Academic literature on the topic 'Oleuropein aglycone'

Olives affected by active and damaging infestation (olive fruit fly Bactrocera oleae (Rossi)) were assayed for their chemical composition. Biophenols were determined by HPLC, sterols, triterpenic dialcohols, and fatty acids by gas chromatography analysis. The acquired data were statistically analyzed. Oils produced from “Istrska belica” fruit affected by active infestation compared to the oils made from fruit affected by damaging infestation showed higher amounts of total oleuropein biofenols (377.3 versus (vs.) 106.6 mg/kg), total biophenols (755 vs. 377 mg/kg), lignans (85.3 vs. 32.9 mg/kg), the dialdehydic form of decarboxymethyl oleuropein aglycone (DMO-Agl-dA) (148.3 vs. 49.0 mg/kg), its oxidized form (DMO-Agl-dA)ox (35.2 vs. 8.5 mg/kg), the dialdehydic form of oleuropein aglycone (O-Agl-dA) (61.1 vs. 8.0 mg/kg), the dialdehydic form of ligstroside aglycone (L-Agl-dA) (63.5 vs. 28.0 mg/kg), the aldehydic form of oleuropein aglycone (O-Agl-A) (40.6 vs. 8.4 mg/kg), and lower amounts of tyrosol (Tyr) (6.0 vs. 13. 9 mg/kg) and the aldehydic form of ligstroside aglycone (L-Agl-A) (13.8 vs. 40.3 mg/kg). Higher values of stigmasterol (2.99%) and lower values of campesterol (2.25%) were determined in oils affected by damaging infestation; an increase in triterpenic dialcohols was also observed (3.04% for damaging and 1.62% for active infestation). Oils affected by damaging infestation, compared to active infestation, showed lower amounts of oleic acid (73.89 vs. 75.15%) and higher amounts of myristic (0.013 vs. 0.011%), linoleic (7.27 vs. 6.48%), and linolenic (0.74 vs. 0.61%) acids.

Olive oil is an important product in the Mediterranean diet, due to its health benefits and sensorial characteristics. Picholine marocaine is the most cultivated variety in Morocco. The present research aims to evaluate the phenolic compounds, vitamin E and fatty acids of commercial Picholine marocaine virgin olive oils (VOOs) from five different North Moroccan provinces (Chefchaouen, Taounate, Errachidia, Beni Mellal and Taza), using HPLC-photodiode array (PDA)/electrospray ionization (ESI)-MS, normal phase (NP)-HPLC/ fluorescence detector (FLD) and GC-flame ionization detector (FID)/MS, respectively. The obtained results showed an average content of 130.0 mg kg−1 of secoiridoids (oleuropein aglycone, 10-hydroxy-oleuropein aglycone and ligstroside aglycone, oleocanthal and oleacein), 108.1 mg kg−1 of phenolic alcohols (tyrosol and hydroxytyrosol), 34.7 mg kg−1 of phenolic acids (caffeic acid, ferulic acid and elenolic acid), and 8.24 mg kg−1 of flavonoids (luteolin, luteolin glucoside, apigenin). With regard to vitamin E, α-tocopherol was the most abundant vitamin E (57.9 mg kg−1), followed by α-tocotrienol (2.5 mg kg−1), γ-tocopherol (4.5 mg kg−1) and β-tocopherol (1.9 mg kg−1), while δ-tocopherol was not detected. Moreover, 14 fatty acids were found and, among them, oleic acid (76.1%), linoleic acid (8.1%) palmitic acid (8.7%) and stearic acid (2.5%) were the major fatty acids detected. Finally, heat map and principal component analysis allowed us to classify the studied provinces in terms of VOO chemical composition: Chefchaouen (tyrosol and hydroxytyrosol), Taounate (oleuropein aglycone), Errachidia (ferulic acid, w-3 and w-6), Beni Mellal (oleocanthal) and Taza (luteolin and oleic acid).

Abstract β-Sitosteryl-D-glucoside and oleuropein isolated from the olive tree (Olea europaea) and their hydrolysed derivatives were tested by a feeding stimulative activity bioassay using the olive weevil (Dyscerus perforatus). Although the steroidal glucoside showed potent feeding stimulative activity, the activity of the aglycone (β-sitosterol) was significantly lower than that of the glucoside. On the other hand, the difference in the activity between oleuropein, a secoiridoid glucoside, and the hydrolysed derivatives was not significant.

Oleuropein, a glycosylated secoiridoid present in olive leaves, is known to be an important antioxidant phenolic compound. We studied the antioxidant effect of low doses of oleuropein aglycone (3,4-DHPEA-EA) and oleuropein aglycone peracetylated (3,4-DHPEA-EA(P)) in murine C2C12 myocytes treated with hydrogen peroxide (H2O2). Both compounds were used at a concentration of 10 μM and were able to inhibit cell death induced by the H2O2 treatment, with 3,4-DHPEA-EA(P) being more. Under our experimental conditions, H2O2 efficiently induced the phosphorylated-active form of JNK and of its downstream target c-Jun. We demonstrated, by Western blot analysis, that 3,4-DHPEA-EA(P) was efficient in inhibiting the phospho-active form of JNK. This data suggests that the growth arrest and cell death of C2C12 proceeds via the JNK/c-Jun pathway. Moreover, we demonstrated that 3,4-DHPEA-EA(P) affects the myogenesis of C2C12 cells; because MyoD mRNA levels and the differentiation process are restored with 3,4-DHPEA-EA(P) after treatment. Overall, the results indicate that 3,4-DHPEA-EA(P) prevents ROS-mediated degenerative process by functioning as an efficient antioxidant.

A set of oleuropein aglycone derivatives were synthesized by transacetalization under mild and environmental friendly conditions. The antioxidant activities of the obtained compounds exhibited a dependence on their level of lipophilicity thus demonstrating their potential application as a preservative in fatty foods.

Mounting evidence supports the beneficial effects of the Mediterranean diet in preventing age-related dysfunctions, neurodegenerative diseases and in attenuating AD-like pathology and cognitive deterioration. We aimed to test the effect of Oleuropein Aglycone, the main polyphenol found in olive oil, on Aß aggregation using a rat model and a transgenic mouse model of Aß deposition. Following the modulatory effect of Oleuropein Aglycone on the autophagic flux, we investigated the role of autophagy in neurodevelopment through knockout autophagic genes in zebrafish.

Macroautophagy, also referred to as autophagy, is an intracellular process aimed to degrade and recycle cytoplasmic components, including long-lived proteins and damaged organelles. Due to the pivotal role of autophagy in maintaining cellular proteostasis, its dysfunction is associated with a wide number of human diseases such as cancer, cardiomyopathies and neurodegenerative disorders. In these pathological conditions, autophagy is initially activated as a survival mechanism but subsequently becomes defective, leading to cell damage. Many recent studies aim to better understand why autophagy is compromised in pathological conditions. Consequently restoration of defective autophagy now appears as an important therapeutic strategy in disease contexts. Several small molecules acting as autophagy modulators, such as plant polyphenols, or natural compounds present in fruit and vegetables, have been proposed as potential therapeutic applications. Plant polyphenols are able to regulate autophagy through different pathways. In particular, resveratrol and epigallocatechin-3 gallate (EGCG) stimulate the autophagic pathway via CamKK-AMPK-mTOR signalling. Polyphenols can also activate the sirtuins (SIRT), family of class III histone deacetylases, which are also involved in autophagy modulation. SIRT-induction results in many cellular outcomes and is considered responsible for the epigenetic effects of polyphenols. Oleuropein is the main polyphenol found in the olive tree and its main product, olive oil. Our previous studies have highlighted the beneficial effects of oleuropein aglycone (OLE), both in neuroblastoma cell lines (N2a) and in TgCRND8 mice, a model of Aβ deposition. In the latter, food supplementation with OLE resulted in remarkable plaque reduction and in the reduction of cognitive impairment when compared to non-OLE fed littermates. These protective effects were strongly correlated to an increased activation of autophagy in OLE fed mice. In light of the benefits associated with the upregulation in autophagy, the aim of this thesis was to investigate the cellular and molecular effectors of OLE-induced autophagy in vitro, by use of cultured human neuroblastoma cells (SH-SY5Y) and in vivo, using our TgCRND8 mice. Our in vitro results showed that OLE supplementation induces a rapid release of Ca2+ from the endoplasmic reticulum stores which, in turn, activates CAMKKβ with subsequent phosphorylation and activation of AMPK. The interplay between AMPK activation and mTOR inhibition shown in the OLE-fed animal model supports the idea that autophagy activation by OLE proceeds through mTOR inhibition. SIRT1 activation, another mechanism that synergizes with OLE-induced Ca2+-CaMKKβ-AMPK-mTOR signalling was also found in N2a cells. Given our findings for OLE dependent promotion of autophagy in our in vitro and in vivo neurodegeneration models, we aimed to determine whether OLE promotion of autophagy is ubiquitous and could protect against other pathological conditions displaying autophagy dysfunction. We selected an in vitro model of cardiomyopathy characterized by overexpression of monoamine oxidase-A (MAO-A). It is well established that catecholamine and serotonin degradation by MAO-A produces H2O2, which then disrupts nuclear translocation of TFEB, a master regulator of autophagy, causing autophagosome accumulation and ultimately cell death. Using this model we have shown that OLE treatment counteracts the effects of the MAO-A/H2O2 axis by improving mitochondrial function and decreasing cell necrosis. We demonstrate that these protective outcomes are, at least in part, related to the activation in autophagy. Indeed, increased autophagy observed in cardiac cells treated with OLE was a measure of the increase in autophagic vacuoles and autophagy-specific marker (LC3II) expression. Double immunofluorescence imaging of RFP-GFP-LC3 after 6 h of OLE treatment showed an increase of the autophagic flux; in addition, nuclear translocation of TFEB in OLE-treated cells was also observed. Together these data suggest that OLE treatment evokes transcriptional regulation of autophagy. In conclusion, our findings demonstrate that the underlying molecular mechanism of OLE stimulated autophagy includes the activation of the Ca2+-CaMKK-AMPK-mTOR signalling pathway. The identified molecular underpinnings of OLE treatment are indeed similar to other plant polyphenols such as resveratrol and EGCG. We show further that SIRT1-activation could synergize to maintain OLE-induced autophagy. TFEB translocation to the nucleus supports the importance of the transcriptional regulation of autophagy, findings that warrent further investigation. The results of this thesis add to the growing knowledge base of the molecular mechanisms of OLE-induced autophagy and provide strong evidence that similar to other plant polyphenols OLE can be a potential therapeutic against age-related diseases associated with autophagy dysfunction, including neurodegeneration and cardiovascular diseases.