure of SY-SY5Y cells with MZADC, a substantial decline in cell viability was observed, accompanied by a concentration-dependent increase in intracellular reactive oxygen species (ROS) levels. Additionally, MZADC induced cellular oxidative stress, leading to elevated malonic dialdehyde (MDA) and superoxide dismutase (SOD) concentrations while decreasing glutathione (GSH) levels. Furthermore, MZADC induced apoptosis at varying doses (20, 40, and 60 μg/mL), and this effect was associated with increased Caspase-3, Bax expressions, and reduced Bcl2 and Bcl2/Bax expressions. In addition, the investigation revealed that MZADC induced autophagy inhibition in SH-SY5Y cells by activating the mTOR signaling pathway, resulting in a decrease in LC3II/LCI and Beclin-1, while increasing p-mTOR/mTOR, p62. Conclusion Consequently, this study suggests that MZADC triggers the mTOR pathway through oxidative stress in SH-SY5Y cells, ultimately leading to apoptosis. Understanding the toxicity mechanisms associated with ZADC can offer a valuable theoretical and experimental basis for its development and utilization.

BACKGROUND:With the increasing awareness of the safety of traditional Chinese medicine and food, as well as in-depth studies on the pharmacological activity and toxicity of Zanthoxylum armatum DC. (ZADC), it has been found that ZADC is hepatotoxic. However, the toxic substance basis and mechanism of action have not been fully elucidated. Hydroxy-α-sanshool (HAS) belongs to an amide compound in the fruits of ZADC, which may be hepatotoxic. However, the specific effects of HAS, including liver toxicity, are unclear. PURPOSE:The objectives of this research was to determine how HAS affects hepatic lipid metabolism, identify the mechanism underlying the accumulation of liver lipids by HAS, and offer assurances on the safe administration of HAS. METHODS:An in vivo experiment was performed by gavaging C57 BL/6 J mice with various dosages of HAS (5, 10, and 20 mg/kg). Biochemical indexes were measured, and histological analysis was performed to evaluate HAS hepatotoxicity. Hepatic lipid levels were determined using lipid indices and oil red O (ORO) staining. Intracellular lipid content were determined by biochemical analyses and ORO staining after treating HepG2 cells with different concentrations of HAS in vitro. Mitochondrial membrane potential, respiratory chain complex enzymes, and ATP levels were assessed by fluorescence labeling of mitochondria. The levels of proteins involved in lipogenesis and catabolism were determined using Western blotting. RESULTS:Mice in the HAS group had elevated alanine and aspartate aminotransferase blood levels as well as increased liver index compared with the controls. The pathological findings showed hepatocellular necrosis. Serum and liver levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol levels were increased, whereas high-density lipoprotein cholesterol levels decreased. The ORO staining findings demonstrated elevated liver lipid levels. In vitro experiments demonstrated a notable elevation in triglyceride and total cholesterol levels in the HAS group. ATP, respiratory chain complex enzyme gene expression, mitochondrial membrane potential, and mitochondrial number were reduced in the HAS group. The levels of lipid synthesis-associated proteins (ACC, FASN, and SREBP-1c) were increased, and lipid catabolism-associated protein levels (PPARα and CPT1) and the p-AMPK/AMPK ratio were decreased in vivo and in vitro. CONCLUSION:HAS has hepatotoxic effects, which can induce fatty acid synthesis and mitochondrial function damage by inhibiting the AMPK signaling pathway, resulting in aberrant lipid increases.

Alkaloids are naturally occurring compounds with complex structures found in natural plants. To further improve the understanding of plant alkaloids, this review focuses on the classification, toxicity and mechanisms of action, providing insight into the occurrence of alkaloid-poisoning events and guiding the safe use of alkaloids in food, supplements and clinical applications. Based on their chemical structure, alkaloids can be divided into organic amines, diterpenoids, pyridines, isoquinolines, indoles, pyrrolidines, steroids, imidazoles and purines. The mechanisms of toxicity of alkaloids, including neurotoxicity, hepatoxicity, nephrotoxicity, cardiotoxicity and cytotoxicity, have also been reviewed. Some cases of alkaloid poisoning have been introduced when used as food or clinically, including accidental food poisoning, excessive consumption, and poisoning caused by the improper use of alkaloids in a clinical setting, and the importance of safety evaluation was illustrated. This review summarizes the toxicity and mechanism of action of alkaloids and provides evidence for the need for the safe use of alkaloids in food, supplements and clinical applications.