The foundation of atherosclerotic cardiovascular disease (ACVD) comprises a triad of dyslipidemia, inflammation, and thrombosis. High levels of Low-Density Lipoprotein (LDL) contribute to endothelial dysfunction and inflammation, ultimately leading to atherothrombosis, impaired blood flow, and tissue ischemia/necrosis, making it the most serious form of atherosclerosis. Preventative measures are crucial when it comes to cardiovascular diseases, and Fucoidan can serve as a supplement to prevent most of them. Fucoidan, a sulfated polysaccharide component found in brown algae, is associated with diverse biological activities.
Hence, I would like to share the following study with you: “Fucoidan’s as a Potential Nutraceutical in Combating Atherosclerotic Cardiovascular Diseases” by Weslley F Braga et al.. This study describes several ‘in vitro’ and experimental studies that illustrate Fucoidan actions that may be beneficial in controlling ACVD.
Fucoidan reduces blood lipids, increases LDL receptors, decreases scavenger receptors, inhibits immune cell migration and activation, cytokine production, reduces platelet aggregation, and inhibits fibrinolysis. Fucoidan is an fantastic dietary supplement that can be utilized as an adjuvant in preventing or treating ACVD. However, future clinical studies are needed to verify these effects in humans.
Because of their similarity to heparin, several species of fucoidan were previously tested for their ability to stimulate fibrinolytic and anticoagulant molecules by Min SK et al., which showed a thrombotic effect. In addition, the research indicates that Fucoidan is capable of stimulating tissue plasminogen activator (tPA), which is not the case with heparin. It protects plasmin activity from α2-plasmin inhibitors, and initiates fibrinolysis by reducing fibrin polymer formation.
According to a study by Huang L et al., when mice were fed a High-Fat Diet (HFD) and given Fucoidan, the levels of Total Cholesterol (TC), Triglycerides (TG), and Low-Density Lipoprotein Cholesterol (LDL-C) were decreased. On the other hand, high-density lipoprotein cholesterol (HDL-C) concentrations were increased. In another study by Thomes P et al., fucoidan administration reduced hypertriglyceridemia and hypercholesterolemia in an isoproterenol-induced myocardial infarction model by lowering LDL-C and increasing HDL-C levels. The research also discovered that Fucoidan was not only linked with the benefits mentioned earlier but also with decreased levels of lipid peroxidation, reducing cardiac enzyme release and myocardial damage.
Studies have shown that Fucoidan possesses powerful antioxidant effects, as it can scavenge hypochlorous superoxide radicals and inhibiting the formation of superoxide radicals, hydroxyl radicals, and lipid peroxides in both in vitro and in vivo assays. Antioxidant activity, like antithrombotic activity, depends on its molecular weight and sulfate content. In addition, ‘in Vivo’ studies using LDL receptor-knockout (LDLR-/-), mice showed that oxLDL receptor (LOX-1) and reactive oxygen species (ROS)-related proteins were negatively regulated in the aorta after fucoidan supplementation. Also, these results suggest that Fucoidan reduces oxidative stress and atherogenesis in animal models. Similar results were obtained in streptozotocin-induced diabetic mice that showed reduced ROS production in aortic smooth muscle cells after fucoidan treatment.
It has been demonstrated in various studies that Fucoidan works as a strong inhibitor of leukocyte migration and platelet activation by binding to L-selectin and P-selectin, and this is why it is referred to as a ‘selectin blocker’. Thus Fucoidan probably works similarly to heparin sulfate, exhibiting a spatial structure of sulfated sugars similar to fucosylated, sialylated, or sulfated oligosaccharides on the cell surface. Fucoidan also suppresses the activity of several inflammatory mediators. A key action is inhibiting nuclear factor-kappa B (NF-κB) signaling. NF-κB is a key transcription factor involved in inflammatory responses. The activation of NF-κB by multiple stimuli, like infections or injuries, leads to the release of the protein from inhibitors and its translocation to the nucleus, where it triggers the transcriptional induction of genes linked to inflammation.
Several studies have shown that Fucoidan downregulated NF-κB and MAPK (ERK, JNK, p38) pathways. Moreover, the transcriptional activity of oncogenes C-Fos or C-Jun is reduced by Fucoidan, resulting in the inhibition of activator protein 1 (AP-1) transactivation. AP-1 regulates gene expression triggered by stimuli, such as cytokines and infections. Thus, Fucoidan inhibits the production of proinflammatory cytokines and the AP-1 response regulated by these mediators. The results were established in a model of myocardial ischemia or reperfusion injury. Fucoidan supplementation reduced myocardial lesion area, damage, and leukocyte infiltration. They showed that the major biological functions of Fucoidan with antiatherogenic events are shown in Figure 1. On a positive note, Fucoidan has several physical actions and may be an adjuvant to prevent or treat ACVD and reduce dyslipidemia, inflammation, and thrombus formation.
Source: Sci & Tech Res 21 (3)-2019. BJSTR. MS.ID.003615. DOI: 10.26717/BJSTR.2019.21.003616