Peptic ulcer disease remains clinically important despite effective Helicobacter pylori (H. pylori) eradication and acid-suppressive therapy. Gastric injury reflects an imbalance between aggressive factors, including acid-pepsin activity, H. pylori, non-steroidal anti-inflammatory drugs (NSAIDs), ethanol, oxidative stress, inflammation, apoptosis, and microvascular disturbance and protective mechanisms such as mucus-bicarbonate secretion, prostaglandin signaling, nitric oxide-regulated blood flow, epithelial restitution, and endogenous antioxidant defenses. Bixa orellana L. (annatto or achiote) is a tropical medicinal plant whose seed arils are rich in the apocarotenoids bixin and norbixin, whereas its leaves contain variable phenolics, flavonoids, tannins, terpenoids, alkaloids, and other constituents depending on geography, maturity, and extraction method. This critical narrative review uses a structured search and qualitative evidence-appraisal framework to evaluate extract-specific phytochemistry, direct gastric evidence, indirectly relevant gastrointestinal and vascular evidence, mechanistic plausibility, safety, quality control, and translational readiness. The available literature supports B. orellana as a biologically plausible preclinical mucosal-protective candidate, particularly for prevention of acute chemical injury; however, it does not establish clinical efficacy or chronic ulcer-healing activity. Confidence is limited by the small number of direct gastric studies, incomplete chemical characterization, inconsistent separation of leaf and seed evidence, limited dose-response testing, narrow model selection, and insufficient mechanistic and histological endpoints. Future studies should use authenticated plant material, voucher specimens, chromatographic fingerprints, quantitative markers, complementary prevention and healing models, acute and repeated-dose toxicology, mucus and prostaglandin measurements, oxidative and inflammatory biomarkers, and blinded histological scoring before human investigation is justified.
Inflammation is a protective physiological response that may cause tissue damage when prolonged. Copper–amino acid complexes, including Cu(L-alanine)₂, have been reported to possess various biological activities. However, their anti-inflammatory potential remains underexplored. This study evaluated the in vivo anti-inflammatory effects of Cu(L-ala)₂ using three experimental models in rats: acetic acid-induced peritoneal vascular permeability, carrageenan-induced paw edema, and nitric oxide (NO) production in paw tissue. Rats were divided into four groups (n = 6) and treated with vehicle control (1% DMSO), indomethacin (10 mg/kg), or Cu(L-ala)₂ at doses of 2 or 20 mg/kg. Acetic acid markedly increased vascular permeability, which was significantly inhibited by Cu(L-ala)₂ by 74.1% (2 mg/kg) and 81.23% (20 mg/kg). In the paw edema model, both doses significantly reduced inflammation compared with the control, with the 2 mg/kg dose showing the greatest inhibition (63.79%) at 1 hour. In contrast, Cu(L-ala)₂ produced only a moderate reduction in NO levels, reaching statistical significance only at 20 mg/kg (27.56%), while indomethacin showed a stronger effect (46.28%). Overall, Cu(L-ala)₂ demonstrated significant anti-inflammatory activity by reducing vascular permeability and edema formation. However, its limited effect on NO production suggests that its mechanism of action may be largely NO-independent. Further studies are required to clarify its molecular targets, dose–response behavior, and therapeutic potential.
Neurodegenerative diseases, like Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), and ischemic stroke (IS), are a major global health challenge because of their complex, multifactorial pathology, and the lack of effective disease-modifying therapies. In recent years, aquaculture-derived marine bioactive molecules like fucoidan, phlorotannins, fucoxanthin, laminarin, alginate oligosaccharides, and C-phycocyanin have developed as promising agents for neuroprotection with their structural diversity and multi-target biological activity. This review showcase predominantly preclinical evidence, including in silico molecular docking analyses, in vitro functional assays, and in vivo animal models, to critically understand the receptor-mediated mechanisms with the neuroprotective actions of marine bioactives originated from aquaculture systems. Available studies shows these compounds can modulate large neuro-receptor systems, like cholinergic, dopaminergic, GABAergic, glutamatergic, toll-like, and nuclear receptors, leading in attenuation of oxidative stress, lowering of neuro-inflammation, regulation of neurotransmission, and conservation of mitochondrial and synaptic function. However, the positive approach of mechanistic evidence varies across compounds and receptor classes, with large interactions assisted by functional outcomes instead of direct receptor-binding validation. The review even discusses emerging and enabling technologies like brain organoids, multi-electrode array platforms, omics-based profiling, and artificial intelligence assisted drug discovery, which are increasingly utilized to refine mechanistic understanding and optimize marine-derived products. Importantly, current evidence stay largely preclinical, with little human studies and a lack of validated receptor-specific biomarkers. Overall, this review provides a well-balanced, evidence-based assessment of aquaculture-derived marine bioactive as potential neurotherapeutic agents.
The complex interdependence between cancer and diabetes has become a major subject of research in molecular medicine since multiple data points indicate that these two conditions have some molecular processes and regulatory pathways in common. The complex relationship between epigenetic and genetic modifications linking these two prevalent diseases was explored in this comprehensive study. Molecular fingerprints such as abnormal DNA methylation, histone modifications, and non-coding RNA dysregulation have become known in recent times as a result of breakthroughs in the multi-omics technology. We systematically analyze the prevalent risk factors such as obesity, chronic inflammation, and oxidative stress that cause these two diseases through various yet similar biological processes. Particular emphasis is put on such important signaling pathways as insulin/IGF, PI3K/AKT/mTOR, and AMPK cascades that are fundamental in both diseases. We also provide an overview of new technologies that can enhance our knowledge of the molecular etiology of these diseases, such as single-cell sequencing and artificial intelligence. These observations are evaluated clinically from the perspective of biomarkers discovery, therapeutic targeting, and personalized medicine modalities. Lastly, we discuss future research for this study and future potential therapies based on the focus on similar biological pathways. This review offers insightful commentary on the field of cancer and diabetes intersection that can help to create more rational treatment regimens for both diseases.
