2026-05-01 2026, Volume 16 Issue 5

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  • research-article
    Wong Yi En, Tan Sun Wern, Ashok Kumar Mandal, Dharmani Devi Murugan

    Exploring natural products as therapeutic alternatives to synthetic drugs has garnered increasing research interest due to their reduced side effects and lower toxicity. Bioactive compounds derived from natural products exhibit a diverse range of pharmacological effects that help reduce cardiovascular risk, primarily by modulating key metabolic pathways. These natural compounds have demonstrated efficacy in mitigating cardiovascular risk factors such as hypertension, hyperglycemia, hyperlipidemia, obesity, and liver injury by modulating metabolism within the biological systems. Mechanistically, natural products exert their effects through coordinated regulation of systemic energy homeostasis, lipidomic and phospholipid balance, amino acid metabolism, mitochondrial bioenergetics, and gut microbiota-derived metabolites. Such modulation results in measurable changes in metabolite profiles across various biological samples, including blood, urine, feces, and tissues. Among the various mechanistic pathways involved in cardiovascular regulation, the metabolic pathway offers a more dynamic and integrative perspective of disease progression and therapeutic response, enabling identification of key metabolites and biomarkers that reflect systemic physiological changes. Furthermore, metabolomics-based approaches provide powerful tools to uncover subtle biochemical alterations that may precede overt pathological changes, making it a valuable focus in natural product therapeutics in cardiovascular research. This review focuses on current evidence on metabolite alterations associated with cardiovascular risk factors and illustrates how natural products reprogram metabolic networks to mitigate disease, providing a systems-level framework for understanding their cardioprotective effects.

  • research-article
    Khaled M. M. Koriem, Mahmoud S. S. Arbid

    Objective: To determine whether soybean oil can ameliorate 4-octylphenol-induced alterations in female hormones, minerals, ovarian antioxidants, and inflammatory cytokines in female rats.

    Methods: Thirty-six female rats were divided into six groups: control, soybean oil (1 mL/rat), soybean oil (2 mL/rat), 4-octylphenol, 4-octylphenol plus soybean oil (1 mL/rat), and 4-octylphenol plus soybean oil (2 mL/rat). Levels of female hormones, serum minerals, ovarian antioxidants, and inflammatory markers were assessed. Ovarian Na+/K+-ATPase activity and nuclear factor kappa B were also detected.

    Results: Soybean oil restored female hormones, serum minerals, Na+/K+-ATPase activity, and ovarian antioxidants, while lowering ovarian inflammatory markers and nuclear factor kappa B levels in 4-octylphenol-exposed female rats. Moreover, soybean oil upregulated p53 expression while downregulating Bcl-2 expression.

    Conclusions: Soybean oil treatment improves female hormones, minerals, ovarian oxidative stress and inflammation in 4-octylphenol-exposed rats.

  • research-article
    Maha Hamadien Abdulla, Mansoor-Ali Vaali-Mohammed, Sabine Matou Nasri, Noura S. Alhassan, M. Meeramaideen, Abdullah Al Obeed, Wagdy M. Eldehna, Rofaida Salem, Thamer Traiki, Khayal Al Khayal

    Objective: To investigate the anticancer effects of a novel benzofuran-isatin conjugate [N’-(5-methoxy-2-oxoindolin-3-ylidene)-3-methylbenzofuran-2-carbohydrazide (conjugate 5d)] against human colorectal adenocarcinoma (CRC) HT29 and metastatic SW620 colorectal cancer cells.

    Methods: The cytotoxic properties of conjugate 5d were evaluated using the MTT assay. Its anti-oncogenic effects were assessed by real-time monitoring of cell proliferation, migration, and invasion, and by performing a clonogenic assay. Flow cytometry was also used to assess the apoptotic status and cell cycle. Apoptosis, cell cycle, and epithelial-mesenchymal transition-related protein and gene expression levels were also measured.

    Results: Conjugate 5d exhibited cytotoxic effects on both CRC cells and enhanced the cytotoxic efficacy of 5-fluorouracil, irinotecan, and oxaliplatin. Conjugate 5d also induced apoptosis by modulation of anti-apoptotic (i.e., Bcl-xl) and pro-apoptotic (i.e., Bax, p53, cytochrome c) proteins, and MMP loss. Docking studies predicted molecular interactions of conjugate 5d with anti-apoptotic Bcl-2, revealing conjugate 5d as a potential Bcl-2 inhibitor. Regarding the oncogenic process, conjugate 5d inhibited CRC cell proliferation, migration, invasion, and colony formation, upregulated E-cadherin expression, and downregulated N-cadherin expression.

    Conclusions: Conjugate 5d shows significant anticancer effects against HT29 and SW620 cells by exerting pro-apoptotic and antimetastatic activities. It also enhances the cytotoxic efficacy of conventional chemotherapeutic drugs in CRC cell lines. However, in vivo studies should be conducted to further confirm its efficacy.