Lipid and color stability of the meat and sausages of broiler fed with calcium anacardate.

BACKGROUND: Anacardic acid, a phenolic compound, represents 90% of cashew nut shell liquid, which is a byproduct from the industrial processing of cashew nuts. This study aimed to add calcium anacardate (CA) to broilers' diets as a source of anacardic acid, to evaluate its antioxidant effect in breast meat and in processed meat products (sausages). For this purpose, birds were fed according to the following treatments: diet without antioxidant and diets containing 2.5, 5.0, 7.5, or 10.0 g kg-1 CA. Chicken breast meat was stored frozen for 90 days. The thigh and drumsticks were used to produce chicken sausages that were kept in refrigerated conditions for 90 days. Lipid oxidation and color stability were assessed every 30 days. RESULTS: For breast meat, a 2.5 g kg-1 concentration of CA was insufficient to retard lipid oxidation, whereas 10.0 g kg-1 gave rise to a pro-oxidant effect and 5.0 g kg-1 slowed the oxidation up to 50 days. A level of 7.5 g kg-1 of CA was effective in retarding oxidation, favoring colour stability during the 90-days frozen storage. For sausages, 2.5 g kg-1 of calcium anacardate in broiler diets was sufficient to retard lipid oxidation. Calcium anacardate 7.5 g kg-1 provided greater redness in the sausages compared with the control and with the other treatments containing 5.0 and 10.0 g kg-1 . CONCLUSIONS: Calcium anacardate is a potential natural antioxidant for breast meat and sausages in storage when added to broilers' diets. © 2018 Society of Chemical Industry.

Peripheral antinociceptive action of mangiferin in mouse models of experimental pain: role of endogenous opioids, K(ATP)-channels and adenosine.

This study aimed to assess the possible systemic antinociceptive activity of mangiferin and to clarify the underlying mechanism, using the acute models of chemical (acetic acid, formalin, and capsaicin) and thermal (hot-plate and tail-flick) nociception in mice. Mangiferin at oral doses of 10 to 100 mg/kg evidenced significant antinociception against chemogenic pain in the test models of acetic acid-induced visceral pain and in formalin- and capsaicin-induced neuro-inflammatory pain, in a naloxone-sensitive manner, suggesting the participation of endogenous opiates in its mechanism. In capsaicin test, the antinociceptive effect of mangiferin (30 mg/kg) was not modified by respective competitive and non-competitive transient receptor potential vanilloid 1 (TRPV1) antagonists, capsazepine and ruthenium red, or by pretreatment with L-NAME, a non-selective nitric oxide synthase inhibitor, or by ODQ, an inhibitor of soluble guanylyl cyclase. However, mangiferin effect was significantly reversed by glibenclamide, a blocker of K(ATP) channels and in animals pretreated with 8-phenyltheophylline, an adenosine receptor antagonist. Mangiferin failed to modify the thermal nociception in hot-plate and tail-flick test models, suggesting that its analgesic effect is only peripheral but not central. The orally administered mangiferin (10-100 mg/kg) was well tolerated and did not impair the ambulation or the motor coordination of mice in respective open-field and rota-rod tests, indicating that the observed antinociception was unrelated to sedation or motor abnormality. The findings of this study suggest that mangiferin has a peripheral antinociceptive action through mechanisms that involve endogenous opioids, K(ATP)-channels and adenosine receptors.

Mangiferin ameliorates 6-hydroxydopamine-induced cytotoxicity and oxidative stress in ketamine model of schizophrenia.

BACKGROUND: Accumulating evidence indicates that mangiferin (MGF), a natural xanthone, by virtue of its antioxidant and antiinflammatory properties is neuroprotective. Here we sought to verify the cytoprotective role of MGF on cultured rat primary mesencephalic cells exposed to 6-hydroxydopamine (6-OHDA) in vitro, and the MGFs anti-inflammatory potential in mouse model of ketamine-induced schizophrenia in vivo. METHODS: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-assay was performed tomeasure cell viability inmesencephalic cell cultures exposed to neurotoxin (6-OHDA, 40 µM). Schizophrenia was induced in mice by ketamine (50 mg/kg, ip, twice a day, for 7 days). The treatment effects of MGF (50 mg/kg, po, for 7 days) were verified on locomotor behavioral changes in open-field test, and on the oxidant stress-related increase in lipid-peroxidation (malondialdehyde) and interleukin-6 (IL-6) levels in brain tissues. RESULTS: MGF (10-100 µM) produced no per se effect on cell viability as measured by MTT assay, but significantly prevented the 6-OHDA-induced cell death in a concentration-dependent manner. Acridine orange/ethidium bromide (AO/EtBr) staining confirmed the absence of 6-OHDA-induced morphological changes characteristic of apoptosis/necrosis. In open-field test, ketamine-induced impaired locomotor activity and behavioral changes such as grooming and stereotyped but not rearing were effectively ameliorated by MGF pretreatment. Also, ketamine-associated increase in brain tissue levels of IL-6 and MDA were significantly lowered in MGF-pretreated mice. CONCLUSION: Mangiferin has a neurocytoprotective role related, at least in part, to an antioxidant and anti-inflammatory mechanism, which could be explored for more effective therapies of schizophrenia and other neurodegenerative diseases.

Protective effect of anacardic acids from cashew (Anacardium occidentale) on ethanol-induced gastric damage in mice.

Cashew nut-shell liquid and the contained anacardic acids (AAs) have been shown to possess antioxidant, lipoxygenase inhibitory, anti-Helicobacter pylori and antitumor properties. Despite these known effects, hitherto there were no published reports on their likely gastroprotective effects. The present study was designed to verify whether AAs afford gastroprotection against the ethanol-induced gastric damage and to examine the underlying mechanism(s). Gastric damage was induced by intragastric administration of 0.2mL of ethanol (96%). Mice in groups were pretreated orally with AAs (10, 30 and 100mg/kg), misoprostol (50 microg/kg), or vehicle (2% Tween 80 in saline, 10mL/kg), 45min before ethanol administration. They were sacrificed 30min later, the stomachs excised, and the mucosal lesion area (mm(2)) measured by planimetry. Gastroprotection was assessed in relation to inhibition of gastric lesion area. To study the gastroprotective mechanism(s), its relations to capsaicin-sensitive fibers, endogenous prostaglandins, nitric oxide and ATP-sensitive potassium channels were analysed. Treatments effects on ethanol-associated oxidative stress markers GSH, MDA, catalase, SOD, and total nitrate/nitrite levels as an index of NO were measured in gastric tissue. Besides, the effects of AAs on gastric secretory volume and total acidity were analysed in 4-h pylorus-ligated rat. AAs afforded a dose-related gastroprotection against the ethanol damage and further prevented the ethanol-induced changes in the levels of GSH, MDA, catalase, SOD and nitrate/nitrite. However, they failed to modify the gastric secretion or the total acidity. It was observed that the gastroprotection by AAs was greatly reduced in animals pretreated with capsazepine, indomethacin, l-NAME or glibenclamide. These results suggest that AAs afford gastroprotection principally through an antioxidant mechanism. Other complementary mechanisms include the activation of capsaicin-sensitive gastric afferents, stimulation of endogenous prostaglandins and nitric oxide, and opening of K(+)(ATP) channels. These combined effects are likely to be accompanied by an increase in gastric microcirculation.

Gastroprotective effect of lupeol on ethanol-induced gastric damage and the underlying mechanism.

The effect of lupeol, a natural pentacyclic triterpene on ethanol-induced gastric damage in mice was evaluated. The gastroprotection was assessed by determination of changes in mean gastric lesion area, quantification of mucosal non-protein sulfhydryls (NP-SH), and characterized using drugs that influence the endogenous prostaglandins, alpha(2)-adrenoceptors, nitric oxide, K(ATP)-channels, and intracellular calcium. Orally administered lupeol (3, 10, and 30 mg/kg) significantly and dose-dependently attenuated the ethanol-induced gastric damage by 39-69%, whereas the positive control N-acetylcysteine (NAC, 300 mg/kg, i.p.) afforded 32% protection. Both lupeol and NAC restored the NP-SH depleted by ethanol but the lupeol effect was only marginal. Lupeol gastroprotection was attenuated by indomethacin and L-NAME, the respective COX and NO-synthase inhibitors and was weakly sensitive to alpha(2)-adrenergic antagonist yohimbine and K(ATP)-channel blocker glibenclamide, but more profoundly to calcium blocker verapamil. These pharmacological effects of lupeol may synergistically contribute to alleviating the ethanol-associated gastric damage, which is multifactorial.

Discovery of novel Trypanosoma cruzi glyceraldehyde-3-phosphate dehydrogenase inhibitors.

Based on its essential role in the life cycle of Trypanosoma cruzi, the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH) has been considered a promising target for the development of novel chemotherapeutic agents for the treatment of Chagas' disease. In the course of our research program to discover novel inhibitors of this trypanosomatid enzyme, we have explored a combination of structure and ligand-based virtual screening techniques as a complementary approach to a biochemical screening of natural products using a standard biochemical assay. Seven natural products, including anacardic acids, flavonoid derivatives, and one glucosylxanthone were identified as novel inhibitors of T. cruzi GAPDH. Promiscuous inhibition induced by nonspecific aggregation has been discarded as specific inhibition was not reversed or affected in all cases in the presence of Triton X-100, demonstrating the ability of the assay to find authentic inhibitors of the enzyme. The structural diversity of this series of promising natural products is of special interest in drug design, and should therefore be useful in future medicinal chemistry efforts aimed at the development of new GAPDH inhibitors having increased potency.

Terpenóides e avaliação do potencial antimalárico, larvicida, anti-radicalar e anticolinesterásico de Pouteria venosa (Sapotaceae) / Terpenoids and evaluation of the antimalarial, larvicidal, anti-radicalar and anticholinesterase potential of Pouteria venosa (Sapotaceae)

O presente trabalho descreve o isolamento de quatro triterpenos (taraxerol, ácido ursólico, ácido 3b,19a,23-triidroxiurs-12-en-28-óico e ácido 2a,3a,19a,23-tetraidroxiurs-12-en-28-óico) e um fitoesteróide (espinasterol), bem como a avaliação do potencial antimalárico (cepa NK-65 do Plasmodium berghei), larvicida (larvas do 4º instar do Aedes aegypti), anti-radicalar (2,2-difenil-1-picril-hidrazila, DPPH) e anticolinesterásico de extratos das folhas, cascas do caule e caule de Pouteria venosa (Mart.) Baehni. Todos os compostos isolados estão sendo descritos pela primeira vez nesta espécie e foram identificados com base na análise de dados espectrais (IV e RMN, incluindo APT e DEPT), bem como pela comparação com dados descritos na literatura.

This work describes the isolation of four triterpenes (taraxerol, ursolic acid, 3b,19a,23-trihydroxyurs-12-en-28-oic acid and 2a,3a,19a,23-tetrahydroxyurs-12-en-28-oic acid) and a phytosteroid (spinasterol), as well as a preliminary evaluation of antimalarial (NK-65 strains of Plasmodium berghei), larvicidal (4th instar of Aedes aegypti), anti-radicalar (2,2-diphenyl-1-pycryl-hydrazyl, DPPH) and anticholinesterase activities of Pouteria venosa (Mart.) Baehni extracts from leaves, stem barks and stems. All isolated compounds are being described for the first time in this species and were identified on basis of the spectral data (IR and NMR, including APT, DEPT), as well as by comparison with literature data.