Faculty of Basic Medical Sciences
Permanent URI for this communityhttp://repository.oouagoiwoye.edu.ng:4000/handle/123456789/11
Browse
7 results
Search Results
Item EFFECTS OF DIETARY SUPPLEMENTATION WITH SESAMUM INDICUM L. SEED ON PLASMA LIPID PROFILE AND OXIDATIVE STRESS BIOMARKERS IN HYPERLIPIDEMIC RATS(2026-07-20) Ajibode, Bamidele AinaHyperlipidemia is a major metabolic disorder associated with cardiovascular diseases (CVDs), atherosclerosis, and oxidative stress. Due to the cost and hepatotoxic risks associated with statins, safer natural alternatives are increasingly needed. This study evaluated the modulatory potential of a Sesamum indicum (sesame)-supplemented diet on lipid profile and oxidative stress biomarkers in hyperlipidemic male rats. Forty rats (95.37 ± 9.79) were randomized into four groups (n = 10): Basal Control, HFD Untreated, HFD + Sesame (50% fortification), and HFD + Atorvastatin (0.02 mg/kg/day Per os). Following an 8-week protocol (4-week induction and 4-week treatment), plasma lipid profile and oxidative stress biomarkers (SOD, CAT, GPx, GST, GSH, and MDA) were assessed after ethical sacrifice of animals. HFD feeding significantly (p < 0.05) increased body weight compared to the basal control, whereas both atorvastatin administration and sesame diet reversed the obesogenic effect. HFD increased total cholesterol (TC) in untreated rats to 29.17 ± 1.39 mg/dL compared to 16.96 ± 1.26 mg/dL observed in the basal control group, while atorvastatin and sesame significantly reduced circulating TC to 22.18 ± 2.01 mg/dL and 21.62 ± 1.56 mg/dL respectively. Similarly, HFD increased triglycerides (TRIG) in untreated rats to 196.26 ± 12.12 mg/dL compared to a value of 75.18 ± 9.81 mg/dL observed in the basal control; however, sesame reduced TRIG 124.38 ± 10.07 mg/dL which is comparable to 126.18 ± 8.93 mg/dL observed in rats administered atorvastatin. HFD also increased LDL-C in untreated rats to 59.03 ± 7.21 mg/dL which is comparable to 23.17 ± 2.58 mg/dL observed in the basal control whereas sesame and atorvastatin significantly lowered LDL-C to 26.18 ± 2.16 mg/dL and 28.09 ± 3.08 mg/dL respectively. Both interventions similarly reversed HFD-induced reductions in HDL-C. Hyperlipidemia disrupted antioxidant defenses, reducing SOD (16.26 ± 2.01 U/L), CAT (19.8 ± 2.73 U/L), GST (56.15 ± 5.16 U/L), GPx (31.24 ± 2.61 U/L), and GSH (0.51 ± 0.01 μM) relative to baseline values of 40.36 ± 4.81 U/L, 56.27 ± 2.92 U/L, 72.31 ± 6.03 U/L, 56.86 ± 3.51 U/L, and 1.47 ± 0.03 μM, respectively. Sesame diet restored antioxidant enzyme activities and GSH level to near-normal levels which is comparable to the values observed in rats administered atorvastatin, while it significantly reduced MDA concentrations. In conclusion, this study indicates that dietary sesame supplementation improved lipid metabolism and reduced oxidative stress in hyperlipidemic rats, underscoring its potential as a low-cost functional food for promoting metabolic health and managing hyperlipidemia. Key words: Hyperlipidemia, oxidative stress, antioxidant enzymes, lipid profile, sesame.Item A MULTI-TARGET INVESTIGATION INTO THE THERAPEUTIC MECHANISMS OF ACTION OF LUTEOLIN IN COLORECTAL CANCER(2026) Omirin, Emmanuel SundayColorectal cancer (CRC) is still one of the major causes of mortality, particularly in nations with low-to-middle income, due to late diagnosis and limited access to therapeutics that are effective, affordable and less toxic. Multi-target anticancer potential of luteolin has been reported, yet its mechanisms in CRC are not well understood because most of the studies rely on one-target or one-pathway analysis. Consequently, this study used a multipronged approach including network pharmacology (NP), molecular docking, and In vivo experimentation to investigate the therapeutic potential of luteolin against CRC. Targets of luteolin and CRC were retrieved from online databases with intention to identify shared interactome. Hub genes were identified from protein-protein interaction network using STRING and cytoscape. Stability of luteolin and its targets were validated by docking and subsequent 100ns simulation. In vivo efficacy was verified in an azoxymethane (AOM)-induced Drosophila model of CRC. NP identified 379 shared targets existed between luteolin and CRC, including hub genes like AKT1, mTOR, TP53 and BCL2. Following enrichment analysis, the main targets are those in PI3K/Akt, Wnt and MAPK signaling pathways. Molecular docking predicted high binding energies - caspase-3 (-9.761 kcal/mol), AKT1 (-8.613 kcal/mol) and mTOR (-7.92 kcal/mol). Complexes were predicted to be favourable using MMGBSA, the major complex being predicted for AKT1 (-54.22 kcal/mol). MD simulations (100ns) demonstrated high structural integrity as the mean RMSD of the caspase-3 complex with luteolin was 1.8 Å and the variation of residues was small. In vivo data revealed luteolin significantly reduced tumour burden in all the groups supplemented with the diet compared to the AOM-only groups, achieving an exceptional result. End-point PCR analysis verified the predicted mechanism, as luteolin significantly (p < 0.05) down regulated oncogenic markers including mTOR, AKT1, c-MYC, and the anti-apoptotic BCL2. Luteolin up regulated critical pro-apoptotic and regulatory genes, specifically TP53, CDKN1A (dap), CASP3 (drice), and CASP9 (dronc). Luteolin disrupts CRC hallmarks by simultaneously inhibiting survival signaling and triggering apoptosis through a stable, multi-target interactome. These data scientifically position luteolin as a potent, multi-target chemopreventive agent which should be further investigated in a more physiologically relevant mammalian model of CRC. Key Words: Colorectal carcinogenesis, Luteolin, Network pharmacology, PI3K/Akt pathway, Drosophila.Collection Collection Collection Collection Collection