The low constitutive activation of Liver X receptor, an endogenous nuclear receptor with two subtypes (α and β), is a condition lying at the crossroad of cancer and cardiovascular disease. Both natural and synthetic Liver X receptor agonists have reportedly shown remarkable antiproliferative and atheroprotective effects but the repeated doses of its synthetic ones are also paradoxically associated with hyperlipidaemic effects and neurotoxicity, though attributed to the alpha subtype. This highlights the need for novel, safe, and potent LXR-beta-selective agonists. Hypocholesterolaemic effects of black theaflavins have been widely reported, but data on the exact theaflavin compound (s) responsible for these effects is currently lacking. Neither is information on the possible modulatory effects of the compound (s) on LXR-beta nor its possible implications in the context of drug development for cardiovascular diseases and cancers is explored. On this account, we investigated the potential interaction of four main theaflavin monomers (TF1, TF2A, TF2B & TF3) with human LXR-beta through robust computational modelling that entails molecular docking, free energy calculations and molecular dynamics simulations. The ligands were further profiled (in silico) for absorption, distribution, metabolism, excretion, and toxicological properties. Our result revealed theaflavin TF2B as a putative LXR-beta agonist, possibly responsible for the widely observed hypocholesterolaemic effect in black tea. This finding, while encouraging, needs to be experimentally verified in wet studies. Communicated by Ramaswamy H. Sarma

This study validates the antidiabetic efficacy of Enantia chlorantha stem bark and the possible therapeutic implications of the co-administration of lisinopril and E. chlorantha in type 2 diabetic rats. E. chlorantha stem bark was extracted by cold maceration. The inhibitory effect of the plant on carbohydrate metabolizing enzymes and its antioxidative potentials were assessed in vitro. The extract exhibited a-amylase and a-glucosidase inhibitory activities and also showed antioxidative properties in vitro. Administration of the extract normalized fasting hyperglycemia in vivo by showing 47.24% reduction in blood glucose levels relative to untreated diabetic rats. Co-administration of E. chlorantha and lisinopril restored serum glucose and serum lipid profile levels. E. chlorantha stem bark displayed antidiabetic potentials as compared with a standard antidiabetic drug (metformin). The study also showed that the plant contained some bioactive compounds which we hypothesize might be responsible for the observed activities. Co-administration of the plant with lisinopril conferred no significant therapeutic advantage on the serum glucose level and lipid profile.

Pharmaceutical treatments for inflammation and ulcers often have side effects, prompting interest in plant-based alternatives. This study investigates the anti-inflammatory and anti-ulcerogenic potential of ethanol extract of Carica papaya leaves using in vitro assays and molecular docking. The leaves were subjected to ethanol extraction, after which the resulting extract underwent GC-MS analysis and in vitro assays. The phytochemicals identified from the GC-MS profile were subsequently analyzed through molecular docking studies for further evaluation. The extract demonstrated significant anti-inflammatory activity by inhibiting protein denaturation (IC₅₀: 180.70±2.25 µg/ml), membrane stabilization (IC₅₀: 192.60±2.29 µg/ml), and proteinase activity (IC₅₀: 1289.00±3.11 µg/ml). Its anti-ulcerogenic potential was evident in its inhibitory effects on H⁺/K⁺-ATPase (IC₅₀: 196.10±2.29 µg/ml) and urease (IC₅₀: 700.90±2.85 µg/ml), suggesting a role in gastric protection. Gas Chromatography-Mass Spectrometry (GC-MS) analysis identified biologically active compounds, such as phenolic acids and long-chain fatty acid esters, known for their anti-inflammatory and gastroprotective properties. Molecular docking analyses additionally confirmed the therapeutic potential of 2,3-Benzofurandione 2-monooxime, 3-(4-Nitrophenyl) propiolic acid, and Phthalic acid, di-(1-hexen-5-yl) by demonstrating strong interactions with cyclooxygenase-2 (COX-2) and H⁺/K⁺-ATPase enzymes, with binding affinities comparable to standard drugs like celecoxib and omeprazole respectively. These results offer scientific validation supporting the traditional use of C. papaya leaves in managing inflammatory and ulcerative conditions. Further in vivo studies and clinical trials are necessary to confirm their efficacy and safety for therapeutic applications.

Aim: The present study was conducted to investigate the preventive/curative effect of aqueous seed extract Syzygium aromaticum in alloxan-induced diabetes in rats. Study Design: Twenty Wistar rats were randomly divided into four groups. The first group served as a control (received 1 ml of normal saline). The second group served as Diabetic control (received 1 ml of normal saline). The third group served as test 1 (pre-treated with 500 mg/kg body weight (b.w.) of aqueous Syzygium aromaticum seeds extract for seven days prior to diabetic induction and post-treated with aqueous seeds extract of Syzygium aromaticum after diabetic induction) and the fourth group served as test 2 (post-treated with 500 mg/kg b.w. of aqueous seed extract of Syzygium aromaticum after diabetic induction) in a daily oral dose for 14 days. Results: Treatment of rats with aqueous seed extract of Syzygium aromaticum in a daily dose of 500 mg/kg significantly mitigates the induced changes in the glucose and lipid profile parameters. Histopathological examination of the pancreas showed the destruction of β-cells in the diabetic control group and recovery of damaged tissues when treated with 500 mg/kg b.w. of aqueous seeds extract of Syzygium aromaticum. Conclusion: The present study suggests that aqueous seed extract S. aromaticum seeds extract at a dose of 500 mg/kg body weight brings about regeneration of the B-cells of the pancreas and significant beneficial effects in various physiological parameters in alloxan-induced diabetes.