No abstract

Olive (Olea europaea) leaf, an important traditional herbal medicine, displays cardioprotection that may be related to the cellular redox modulating effects of its polyphenolic constituents. This study was undertaken to investigate the protective effect of the ethanolic and methanolic extracts of olive leaves compared to the effects of oleuropein, hydroxytyrosol, and quercetin as a positive standard in a carbonyl compound (4-hydroxynonenal)-induced model of oxidative damage to rat cardiomyocytes (H9c2). Cell viability was detected by the MTT assay; reactive oxygen species production was assessed by the 2',7'-dichlorodihydrofluorescein diacetate method, and the mitochondrial membrane potential was determined using a JC-1 dye kit. Phospho-Hsp27 (Ser82), phospho-MAPKAPK-2 (Thr334), phospho-c-Jun (Ser73), cleaved-caspase-3 (cl-CASP3) (Asp175), and phospho-SAPK/JNK (Thr183/Tyr185) were measured by Western blotting. The ethanolic and methanolic extracts of olive leaves inhibited 4-hydroxynonenal-induced apoptosis, characterized by increased reactive oxygen species production, impaired viability (LD50: 25 µM), mitochondrial dysfunction, and activation of pro-apoptotic cl-CASP3. The ethanolic and methanolic extracts of olive leaves also inhibited 4-hydroxynonenal-induced phosphorylation of stress-activated transcription factors, and the effects of extracts on p-SAPK/JNK, p-Hsp27, and p-MAPKAPK-2 were found to be concentration-dependent and comparable with oleuropein, hydroxytyrosol, and quercetin. While the methanolic extract downregulated 4-hydroxynonenal-induced p-MAPKAPK-2 and p-c-Jun more than the ethanolic extract, it exerted a less inhibitory effect than the ethanolic extract on 4-hydroxynonenal-induced p-SAPK/JNK and p-Hsp27. cl-CASP3 and p-Hsp27 were attenuated, especially by quercetin. Experiments showed a predominant reactive oxygen species inhibitory and mitochondrial protecting ability at a concentration of 1-10 µg/mL of each extract, oleuropein, hydroxytyrosol, and quercetin. The ethanolic extract of olive leaves, which contains larger amounts of oleuropein, hydroxytyrosol, verbascoside, luteolin, and quercetin (by HPLC) than the methanolic one, has more protecting ability on cardiomyocyte viability than the methanolic extract or each phenolic compound against 4-hydroxynonenal-induced carbonyl stress and toxicity.

Quorum sensing (QS) and biofilm formation are important mechanisms related to antibiotic resistance of many pathogens. Alternative treatments are needed to prevent recurrent or chronic infections caused by multi-resistant pathogens. Therefore, the aim of this study is to investigate and compare the inhibitory potential of the dietary phytochemicals: curcumin, quercetin, apigenin, pyrogallol, gallic acid and luteolin against QS of and biofilm formation by Chromobacterium violaceum ATCC 12472 and the swimming and swarming abilities of Pseudomonas aeruginosa PAO1. Anti-QS potential of the phytochemicals was evaluated qualitatively and quantitatively using C. violaceum via the disk diffusion assay based on violacein pigment inhibition at the subminimal inhibitory concentrations ranging from 46.87 to 750 µg/mL. The results of anti-QS and antibiofilm activities on C. violaceum demonstrated that all the phytochemicals except pyrogallol and gallic acid inhibited violacein production (from (11.0±0.1) to (88.2±0.1) %) in a concentration-dependent manner. In addition, the biofilm formation was also significantly inhibited (p<0.05) in the presence of all the phytochemicals ((1.38±0.08)–(84.2±0.2) %). In the present study, the results revealed that quercetin, curcumin, apigenin and luteolin could be promising QS and biofilm inhibitory agents against the C. violaceum 12472 biosensor system. Our findings also suggest that all the phytochemicals, especially curcumin, quercetin and pyrogallol, might be anti-pathogenic agents against P. aeruginosa PAO1 infections due to the ability to control QS. However, more comprehensive studies at the molecular level, explaining their anti-QS mechanisms, need to be conducted to confirm these results and identify the genes involved.

According to our findings, owing to its antioxidant and cytotoxic potential, EtAc extract might include anticancer agents for acute promyelocytic leukemia.

Current evidence has demonstrated the immunomodulatory efficacy of omega-3 polyunsaturated fatty acids (PUFAs) in glial cells, suggesting their therapeutic potential for diseases in the central nervous system (CNS). However, conjugated omega-5 PUFAs have also attracted considerable attention because of their suggested anti-inflammatory effects. In the present study, the effect of pomegranate (Punica granatum L.) seed oil (PSEO) (a rich source of omega-5 PUFAs) on the activation of cultured BV-2 microglia was investigated within a 24-hour incubation period. PSEO (25 μg/ml) showed only a slightly smaller inhibitory effect on LPS-stimulated NO production (243 ± 12.5 % of control, p<0.001 vs. 437 ± 9.2 % in stimulated cells) and TNF-α release (87.1 ± 5.62 pg/ml vs. 229 ± 24.4 pg/ml in stimulated cells), as well as iNOS expression (7.36-fold of control, p < 0.01, vs. 17.5-fold increase in stimulated cells) compared to a standardized omega-3 PUFAs mixture (25 μg/ml) and the flavonoid quercetin (25 μmol/l). Unlike quercetin and stobadine, only the PUFA preparations effectively prevented apoptosis of microglia (as confirmed by the suppression of caspase 3 activation) exposed to the toxic concentration of LPS. The PUFA preparations did not provide a notable suppression of the intracellular oxidant generation and did not influence the intracellular distribution of cholesterol (as confirmed by filipin staining). However, they appeared to affect the morphology of activated cells. In conclusion, our data point to the first evidence of immunomodulation and cytoprotection of BV-2 microglia by the pomegranate seed oil, indicating that it may be (comparably to omega-3 PUFAs) efficient against microglia-mediated neuroinflammation while preventing the premature depletion of these immune effector cells in the brain.