Fucoidan, a marine polysaccharide, has demonstrated potential in treating cardiovascular diseases, including coronary artery disease (CAD). CAD treatment includes lowering blood coagulation, blood fat levels, and having heart-protective activity. This study aimed to evaluate the potential of fucoidan compounds isolated from brown algae (Sargassum polycystum C. Agardh) on anticoagulant effects through measurements of PT, APTT, and TT, as well as lipid profile, body weight, heart and aortic mass index, LDH, and CK-MB, as well as in Wistar rats (Rattus norvegicus). A total of 36 animals were divided into six groups. Group I received a standard diet without treatment; Group II received 0.5% CMC; Group III was treated with simvastatin at 20 mg/kg BW; and Groups IV, V, and VI received fucoidan at doses of 30 mg/200 g BW, 40 mg/200 g BW, and 50 mg/200 g BW, respectively. Statistical analysis of the lipid profile showed that all fucoidan doses significantly reduced total cholesterol and triglyceride levels, although HDL levels were not increased. Organ weight analysis revealed a significant reduction (p < 0.05) in aortic weight in all treated groups, while no significant changes were observed in body or heart weight. Seven days of fucoidan administration also significantly reduced CK-MB and LDH serum levels (p < 0.05). In conclusion, fucoidan compounds Sargassum polycystum C. Agardh at all tested doses show potential in the treatment of CAD by lowering total cholesterol and triglyceride levels, reducing aortic weight, prolonging coagulation times (PT, APTT, and TT), and decreasing CK-MB and LDH levels.
A complex metabolic condition i.e. obesity is linked to a number of health issues, such as Diabetes, metabolic dysfunctions and cardiovascular disorders etc. Body weight control has often been misunderstood, with eating habits and exercise levels portrayed as personal preferences, usually associated with self-control or lack thereof. However, obesity is more than just a matter of choice in food habits, it is characterized by an excess of macrophage infiltration in adipose tissue, adipocyte hypertrophy, and disruptions in normal metabolic functions. An important contributing factor to the rising prevalence of obesity is disturbed eating patterns, frequently driven by cravings rather than actual hunger. Hypothalamus, particularly the arcuate nucleus plays an important role in regulating hunger and energy homeostasis in the body. The arcuate nucleus regulates appetite through two primary pathways: the orexigenic (appetite-stimulating) and anorexigenic (appetite-suppressing) systems. Remarkably, the endocannabinoid system (ECS) plays a key role in modulating both homeostatic and non-homeostatic aspects of food intake through its cannabinoid receptor 1 and 2 by interacting with various hypothalamic regions controlling hunger feeding patterns of hedonic and reward feeding. This review focuses on the role of ECS control on hypothalamic regulation of appetite, & hedonic or reward feeding patterns. A deeper understanding of these pathways is essential for addressing the growing prevalence of obesity and its associated health risks.
Caloric restriction (CR) is among the most effective non-genetic strategies to extend lifespan and delay age-related metabolic decline. Yet, the molecular mediators linking CR to hepatic protection remain incompletely understood. Here, we performed age-stratified targeted oxylipin (lipid mediator) profiling of livers from ad libitum (AL) and CR mice across adulthood and aging. In AL-fed mice, similar to 9 months emerged as an inflection point where oxylipin networks shifted toward a pro-inflammatory state, marked by transient elevations in PGE(2), 11-keto-TXB2, 20-HETE, and 5-oxo-ETE, with concomitant loss of pro-resolving/hydroxy-dihydroxylated mediators. Later life was characterized by depletion of CYP-derived epoxides and accumulation of soluble epoxide hydrolase (sEH)-generated diols, indicating impaired epoxide-to-diol coupling and resolution capacity. Lifelong CR dynamically reprogrammed these trajectories, blunting mid-life inflammatory surges, preserving EPA-derived epoxy-fatty acids (eg., EpETEs), and inducing the redox enzyme CYB5R3, which may sustain CYP epoxygenase activity (and epoxide output) despite reduced enzyme abundance. These oxylipin changes coincided with reduced hepatic lipid accumulation and a more favorable systemic metabolic profile in CR mice. Collectively, these findings identify age-and diet-associated remodeling of the hepatic COX/LOX/CYP oxylipin network, particularly the epoxide-diol profile, and nominate CYB5R3-associated redox regulation as a hypothesis for future mechanistic investigation.
Linoleic acid-derived epoxyoctadecenoic acids (EpOMEs) have been implicated in inflammatory and metabolic diseases, yet their direct effects on colonic homeostasis under normal physiological conditions remain unclear. In this study, we investigated whether EpOMEs exposure alters colonic crypt structure, immune activation, and gut microbiome composition in C57BL/6 mice. We found that EpOMEs administration shortened colonic crypt length and reduced the expression of antimicrobial peptide genes, including Defb1 and Reg3g, indicating impaired epithelial architecture and weakened antimicrobial defense. EpOMEs also promoted macrophage accumulation in the colon and elevated expression of pro-inflammatory cytokines. Furthermore, 16S rRNA gene sequencing revealed that EpOMEs exposure altered gut microbial composition, characterized by reduced microbial diversity, decreased abundance of potentially beneficial taxa including Muribaculaceae and Akkermansia, and enrichment of inflammation-associated Romboutsia. Together, these findings demonstrate that EpOMEs exposure is associated with impaired epithelial structure, enhanced macrophage-associated inflammatory responses, and gut micro-biome dysbiosis. This study could provide new insight into how linoleic acid-derived lipid mediators may contribute to the early stages of gut dysfunction and increase susceptibility to associated inflammatory disorders.
The anti-inflammatory potential of Oroxylum indicum (OI), a traditional medicinal plant, was evaluated through in vitro, ex vivo, and molecular docking studies. The stem bark extract exhibited a significant, dose-dependent inhibition of protein denaturation in both egg albumin and bovine serum albumin assays at concentrations of 10, 30, and 100µg/mL. Molecular docking revealed strong binding affinities of key bioactive compounds, especially Oroxylin B (docking score -8.79), to the cyclooxygenase-2 (COX-2) enzyme, suggesting a mechanistic basis for anti-inflammatory effects. The extract exhibited no cytotoxicity on human lymphocytes across tested concentrations (20-200µg/mL) in the MTT assay, indicating safety. Ex vivo, OI extract significantly reduced COX-2 enzyme levels from 124.66 ± 0.16ng/mL in radiation controls to 107.33 ± 0.10ng/mL, comparable to diclofenac (106.36 ± 0.08ng/mL). Furthermore, IL-6 and TNF-alpha pro-inflammatory cytokine levels were substantially elevated by radiation but significantly decreased upon treatment with OI extract; IL-6 levels were reduced to 21.74 ± 0.95pg/mL compared to 27.45 ± 0.82pg/mL in radiation controls and TNF-alpha levels were similarly lowered, comparable to the diclofenac-treated group. These findings support the notion that the extract derived from the stem bark of Oroxylum indicum holds considerable strong possibility as a natural anti-inflammatory agent with modulatory effects on key inflammatory enzymes and cytokines, meriting further pharmacological and clinical evaluation.
