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Essential oils (EOs) are mixtures of secondary plant metabolism compounds with potential lipid-lowering activity and antioxidant properties. They may therefore be considered as add-on therapy for the prevention and treatment of cardiovascular diseases. EOs of Origanum × paniculatum (OpEO) , Lippia alba (chemotype linalool) (LaLEO) , Clinopodium nepeta (CnEO) and Eucalyptus globulus (EgEO), were evaluated on THP-1 foam cell macrophages as a cellular model of atherogenesis. Cell viability was determined by the MTT assay, lipid content by thin-layer chromatography, and Oil Red O staining. Antioxidant activity was evaluated by TBARS on low-density lipoprotein lipid peroxidation, and by ABTS•+, DPPH•, and FRAP assays. EOs were characterised by gas chromatography–mass spectrometry and a predictive multivariate data analysis was performed by partial least square regression (PLS) to identify the components related to antiatherogenic potential. OpEO reduced foam cell viability (IC50 = 45 µl/l) and cholesterol and triacylglycerol content and demonstrated antioxidant activity. In contrast, LaLEO increased lipid content and showed a prooxidant capacity with low reduction of cell viability (IC50 = 340 µl/l). CnEO showed prooxidant activity and reduction of cell viability (IC50 = 130 µl/l) without changes in lipid content. EgEO showed antioxidant activity, lipid increase, and low cytotoxicity (IC50 = 770 µl/l). PLS analysis suggests that cis-sabinene hydrate is responsible for cell viability inhibition, thymol and β-cis-terpineol decrease lipid content and possess antioxidant activity, and linalool increases lipid levels and has prooxidant capacity. OpEO is a promising natural product for therapy against atherosclerosis, with cis-sabinene hydrate, thymol, and β-cis-terpineol as potential active principles. [Display omitted] • Essential oils with or without potential antiatherogenic effects. • Origanum x paniculatum essential oil reduces viability and lipids in foam cells. • Origanum x paniculatum essential oil inhibits low density lipoprotein oxidation. • Lippia alba (chemotype linalool) essential oil increases lipids in foam cells. • Lippia alba (chemotype linalool) shows prooxidant activity. [ABSTRACT FROM AUTHOR]

Neurodegenerative disorders are characterized by the progressive accumulation of misfolded protein aggregates that eventually lead to the loss of selected neuronal populations. Immunotherapy has been shown in the recent years as a promising approach for targeting, clearing, and reducing the accumulation of protein aggregates. Alzheimer's disease (AD), which is the most common neurodegenerative disorder, has been the focus of numerous immunotherapeutic studies because the extracellular nature of the amyloid-β (Aβ) peptide. The aim of the current work is to dissect the state-of-the-art of anti-Aβ immunotherapy for AD. The rationale behind anti-Aβ antibodies, what has happened in clinical trials, and which strategies have been designed to avoid side-effects and improve the efficacy of those antibodies are presented. [ABSTRACT FROM AUTHOR]

Background Geraniol (G) is a natural isoprenoid present in the essential oils of several aromatic plants, with various biochemical and pharmacologic properties. Nevertheless, the mechanisms of action of G on cellular metabolism are largely unknown. Hypothesis/Purpose We propose that G could be a potential agent for the treatment of hyperlipidemia that could contribute to the prevention of cardiovascular disease. The aim of the present study was to advance our understanding of its mechanism of action on cholesterol and TG metabolism. Study Design/Methods NIH mice received supplemented diets containing 25, 50, and 75 mmol G/kg chow. After a 3-week treatment, serum total-cholesterol and triglyceride levels were measured by commercial kits and lipid biosynthesis determined by the [ 14 C] acetate incorporated into fatty acids plus nonsaponifiable and total hepatic lipids of the mice. The activity of the mRNA encoding HMGCR—the rate-limiting step in cholesterol biosynthesis—along with the enzyme levels and catalysis were assessed by real-time RT-PCR, Western blotting, and HMG-CoA-conversion assays, respectively. In-silico analysis of several genes involved in lipid metabolism and regulated by G in cultured cells was also performed. Finally, the mRNA levels encoded by the genes for the low-density-lipoprotein receptor (LDLR), the sterol-regulatory-element-binding transcription factor (SREBF2), the very-low-density-lipoprotein receptor (VLDLR), and the acetyl-CoA carboxylase (ACACA) were determined by real-time RT-PCR. Results Plasma total-cholesterol and triglyceride levels plus hepatic fatty-acid, total-lipid, and nonsaponifiable-lipid biosynthesis were significantly reduced by feeding with G. Even though an up-regulation of the mRNA encoding HMGCR occurred in the G treated mouse livers, the protein levels and specific activity of the enzyme were both inhibited. G also enhanced the mRNAs encoding the LDL and VLDL receptors and reduced ACACA mRNA, without altering the transcription of the mRNA encoding the SREBF2. Conclusions The following mechanisms may have mediated the decrease in plasma lipids levels in mice: a down-regulation of hepatocyte-cholesterol synthesis occurred as a result of decreased HMGCR protein levels and catalytic activity; the levels of LDLR mRNA became elevated, thus suggesting an increase in the uptake of serum LDL, especially by the liver; and TG synthesis became reduced very likely because of a decrease in fatty-acid synthesis. [ABSTRACT FROM AUTHOR]

Highlights: [•] Linalool, 1,8-cineole and simvastatin inhibit cholesterogenesis and proliferation. [•] The three compounds in pairwise combination inhibited synergistically. [•] Linalool and 1,8-cineole seemed to block the mevalonate pathway at different points. [•] Both monoterpenes decreased HMGCR levels. [•] HMGCR inhibition alone by monoterpenes did not cause antiproliferative effects. [ABSTRACT FROM AUTHOR]

Graphical abstract Abstract Anti-Aβ immunotherapy has emerged as a promising approach to treat Alzheimer’s disease (AD). The single-chain variable fragment scFv-h3D6 is an anti-Aβ antibody fragment that lacks the Fc region, which is associated with the induction of microglial reactivity by the full-length monoclonal antibody bapineuzumab. ScFv-h3D6 was previously shown to restore the levels of apolipoprotein E (apoE) and apolipoprotein J (apoJ) in a triple-transgenic-AD (3xTg-AD) mouse model. Since apoE and apoJ play an important role in the development of AD, we aimed to study the in vivo effect of the combined therapy of scFv-h3D6 with apoE and apoJ mimetic peptides (MPs). Four-and-a-half-month-old 3xTg-AD mice were treated for six weeks with scFv-h3D6, apoE-MP, apoJ-MP, or a combination of scFv-h3D6 with each of the MPs, or a vehicle, and then the results were compared to non-transgenic mice. Magnetic Resonance Imaging showed a general tendency of the different treatments to protect against the reduction in brain volume. Aβ burden decreased after treatment with scFv-h3D6, apoE-MP, or apoJ-MP, but the effect was not as evident with the combined therapies. In terms of glial reactivity, apoE-MP showed a potent anti-inflammatory effect that was eased by the presence of scFv-h3D6, whereas the combination of apoJ-MP and scFv-h3D6 was not detrimental. ScFv-h3D6 alone did not induce microglial reactivity, as full-length antibodies do; rather, it reduced it. Endogenous apoE and apoJ levels were decreased by scFv-h3D6, but the MPs lead to a simultaneous increase of both apolipoproteins. While apoE-MP and apoJ-MP demonstrated different effects in the combined therapies with scFv-h3D6, they did not improve the overall protective effect of scFv-h3D6 in reducing the Aβ burden, apolipoproteins levels or microglial reactivity. [ABSTRACT FROM AUTHOR]