Marine algae, encompassing both macroalgae and microalgae, have emerged as a promising and prolific source of bioactive compounds with potent anticancer properties. Despite their significant therapeutic potential, the clinical application of these peptides is hindered by challenges such as poor bioavailability and susceptibility to enzymatic degradation. To overcome these limitations, innovative delivery systems, particularly nanocarriers, have been explored. Nanocarriers, including liposomes, nanoparticles, and micelles, have demonstrated remarkable efficacy in enhancing the stability, solubility, and bioavailability of marine algal peptides, ensuring controlled release and prolonged therapeutic effects. Marine algal peptides encapsulated in nanocarriers significantly enhance bioavailability, ensuring more efficient absorption and utilization in the body. Preclinical studies have shown promising results, indicating that nanocarrier-based delivery systems can significantly improve the pharmacokinetic profiles and therapeutic outcomes of marine algal peptides. This review delves into the diverse anticancer mechanisms of marine algal peptides, which include inducing apoptosis, disrupting cell cycle progression, and inhibiting angiogenesis. Further research focused on optimizing nanocarrier formulations, conducting comprehensive clinical trials, and continued exploration of marine algal peptides holds great promise for developing innovative, effective, and sustainable cancer therapies.

The potential of seaweed as a source of bioactive compounds including antioxidants made it a versatile form of ingredient that can be incorporated directly or indirectly in the preparation of foods and beverages. Antioxidant constituents are important in managing and regulating oxidative stress and protecting the human body from severe adverse effects due to the excess release of free radicals or reactive oxygen species that promote the onset of chronic diseases. This study aimed to make a functional beverage containing 20 – 30% Caulerpa racemosa (seaweed), and identify phytocompounds using GC–MS, determine the antioxidant activity, molecular and drug likenees of the identfied compounds. Data showed that the total phenolic content of the juice made with 30% seaweed was 32.2 + 0.5 μg/GAE, vitamin C 2.9 + 0.1 µg/mL while the antioxidant activity (DPPH IC50) was 46.8±3.3 mg/mL. Twenty compounds were identified of which three met the Lipinski’s rule of five. They were then docked with five enzymes involved in oxidative stress and inflammation (cytochrome P450, lipoxygenase, myeloperoxidase, NADPH oxidase, and Xanthin oxidase). Their binding energies (∆G: – 4.1 to – 6.3 Kcal/mol) were comparable to those of known commercial binders (∆G: – 5.0 to – 7.3 Kcal/mol) of each enzyme. Pharmacokinetic analyses showed excellent scores for the three compounds in regard to bioavailability, human intestinal absorption, and blood brain barrier. The sensory test value of the juice showed good odor, taste, and color, with a score between 4.7- 5.9. Overall, the functionalized juice displayed properies that make it potentially useful in the reduction of oxidative stress are related conditions, although in-vivo studies are needed.

Myocardial ischemia–reperfusion (I/R) injury remains a major limitation in cardiovascular therapy, where restoration of blood flow paradoxically initiates oxidative stress, inflammation, mitochondrial dysfunction, and cardiomyocyte death. Although multiple pharmacological strategies have been investigated, clinical translation remains limited by inconsistent efficacy and incomplete pathway coverage. Quercetin, a naturally occurring flavonoid with pleiotropic biological activity, has attracted increasing interest as a potential modulator of I/R‐associated injury. This systematic review evaluated current evidence regarding the cardioprotective effects and mechanistic actions of quercetin in myocardial I/R injury. A structured literature search identified 25 eligible studies comprising predominantly preclinical in vivo animal investigations, together with limited ex vivo, in vitro, and clinical evidence. Across studies, quercetin consistently reduced infarct size, attenuated myocardial injury biomarkers, and improved cardiac functional parameters. Mechanistically, these effects were associated with suppression of oxidative stress and inflammatory signaling, particularly through modulation of ROS generation, NF‐κB activation, PI3K/Akt signaling, mitochondrial dysfunction, and apoptosis‐related pathways. Several studies also demonstrated preservation of endogenous antioxidant systems and mitochondrial integrity. However, substantial heterogeneity in experimental design, limited mitochondrial‐specific analyses, and the scarcity of comparative clinical studies remain major barriers to translation. Collectively, current evidence supports quercetin as a multi‐pathway cardioprotective candidate in myocardial I/R injury, although further standardized and clinically oriented investigations are required to clarify its therapeutic relevance.