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An experimental study has been conducted to investigate the efficacy of geraniol (GNL) isolated from lemomgrass in protecting against cardiac toxicity induced by tilmicosin (TIL) in albino mice. Compared to TIL-treated mice, those supplemented with GNL had a thicker left ventricular wall and a smaller ventricular cavity. Studies of TIL animals treated with GNL showed that their cardiomyocytes had markedly changed in diameter and volume, along with a reduction in numerical density. After TIL induction, animals showed a significant increase in the protein expression of TGF-β1, TNF-α, nuclear factor kappa B (NF-kB), by 81.81, 73.75 and 66.67%, respectively, and hypertrophy marker proteins ANP, BNP, and calcineurin with respective percentages of 40, 33.34 and 42.34%. Interestingly, GNL significantly decreased the TGF-β1, TNF-α, NF-kB, ANP, BNP, and calcineurin levels by 60.94, 65.13, 52.37, 49.73, 44.18 and 36.84%, respectively. As observed from histopathology and Masson's trichrome staining, supplementation with GNL could rescue TIL-induced cardiac hypertrophy. According to these results, GNL may protect the heart by reducing hypertrophy in mice and modulating biomarkers of fibrosis and apoptosis. [ABSTRACT FROM AUTHOR]

Background: Hepatotoxicity caused by CCL4 is well known. Geraniol (GNL) has high antioxidant effect that can induces liver regeneration. However, the protective effect of GNL effect on CCL4-induced hepatorenal toxicity in pregnant mice has not yet been studied. Objective: To investigate whether GNL could protect against oxidative stress induced by CCL4 via the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which is regulated by phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), and has been found to have protective effects on renal and hepatic tissues. Materials and Methods: Forty-eight female albino mice weighing 25-30 g were randomly allocated to 4 groups: Group I served as a control; Group II received a toxicity-inducing single dose of 15 µL of CCL4 on the 4th day after mating; Group III received 40 mg/kg GNL + CCL4 (with GNL from the 1st day of assimilation to delivery); and Group IV received GNL alone from the 1st day of assimilation to the end of the delivery period. GNL was evaluated for its protective effects on hepatotoxicity in CCL4-treated pregnant mice. Litter size, weight, survival rate, and resorption were recorded. In addition, H & E staining was done for liver and kidney pathology as well as biochemical markers and oxidative markers malondialdehyde, superoxide dismutase, and catalase were analyzed. Results: CCL4 significantly reduced survival rate and increased resorption after exposure. Alanine transaminase and aspartate aminotransferase concentrations in the serum, tissue MDA, blood urea nitrogen, and creatinine were increased after CCL4 exposure. GNL improved enzyme and antioxidant levels and prevented CCL4-induced hepatic injury in mice. Caspase-3 cleavage was decreased by GNL, which increased PI3K, phosphorylated AKT, Nrf2, and B-cell lymphoma 2. Conclusion: GNL demonstrates a protective effect against CCl4-induced hepatorenal toxicity, mediated through the activation of the PI3K/AKT signaling pathway and the upregulation of Nrf2. These findings highlight the potential therapeutic implications of GNL in mitigating oxidative stress and inflammation in liver and kidney tissues. [ABSTRACT FROM AUTHOR]

Among the world's leading causes of cardiovascular disease, atherosclerosis is a chronic inflammatory disorder that affects the arteries. Both vasodilation and vasoconstriction, low levels of nitric oxide and high levels of reactive oxygen species and pro-inflammatory factors characterize dysfunctional blood vessels. Hypertension, and atherosclerosis, all start with this dysfunction. Geraniol, a compound of acyclic monoterpene alcohol, found in plants such as geranium, lemongrass and rose, is a primary constituent of essential oils. It shows a variety of pharmacological properties. This study aimed to investigate the impact of geraniol on Ox-LDL-induced stress and inflammation in human umbilical vein endothelial cells. In this study, HUVECs were treated with Ox-LDL or geraniol at different dose concentrations. MTT assay, Western blot, ROS generation and DNA fragmentation were used to evaluate geraniol's effects on Ox-LDL-induced HUVECs inflammation. The results show that geraniol pre-incubation ameliorates Ox-LDL-mediated HUVECs cytotoxicity and DNA fragmentation. The geraniol inhibited the production of pro-inflammatory cytokines by Ox-LDL, including TNF-α, IL-6 and IL-1β. In Ox-LDL-stimulated HUVECs, geraniol suppresses the nuclear translocation and activity of NF-ᴋB as well as phosphorylation of IkBα. Moreover, geraniol activated the PI3K/AKT/NRF2 pathway in HUVECs, resulting in an increase in the expression of HO-1. Taking our data together, we can conclude that, in HUVECs, geraniol inhibits Ox-LDL-induced inflammation and oxidative stress by targeting PI3/AKT/NRF2. [ABSTRACT FROM AUTHOR]

From the butanolic and the ethyl acetate extracts of Rhamnus alaternus L root bark and leaves, three new anthraquinone glycosides, alaternosides A-C (1,4,6,8 tetrahydroxy-3 methyl anthraquinone 1-O-ß-D-glucopyranosyl-4,6-di-O-α-L-rhamnopyranoside (1); 1,2,6,8 tetrahydroxy-3 methyl anthraquinone 8-O-ß-D-glucopyranoside (2) and 1, 6 dihydroxy-3 methyl 6 [2′-Me (heptoxy)] anthraquinone (3)) were isolated and elucidated together with the two known anthraquinone glycosides, Physcion-8-O-rutinoside (4) and emodin-6-O-α-L-rhamnoside (5) as well as with the known kaempferol-7-methylether (6), β-sitosterol (7) and β-sitosterol-3-O-glycoside (8). Their chemical structures were elucidated using spectroscopic methods (1D-, 2D-NMR and FAB-MS). Free radical scavenging activity of the isolated compounds was evaluated by their ability to scavenge DPPH. free radicals. Compounds (3), (4) and (6) showed the highest activity with IC50 values of 9.46, 27.68 and 2.35 μg/mL, respectively. [ABSTRACT FROM AUTHOR]