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Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention

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A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Natural Products".

Deadline for manuscript submissions: 25 September 2026 | Viewed by 22563

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Dr. Lucas Fornari Laurindo

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Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília 17525-902, SP, Brazil
Interests: medicinal plants; bioactive compounds; phytochemicals; phytochemistry; cancer; metabolism; metabolic disorders; pharmacology; inflammation; oxidative stress; cardiovascular diseases; neurodegenerative diseases
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Dr. Sandra Barbalho

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Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília 17525-902, SP, Brazil
Interests: inflammatory diseases; cardiovascular diseases; neurodegenerative diseases; inflammation; medicinal plants; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We warmly welcome you to contribute to our Special Issue. This issue delves into targeting cancer and metabolic diseases with bioactive compounds derived from medicinal plants, advocating for tumor and metabolic disorders, including diabetes, dyslipidemia, obesity, MAFLD, and others, as well as prevention and intervention using these naturally derived remedies. Cancer is a complex and pervasive disease, representing a global health challenge. The disease characterizes the abnormal and uncontrolled proliferation of cells. Often, cancer invades surrounding tissues and metastasizes distant organs. Since cancer is heterogenous and adaptable, there remains a threat due to the limitations of conventional therapies, including drug resistance, severe side effects, and variability in efficacy across different cancer types and individual patterns, resulting in the need for novel therapeutic agents to more precisely target cancer cells or enhance the effectiveness of existing treatments, ultimately minimizing adverse events. On the other hand, metabolic diseases are non-communicable disorders that predispose individuals to an increased mortality rate. Metabolic diseases are also heterogeneous and depend on several factors, such as dietary patterns. In these scenarios, bioactive compounds from medicinal plants emerge as a candidate strategy. They are more cost-effective, present minimal side effects, possess many anticancer activities, and are primarily anti-inflammatory, antioxidant, antidiabetic, hepatoprotective, and antigenotoxic. In addition, they have been used since ancient times, and their effectiveness against the diseases of today’s world must be widely tested. Therefore, this Special Issue aims to publish high-quality research and review articles to elucidate bioactive compounds' anticancer and metabolic-enhancing potential from medicinal plants, advocating for translational research addressing cancer and metabolic disorders prevention and intervention. Synergistic studies between plant compounds and synthetic chemotherapeutic drugs are also welcome regarding cancer therapy. Studies on phytochemicals' antioxidant and anti-inflammatory effects against cancerous cell lineages can also be submitted.

We appreciate your interest in our Special Issue and look forward to receiving your papers. Your contributions will make this project a success!

Dr. Lucas Fornari Laurindo
Dr. Sandra Barbalho
Guest Editors

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Keywords

cancer
metastasis
tumor growth
tumor spread
bioactive compounds
phytochemicals
medicinal plants
phytochemistry
cancer prevention
cancer intervention
metabolic diseases
metabolism
diabetes
MAFLD
dyslipidemia

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Published Papers (9 papers)

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25 pages, 5532 KB

Open AccessArticle

Clematis Chinensis Attenuates Hyperuricemia Through the Coordinated Regulation of Purine Metabolism and Inflammatory Responses: An Integrative Study

by Ze Fu, Hao Ju, Zi-Hao Chen, Yan-Chao Wu and Hui-Jing Li

Pharmaceuticals 2026, 19(6), 830; https://doi.org/10.3390/ph19060830 - 26 May 2026

Viewed by 92

Abstract

Background/Objectives: Hyperuricemia is a metabolic disorder characterized by renal dysfunction and systemic inflammation. While Clematis chinensis Osbeck is traditionally used for gout-related conditions, its chemical basis and precise mechanisms remain poorly understood. This study aimed to characterize the bioactive fraction (CWE-60EF) and elucidate its multi-target regulatory mechanisms against hyperuricemia. Methods: Qualitative and quantitative chemical profiling of CWE-60EF was performed using high-resolution LC-MS/MS. Its anti-hyperuricemic activity was validated using in vitro xanthine oxidase (XOD) inhibition, a zebrafish model, and HK-2 cell injury models. Mechanisms were explored through an integrated approach combining bioinformatics, Mendelian randomization (MR), and molecular docking. Results: A total of 50 compounds, primarily alkaloids and flavonoids (e.g., magnoflorine and phloretin), were characterized in CWE-60EF, and major marker compounds were quantitatively standardized. The fraction significantly inhibited XOD activity and rescued hyperuricemia-associated phenotypes in zebrafish. In HK-2 cells, CWE-60EF suppressed adenosine- and urate-induced cellular injury and the transcriptional expression of pro-inflammatory cytokines (IL-6 and IL-1β). MR analysis provided genetic evidence supporting IL-6 as a causal mediator of gout risk. Integrative analysis revealed that the protective effects of CWE-60EF are mediated through the coordinated regulation of purine metabolism, inflammatory cascades, and urate transporters (URAT1/GLUT9). Conclusions: This study demonstrates that CWE-60EF is a quantitatively standardized bioactive fraction that exerts anti-hyperuricemic, renoprotective, and anti-inflammatory effects by modulating uric acid metabolism and inflammation. By integrating genetic causality with phytochemical validation, our findings provide a novel mechanistic foundation for the traditional application of C. chinensis in hyperuricemic disorders. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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28 pages, 7799 KB

Open AccessArticle

Discovery of Benzophenanthridine Alkaloids from Zanthoxylum nitidum That Target the MDM2–p53 Axis in NSCLC

by Nguyen Manh Cuong, Elizaveta Fefilova, Vu Thanh Loc, Natalia Karpova, Nguyen Xuan Ha, Alexandra Daks, Nguyen Viet Ha, Tran Thu Huong, Sergey Parfenyev, Alexander Nazarov, Oleg Semenov, Yulia Gnennaya, Olga Fedorova, Nickolai A. Barlev and Oleg Shuvalov

Pharmaceuticals 2026, 19(6), 814; https://doi.org/10.3390/ph19060814 - 22 May 2026

Viewed by 193

Abstract

Background/Objectives: Non-small cell lung cancer (NSCLC) accounts for about 85% of lung cancers and is a leading cause of cancer-related deaths worldwide. Pharmacological targeting of the p53–MDM2 interaction to activate wild-type p53 is a promising strategy for treating NSCLC that retain functional p53 (approximately 50% of all cases). Methods: We screened 33 ethnomedicinal Vietnamese plant extracts for their anticancer effects using p53-expressing and p53-null NSCLC cell models, as well as two non-cancerous cell lines for control. We used an array of different experimental approaches including NMR spectroscopy; molecular docking; an MTT test; cell cycle analysis; apoptosis analysis; wound healing, migration, and invasion assays; Real-Time PCR; immunoblotting; and Seahorse energy profiling to characterize and study the effects of these bioactive compounds on NSCLC cells. Results: Ethanol extract of Zanthoxylum nitidum stems and twigs demonstrated potent and selective activity by inducing p53-dependent cell cycle arrest and apoptosis. Phytochemical analysis identified several benzophenanthridine alkaloids as active constituents. Molecular docking revealed their strong in silico binding to MDM2. Notably, nitidine was the most promising compound among the molecules tested. Unlike nutlin, but similar to SP141 (two well-known MDM2 inhibitors), nitidine strongly stabilized p53 while concomitantly attenuating MDM2 at the protein level. Surprisingly, this effect was p53-independent. Additionally, nitidine suppressed the EMT master regulator Snail, and hence disrupted cellular bioenergetics and inhibited migration and invasion of NSCLC cells. Conclusions: Our findings identify Z. nitidum and nitidine as promising sources for developing novel MDM2-targeting therapeutics against NSCLC irrespective of the p53 status. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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12 pages, 5778 KB

Open AccessArticle

Sodium Rutin Ameliorates Non-Alcoholic Fatty Liver Disease and Alleviates Insulin Resistance by Promoting Lipophagy

by Xue Zhang, Shuoshuo Li, Ping Zhang, Chenggang Zhang and Zengqiang Yuan

Pharmaceuticals 2026, 19(4), 604; https://doi.org/10.3390/ph19040604 - 9 Apr 2026

Viewed by 569

Abstract

Background/Objectives: Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder for which there are limited pharmacotherapies. Sodium rutin (NaR), a soluble flavonoid derivative, has shown beneficial metabolic effects, but its role in NAFLD remains unclear. This study investigates whether NaR ameliorates high-fat diet (HFD)-induced NAFLD and insulin resistance through promoting hepatic lipophagy. Methods: Male mice aged 8 weeks old were fed a HFD for 12 weeks with/without NaR supplementation. Body weight was measured every week. After 12 weeks of treatment, GTT and ITT were performed to assess insulin resistance. Then, the tissues were collected and hepatic histology, serum biochemistry, and markers of autophagy and senescence were assessed. Results: NaR treatment significantly attenuated HFD-induced weight gain, reduced visceral fat and liver weights, and ameliorated hepatic steatosis and vacuolization. NaR improved serum lipid profiles; lowered alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase levels; and reduced hepatic cellular senescence. NaR enhanced hepatic autophagy, evidenced by decreased p62 levels, increased LC3-II/LC3-I ratio, and enhanced colocalization of lipid droplets with LC3 and LAMP1 in vivo and in vitro. These changes were accompanied by improved glucose tolerance and insulin sensitivity. Conclusions: NaR effectively alleviates HFD-induced NAFLD and insulin resistance by activating hepatic lipophagy. These findings support NaR as a promising multi-targeted therapeutic candidate for NAFLD. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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19 pages, 8134 KB

Open AccessArticle

Phytochemical Analysis and Anticancer Activity of Salvia chinensis Benth in Colorectal Cancer: An Integrated Transcriptomic and Bioinformatic Study

by Long-Zhu Li, Xin-Yue Li, Zi-Yuan Wang, Tian-Qi Ma, Yan-Chao Wu and Hui-Jing Li

Pharmaceuticals 2026, 19(4), 569; https://doi.org/10.3390/ph19040569 - 2 Apr 2026

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Abstract

Background/Objectives: Salvia chinensis Benth (SJC), as a traditional medicinal plant, has garnered significant attention for its extensive pharmacological activities. However, a systematic investigation of its comprehensive chemical profile and the underlying mechanisms in colorectal cancer (CRC) remains to be elucidated. This study aims to elucidate the active compounds and targets responsible for the anti-colorectal cancer effects of the aqueous extract of SJC. Methods: An integrated strategy was employed. The chemical profile of the SJC aqueous extract was analyzed by UPLC-MS/MS. Its anticancer activities, including effects on cell proliferation, migration, and apoptosis, were evaluated using the HCT-116 CRC cell line. An integrated transcriptomic and bioinformatic approach, followed by protein–protein interaction (PPI) network analysis, was used to identify key molecular pathways and targets. Finally, molecular docking and cellular assays were performed to screen for potential bioactive compounds. Results: A total of 60 natural compounds were tentatively identified in SJC. SJC inhibited the proliferation, migration, and invasion of HCT-116 colorectal cancer cells. Through combined transcriptomic and bioinformatic analysis, four candidate key genes were initially identified. Further PPI network analysis prioritized CXCL8 as a key candidate among the four candidate targets. Molecular docking against CXCL8, together with subsequent cellular experiments, validated naringenin as a potential bioactive constituent contributing to the anti-CRC activity of SJC. Conclusions: This study provides a comprehensive chemical profile of SJC and offers significant insights into its potential anticancer mechanisms in CRC by identifying candidate targets and a potential bioactive constituent. While these findings are preliminary and require further experimental validation through additional CRC cell lines and in vivo models, they establish a solid foundation for future research into the therapeutic applications of SJC for colorectal cancer. These planned studies will help to further elucidate the underlying mechanisms and assess the translational potential of SJC. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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21 pages, 5853 KB

Open AccessArticle

Systematic Investigation of Tumor Immune Microenvironment Modulation by Cynomorium songaricum Against Breast Cancer Through Integrated Chemomics, Network Pharmacology and Molecular Docking

by Ze-An Mao, Mei-Ling Zhang, Zi-Yi An and Wei-Lin Jin

Pharmaceuticals 2026, 19(2), 314; https://doi.org/10.3390/ph19020314 - 13 Feb 2026

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Abstract

Background/Objectives: Breast cancer remains a leading cause of cancer-related mortality in women, with therapeutic resistance frequently arising from tumor heterogeneity and an immunosuppressive tumor immune microenvironment (TIME). While Cynomorium songaricum Rupr. (CS) has been used traditionally in Chinese medicine and exhibits preliminary anti-tumor activity, its bioactive constituents and precise mechanisms against breast cancer remain to be elucidated. Methods: The chemical constituents of CS were systematically profiled using ultra-high-performance liquid chromatography coupled with Q Exactive Orbitrap mass spectrometry (UHPLC-Q-Exactive Orbitrap MS/MS). Network pharmacology and functional enrichment analyses were performed to identify immuno-related targets and pathways, followed by molecular docking to prioritize component–target pairs. Molecular dynamics (MD) simulations were conducted to validate the stability of a representative docked complex and to characterize binding stability, interaction persistence, molecular mechanics/(Poisson–Boltzmann) surface area (MM/(P)BSA) energetics, and principal component analysis (PCA)-based conformational landscapes. Results: We identified 1100 compounds, of which 84 satisfied the in silico drug-likeness criteria, including 12 phenylpropanoids, 4 terpenes, 35 flavonoids, 2 quinones, 1 phenol, 3 alkaloids, and other phytochemicals. Network pharmacology analysis revealed 776 overlapping targets associated with both breast cancer and immune regulation. Functional enrichment analysis underscored significant involvement in immune-related pathways, and molecular docking studies supported high-affinity interactions between the components and their targets. MD analyses further supported a stable bound ensemble for the representative SRC–Tomentogenin complex during the equilibrated window, with persistent pocket occupancy, consistent interaction signatures, favorable MM/(P)BSA binding energetics, and a concentrated low-energy basin on the PCA-based free energy landscape. Conclusions: These findings elucidate the chemical basis of CS and uncover its immunomodulatory mechanism against breast cancer, offering a foundation for developing CS-based immunotherapeutic strategies and supporting multi-target drug discovery from traditional medicines. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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17 pages, 4183 KB

Open AccessArticle

Cuproptosis Contributes to Cisplatin-Induced Nephrotoxicity: Insights into Thymol’s Potential Inhibitory and Protective Effects

by Layla A. Al-Kharashi, Amira M. Badr, Reem T. Atawia, Elshaymaa I. Elmongy, Hanan Henidi, Rehab Ali, Awatif A. Binmughram, Lian Al-Abkka, Nervana Mostafa Kamal Bayoumy and Yasmen F. Mahran

Pharmaceuticals 2025, 18(11), 1686; https://doi.org/10.3390/ph18111686 - 7 Nov 2025

Cited by 2 | Viewed by 1340

Abstract

Background: Cisplatin is a powerful treatment for cancer; however, its clinical application is compromised due to its potential for nephrotoxicity. The development of nephroprotective agents is hindered mainly due to the lack of understanding of the exact underlying mechanism. Additionally, the identification of safe nephroprotective agents that can be used as an adjunct to cisplatin is necessary. Methods: Rats were pretreated with thymol (60 mg/kg, orally) daily for two weeks and received a single cisplatin injection (8 mg/kg, i.p.) on the seventh day to induce nephrotoxicity. Results: Thymol prevented cisplatin-induced renal injury and restored serum creatinine and blood urea nitrogen. The renoprotective activity of thymol was further validated by histopathological studies, as demonstrated by the preserved architectures of the glomeruli, proximal, and distal convoluted tubules. Oxidative stress plays an important role in the pathophysiology of nephrotoxicity. Herein, cisplatin administration increased lipid peroxides and depleted the cellular antioxidant defense mechanisms (GSH, SOD, Nrf2, and HO-1). Interestingly, thymol remarkably ameliorated these alterations and restored oxidative status. We further examined the impact of cisplatin and/or thymol on cuproptosis, a distinct type of cell death associated with the excess intracellular accumulation of copper which is aggravated by oxidative stress. Pretreatment with thymol blunted the cisplatin-induced upregulation of genes associated with cuproptosis, including SLC31A1, DLAT, FDX1, LIAS, and ATP7A, as well as FDX1 protein expression. Furthermore, the molecular docking studies of thymol demonstrated favorable fitting and interactions with the conservative amino acids of FDX-1, DLAT, and ATP7A. This further supports the inhibitory effect of thymol on cuproptosis, which underlies its protective properties. Conclusions: This study illustrates that cuproptosis and oxidative stress play crucial roles in the development and progression of cisplatin-induced nephrotoxicity, and the protective activity of thymol is attributed, at least in part, to blunting these mechanisms. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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24 pages, 9438 KB

Open AccessArticle

Large-Scale Transcriptome Profiling and Network Pharmacology Analysis Reveal the Multi-Target Inhibitory Mechanism of Modified Guizhi Fuling Decoction in Prostate Cancer Cells

by Guochen Zhang, Lei Xiang, Qingzhou Li, Mingming Wei, Xiankuo Yu, Yan Luo, Jianping Chen, Xilinqiqige Bao, Dong Wang and Shiyi Zhou

Pharmaceuticals 2025, 18(9), 1275; https://doi.org/10.3390/ph18091275 - 27 Aug 2025

Cited by 2 | Viewed by 1804

Abstract

Background: Prostate cancer (PCa) is the primary contributor to male cancer-related mortality and currently lacks effective treatment options. The Modified Guizhi Fuling Decoction (MGFD) is used in clinical practice to treat multiple tumors. This research focused on the mechanisms of action (MOA) in MGFD that inhibit PCa. Methods: The impact of MGFD on PCa cells (PC3 and DU145) was examined via Cell Counting Kit-8, wound healing assays, and transwell assays. To determine the MOA, high-throughput sequencing based high-throughput screening (HTS²) was utilized along with network pharmacology. Results: The findings indicated that MGFD suppressed the proliferation, migration, and invasion of PCa cells. We then utilized the HTS² assay to generate 270 gene expression profiles from PCa cells perturbed by MGFD. Large-scale transcriptional analysis highlighted three pathways closely associated with PCa: the TNF signaling pathway, cellular senescence, and FoxO signaling pathway. Through the combination of network pharmacology and bioinformatics, we discovered four primary targets through which MGFD acts on PCa: AKT serine/threonine kinase 1 (AKT1), Caspase-8 (CASP8), Cyclin-Dependent Kinase 1 (CDK1), and Cyclin D1 (CCND1). Finally, molecular docking demonstrated that the potential bioactive compounds baicalein, quercetin, and 5-[[5-(4-methoxyphenyl)-2-furyl] methylene] barbituric acid strongly bind to CDK1, AKT1, and CASP8, respectively. Conclusions: This research shows that MGFD displays encouraging anticancer effects via various mechanisms. Its multi-target activity profile underscores its promise as a potential therapeutic option for PCa treatment and encourages additional in vivo validation studies. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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32 pages, 4062 KB

Open AccessArticle

Chemical Composition and Anti-Lung Cancer Activities of Melaleuca quinquenervia Leaf Essential Oil: Integrating Gas Chromatography–Mass Spectrometry (GC/MS) Profiling, Network Pharmacology, and Molecular Docking

by Eman Fikry, Raha Orfali, Shagufta Perveen, Safina Ghaffar, Azza M. El-Shafae, Maher M. El-Domiaty and Nora Tawfeek

Pharmaceuticals 2025, 18(6), 771; https://doi.org/10.3390/ph18060771 - 22 May 2025

Cited by 4 | Viewed by 2762

Abstract

Background/Objectives: This study investigates the phytochemical composition and anticancer activity of Melaleuca quinquenervia leaf essential oil (MQLEO) from Egypt. Methods: Chemical profiling was performed using GC/MS. Anticancer activity was assessed through cytotoxicity screening against multiple cancer cell lines, with a subsequent evaluation of cell migration, apoptosis, and cell cycle analysis on the most sensitive line (A549). Network pharmacology and molecular docking analyses were employed to identify potential molecular targets and pathways. Results: GC/MS analysis revealed a unique profile dominated by 1,8-cineole (31.57%), α-pinene isomers (both 1R and 1S forms, collectively 21.26%), and sesquiterpene alcohols (viridiflorol: 13.65%; ledol: 4.55%). These results diverge from prior studies, showing a 25.63% decrease in 1,8-cineole and no detectable α-terpineol, suggesting environmental, genetic, or methodological impacts on biosynthesis. In vitro tests revealed selective cytotoxicity against A549 lung cancer cells (IC₅₀ = 18.09 μg/mL; selectivity index = 4.30), meeting NCI criteria. Staurosporine was used as a positive control to validate the assays, confirming the reliability of the methods. MQLEO also inhibited cell migration (62–68% wound closure reduction) and induced apoptosis (24.32% vs. 0.7% in controls). Cell cycle arrest at the G₀-G₁ phase implicated cyclin-dependent kinase regulation. Network pharmacology identified ESR1, CASP3, PPARG, and PTGS2 as key targets, with MQLEO components engaging apoptosis, inflammation (TNF, IL-17), and estrogen pathways. Conclusions: MQLEO demonstrates promising anticancer activity through multiple mechanisms including apoptosis induction, cell cycle arrest, and migration inhibition. The multi-target activity profile highlights its potential as a therapeutic candidate for lung cancer, warranting further in vivo validation and pharmacokinetic studies to advance clinical translation. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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21 pages, 2576 KB

Open AccessSystematic Review

Assessing the Effects of Moderate to High Dosage of Astaxanthin Supplementation on Lipid Profile Parameters—A Systematic Review and Meta-Analysis of Randomized Controlled Studies

by Lucas Fornari Laurindo, Victória Dogani Rodrigues, Dennis Penna Carneiro, Luiz Sérgio Marangão Filho, Eliana de Souza Bastos Mazuqueli Pereira, Ricardo José Tofano, Eduardo Federighi Baisi Chagas, Jesselina Francisco dos Santos Haber, Flávia Cristina Castilho Caracio, Letícia Zanoni Moreira, Vitor Engrácia Valenti and Sandra Maria Barbalho

Pharmaceuticals 2025, 18(8), 1097; https://doi.org/10.3390/ph18081097 - 24 Jul 2025

Cited by 3 | Viewed by 13116

Abstract

Background/Objectives: Astaxanthin, a xanthophyll carotenoid, has garnered significant interest due to its benefits with regard to dyslipidemia. This multifaceted functional food ingredient modulates several key enzymes associated with lipid regulation, including HMG-CoA reductase, CPT1, ACCβ, and acyl-CoA oxidase. It influences key antioxidant molecular pathways like the Nrf2, limiting dyslipidemia occurrence and regulating liver cholesterol uptake through the modulation of liver lipid receptors. Due to the current lack of systematic reviews and meta-analyses assessing moderate to high dosages (6–24 mg/d) of astaxanthin supplementation on lipid dysregulation, the present manuscript aims to fill this gap in the literature. Methods: Following the PRISMA guidelines, we included eight studies comprising eleven results from the PubMed, Springer Link, Science Direct, Cochrane, and Google Scholar databases. The Jamovi (Version 2.6.26, Solid) software was utilized for statistics. Our primary objective was to assess in detail the effects of astaxanthin on LDL-C, HDL-C, triglyceride, and total cholesterol levels. Results: The meta-analysis concludes positive effects of astaxanthin (6–20 mg/d) on HDL-C (0.4200; 95% CI: 0.1081 to 0.7319) and triglyceride (−0.3058; 95% CI: −0.5138 to −0.0978) levels. Unfortunately, astaxanthin (6–20 mg/d) does not appear to significantly influence LDL-C (−0.0725; 95% CI: −0.3070 to 0.1620) and total cholesterol (−0.0448; 95% CI: −0.3369 to 0.2473) levels. Regarding HDL-C, improvements were observed from 55 ± 8 mg/dL (pre-intervention) to 63 ± 8 mg/dL (post-intervention) (p < 0.01) in the 12 mg/d of astaxanthin groups. In the assessment of triglyceride levels, results show a decrease from 151 ± 26 mg/dL (pre-intervention) to 112 ± 40 mg/dL (post-intervention) (p < 0.01) for 18 mg/d astaxanthin supplementation. Conclusions: Further research is necessary to fully harness the potential of astaxanthin, which includes assessing astaxanthin in different subsets of patients, using a GWAS, and in combination with other nutraceuticals to understand the compound’s effectiveness with regard to varying health conditions, genetic and epigenetic factors, and synergistic effects with other compounds. Full article

(This article belongs to the Special Issue Medicinal Plants: Exploring Plant-Based Bioactive Compounds for Cancer and Metabolic Diseases Prevention and Intervention)

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