There is significant promise for propolis as an effective antioxidant and anti-inflammatory agent with particular promise in cardiometabolic health.

PMID: 

Nutrients. 2019 Nov 8 ;11(11). Epub 2019 Nov 8. PMID: 31717277

Abstract Title: 

Evidence on the Health Benefits of Supplemental Propolis.

Abstract: 

Propolis is a honey-related product with reported health benefits such as improved immunity, lowered blood pressure, treated allergies and skin conditions. A literature review and narrative synthesis were conducted to investigate the evidence on the reported health benefits and future direction of propolis products. Using a predefined search strategy we searched Medline (OvidSP), Embase and Central for quantitative and qualitative studies (1990-2018). Citation, reference, hand searches and expert consultation were also undertaken. Studies of randomised control trials and observational data on humans with health-related outcomes were included. Collected data were entered into NVivo software (Version 12, QRS International) and analysed using a thematic framework and a narrative synthesis of emergent themes. A total of 63 publications were discussed. The majority were cell-based and animal studies, with a few key human trials conducted. There is significant promise for propolis as an effective antioxidant and anti-inflammatory agent with particular promise in cardiometabolic health.

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The role of propolis against paclitaxel-induced oligospermia, sperm abnormality, oxidative stress and DNA damage in testes of male rats.

PMID: 

Andrologia. 2019 Nov 25:e13394. Epub 2019 Nov 25. PMID: 31762066

Abstract Title: 

The role of propolis against paclitaxel-induced oligospermia, sperm abnormality, oxidative stress and DNA damage in testes of male rats.

Abstract: 

Paclitaxel (taxol) is one of the most powerful anticancer drugs but it possesses toxic effects on male reproductive system. Propolis, from folkloric remedy, have antioxidant, anti-inflammatory and anticancer effects. The present study established to examine the protective impact of Propolis against malformation of semen induced by taxol. Twenty-four male rats equally divided into four groups. Group I (normal control); group II, administrated Propolis alone; group III, taxol-treated group received taxol; group IV, co-administered of taxol and Propolis extract. After 4 weeks of treatment, the semen were collected and testis 24 hr after the last treatment. Sperm count, motility, viability and sperm morphology were assayed. Tissue supernatants were isolated for oxidative stress, cell energy parameters and 8-OHdG. DNA damage was evaluated using Comet assay in testes. Our results confirmed that taxol-induced significant reduction in sperm count, motility, viability and recorded marked elevation in sperm abnormalities. Also, taxol caused increased in 8-OHdG and DNA damage versus that recorded in control group. Treatment with Propolis improving semen quality and protected testis from detrimental effects of taxol and minimises its toxicity. In conclusions, Oral administration of Propolis modulates the toxic impact of taxol by amelioration semen quality, diminishing oxidation state, DNA damage and preserving cell energy.

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This review describes the beneficial effects of propolis on metabolic disorders.

PMID: 

Molecules. 2019 Dec 1 ;24(23). Epub 2019 Dec 1. PMID: 31805752

Abstract Title: 

Effects of Propolis Extract and Propolis-Derived Compounds on Obesity and Diabetes: Knowledge from Cellular and Animal Models.

Abstract: 

Propolis is a natural product resulting from the mixing of bee secretions with botanical exudates. Since propolis is rich in flavonoids and cinnamic acid derivatives, the application of propolis extracts has been tried in therapies against cancer, inflammation, and metabolic diseases. As metabolic diseases develop relatively slowly in patients, the therapeutic effects of propolis in humans should be evaluated over long periods of time. Moreover, several factors such as medical history, genetic inheritance, and living environment should be taken into consideration in human studies. Animal models, especially mice and rats, have some advantages, as genetic and microbiological variables can be controlled. On the other hand, cellular models allow the investigation of detailed molecular events evoked by propolis and derivative compounds. Taking advantage of animal and cellular models, accumulating evidence suggests that propolis extracts have therapeutic effects on obesity by controlling adipogenesis, adipokine secretion, food intake, and energy expenditure. Studies in animal and cellular models have also indicated that propolis modulates oxidative stress, the accumulation of advanced glycation end products (AGEs), and adipose tissue inflammation, all of which contribute to insulin resistance or defects in insulin secretion. Consequently, propolis treatment may mitigate diabetic complications such as nephropathy, retinopathy, foot ulcers, and non-alcoholic fatty liver disease. This review describes the beneficial effects of propolis on metabolic disorders.

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Arctigenin can improve myocardial infarction by inhibiting the inflammatory phenotype of macrophages/monocytes.

PMID: 

Lab Invest. 2019 Dec 2. Epub 2019 Dec 2. PMID: 31792391

Abstract Title: 

Arctigenin alleviates myocardial infarction injury through inhibition of the NFAT5-related inflammatory phenotype of cardiac macrophages/monocytes in mice.

Abstract: 

In this study, we screened potential natural compounds for the treatment of myocardial infarction (MI) and explored the underlying mechanisms. We built three machine learning models to screen the potential compounds. qPCR, flow cytometry, immunohistochemistry, and immunofluorescence analyses were applied to analyze the pharmacological effects of the compounds on macrophages/monocytes in vivo and in vitro. Arctigenin (AG) was selected as a candidate, and echocardiography, Masson's trichrome staining, and TUNEL staining were utilized to detect the effect of AG on MI in vivo. Transcriptome analysis and subsequent bioinformatics analyses were performed to predict the target of the selected compound. Western blot and luciferase reporter assays were used to confirm the target and mechanism of AG. The reversibility of the effects of AG were verified through overexpression of NFAT5. The results showed that AG can improve cardiac injury after MI by reducing infarct size, improving heart function, and inhibiting cardiac death. In addition, AG suppresses inflammatory macrophages/monocytes and proinflammatory cytokines in vivo and in vitro. Transcriptomic and biological experiments revealed that AG modulates macrophage polarization via the NFAT5-induced signaling pathway. Therefore, our data suggest that AG can improve MI by inhibiting the inflammatory phenotype of macrophages/monocytes through targeting of NFAT5.

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A. lappa extracts are potential candidates for the treatment of inflammatory disorders that are complement-related.

PMID: 

Chem Biodivers. 2019 Oct 25. Epub 2019 Oct 25. PMID: 31654480

Abstract Title: 

Inhibitory Effect of Supercritical Extracts from Arctium lappa L. on the Lectin Pathway of the Complement System.

Abstract: 

The complement system participates in host defense by eliminating microorganisms and triggering inflammation. However, insufficient control or exacerbated complement activation contributes to inflammatory diseases. Since promising antioxidant and anti-inflammatory activities have been identified in Arctium lappa L. extracts, this study aims to explore the effect of A. lappa extracts on the lectin pathway (LP) of complement activation. Four extracts were obtained by supercritical extraction using scCOwith or without ethanol as co-solvent, at different temperatures and pressures (E1: 2.2 mg/mL, E2: 2.6 mg/mL and E3: 2.0 mg/mL, E4: 1.5 mg/mL). To evaluate the effect of A. lappa extracts on the LP activation, an ELISA assay using mannose binding lectin pathway of complement was carried out with C4 detection. All extracts showed a concentration-dependent inhibitory effect on the activation of complement by the LP. The following ICwere observed for E1, E2, E3 and E4: 179.4 μg/mL, 74.69 μg/mL, 119.1 μg/mL and 72.19 μg/mL, respectively. Our results suggest that A. lappa extracts are potential candidates for the treatment of inflammatory disorders that are complement-related.

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Burdock root attenuates preneoplastic lesion development.

PMID: 

Environ Toxicol. 2019 Dec 5. Epub 2019 Dec 5. PMID: 31804025

Abstract Title: 

Burdock (Arctium lappa L.) root attenuates preneoplastic lesion development in a diet and thioacetamide-induced model of steatohepatitis-associated hepatocarcinogenesis.

Abstract: 

Nonalcoholic steatohepatitis (NASH) is considered growing risk factor for hepatocellular carcinoma development in high-income countries. Diet- and chemically induced rodent models have been applied for the translational study of NASH-associated hepatocarcinogenesis due to their morphological and molecular similarities to the corresponding human disease. Arctium lappa L. (burdock) root tea has been extensively consumed in Traditional Chinese Medicine due to its potential therapeutic properties. Indeed, the bioactive compounds of A. lappa root, as the polyphenols, have already showed antioxidant and anti-inflammatory properties in different in vivo and in vitro bioassays. In this study, we investigated whether burdock root ethanolic extract (BRE) administration attenuates NASH-associated hepatocarcinogenesis. Eight-week-old male Wistar rats received choline-deficient high-fat diet for 8 weeks and multiple thioacetamide doses for 4 weeks in order to induce NASH and preneoplastic glutathione-S-transferase pi (GST-P)preneoplastic foci. Subsequently, rats were treated with BRE (100 or 200 mg/kg body weight) or vehicle by oral gavage for 2 weeks. BRE displayed high levels of chlorogenic and caffeic acids and BRE administration reduced total fatty acid and lipid hydroperoxide levels, while increasing the activities of antioxidant superoxide dismutase and catalase enzymes in the liver. Furthermore, burdock intervention diminished the size of GST-Premodeling preneoplastic lesions (PNLs) and displayed a trend on reducing hepatocyte proliferation (Ki-67) inside them. These findings suggest that short-term exposure to BRE alleviated remodeling PNL development in NASH-associated hepatocarcinogenesis.

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Arctium lappa root extract prevents lead-induced liver injury.

PMID: 

Antioxidants (Basel). 2019 Nov 24 ;8(12). Epub 2019 Nov 24. PMID: 31771282

Abstract Title: 

Root Extract Prevents Lead-Induced Liver Injury by Attenuating Oxidative Stress and Inflammation, and Activating Akt/GSK-3β Signaling.

Abstract: 

L () is a popular medicinal plant with promising hepatoprotective activity. This study investigated the protective effect ofroot extract (ALRE) on lead (Pb) hepatotoxicity, pointing to its ability to modulate oxidative stress, inflammation, and protein kinase B/Akt/glycogen synthase kinase (GSK)-3β signaling. Rats received 50 mg/kg lead acetate (Pb(Ac)) and 200 mg/kg ALRE or vitamin C (Vit. C) for 7 days, and blood and liver samples were collected. Pb(Ac)provoked hepatotoxicity manifested by elevated serum transaminases and lactate dehydrogenase, and decreased total protein. Histopathological alterations, including distorted lobular hepatic architecture, microsteatotic changes, congestion, and massive necrosis were observed in Pb(II)-induced rats. ALRE ameliorated liver function and prevented all histological alterations. Pb(II) increased hepatic lipid peroxidation (LPO), nitric oxide (NO), caspase-3, and DNA fragmentation, and serum C-reactive protein, tumor necrosis factor-α, and interleukin-1β. Cellular antioxidants, and Akt and GSK-3β phosphorylation levels were decreased in the liver of Pb(II)-induced rats. ALRE ameliorated LPO, NO, caspase-3, DNA fragmentation and inflammatory mediators, and boosted antioxidant defenses in Pb(II)-induced rats. In addition, ALREactivated Akt and inhibited GSK-3β in the liver of Pb(II)-induced rats. In conclusion, ALRE inhibits liver injury in Pb(II)-intoxicated rats by attenuating oxidative injury and inflammation, and activation of Akt/GSK-3β signaling pathway.

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Gestational exposure to paracetamol in rats induces neurofunctional alterations in the progeny.

PMID: 

Neurotoxicol Teratol. 2019 Oct 20 ;77:106838. Epub 2019 Oct 20. PMID: 31644948

Abstract Title: 

Gestational exposure to paracetamol in rats induces neurofunctional alterations in the progeny.

Abstract: 

Paracetamol (PAR) is an over-the-counter medicine used as analgesic or antipyretic by 40-50% of the pregnant women in different countries. Epidemiologic studies have been associating maternal use of PAR with neurodevelopmental disruption and special attention has been given to its potential to increase the odds for neurodevelopmental disorders, such as attention-deficit hyperactive disorder and autism spectrum disorder. Population-based research do not allow the establishment of causal relationships because variable control is weak. We aimed to evaluate the potential of PAR to induce developmental neurotoxicity in rats. Pregnant Wistar rats were gavaged with PAR (350 mg/kg/day) or water from gestational day 6 until delivery. General toxicity endpoints included dams' body weight and food intake as well as pups' body weight until weaning. Behavioral evaluation occurred at post-natal days 10 (nest seeking test), 27 (behavioral stereotypy), 28 (three chamber sociability test and open field) and 29 (hot plate and elevated plus-maze). Moreover, lipid hidroperoxide (LOOH), reduced glutathione (GSH) and brain derived neurotrophic factor (BDNF) levels were quantified in prefrontal cortex and hippocampus of 22-days-old rats. Gestational exposure to PAR impaired nest seeking behavior, augmented apomorphine-induced behavioral stereotypy and decreased rostral grooming in the elevated plus maze. Exposed female pups presented elevated vertical exploration in the open field test. No alterations were observed in LOOH, GSH or BDNF levels in the prefrontal cortex orhippocampus. Exposure regimen did not affect general toxicity parameters or pups' behavior in the hot plate and sociability tests. These data suggest PAR as a developmental neurotoxicant. Observed alterations may be relevant for neurodevelopmental disorders.

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Nobiletin attenuates acetaminophen-induced hepatorenal toxicity.

PMID: 

J Biochem Mol Toxicol. 2019 Nov 27:e22427. Epub 2019 Nov 27. PMID: 31777137

Abstract Title: 

Nobiletin attenuates acetaminophen-induced hepatorenal toxicity in rats.

Abstract: 

The study aimed to examine the effects of nobiletin on the toxicity model induced with acetaminophen (APAP). For this purpose, 24 adult male rats were equally divided into four groups. The groups were the control group (group 1); dimethyl sulfoxide only, the APAP group (group 2) received a single dose of APAP 1000 mg/kg on the 10th day of experiment; the Nobiletin group (group 3), nobiletin (10 mg/kg) for 10 days; and the APAP + Nobiletin group (group 4), nobiletin (10 mg/kg) for 10 days with a single dose of APAP (1000 mg/kg) administered on the 10th day and the experiment ended after 48 hours. At the end of the study, a significant increase in malondialdehyde, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels and a significant decrease in glutathione levels, glutathione peroxidase activities and nuclear factor erythroid-derived 2-like 2 (Nrf-2) and heme oxygenase-1 (HO-1) expressions were observed with APAP application in liver and kidney tissues. Serum aspartate transaminase (AST), alanine transaminase (ALT), urea, and creatinine levels were also significantly increased in the APAP group. However, nobiletin treatment in group 4 reversed oxidative stress and inflammatory and histopathological signs caused by APAP. It is concluded that nobiletin may be a beneficial substance that confers hepatorenal protection to APAP-induced toxicity via antioxidant and anti-inflammatory mechanisms.

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Betanin exerted a potential anti-inflammatory and antioxidant effect against hepato-renal damage induced by paracetamol and diclofenac over consumption.

PMID: 

Biomarkers. 2019 Nov 26:1-24. Epub 2019 Nov 26. PMID: 31766895

Abstract Title: 

Impact of betanin against paracetamol and diclofenac induced hepato-renal damage in rats.

Abstract: 

Paracetamol (PAR) and diclofenac (DF) are the most popular consumed analgesics and anti-inflammatory medications.This study aimed to explore the protective effect of betanin (Bet) against PAR or DF induced hepato-renal damage in rats.Rats were randomly divided into five groups: Normal control (NC) group rats were given saline only. PAR group rats received PAR (400 mg/kg). PAR/Bet treated group rats administered PAR (400 mg/kg) plus Bet (25mg/kg). DF group rats received DF (10mg/kg). DF/Bet treated group rats administered DF (10mg/kg) plus Bet (25mg/kg). All drugs were given by gavage for 28 consecutive days.PAR and DF administration in high dose and long-time induced liver and kidney injury, disrupted serum lipid profile, enhanced serum levels of inflammatory and oxidative stress markers, triggered DNA fragmentation and caused drastic changes in the histopathological pictures of the two organs. Bet supplementation succeeded to ameliorate most of the biochemical changes and protected DNA from damage as obtained from comet assay. Histological features in H&E taken to different groups also mirrors this findings.Bet exerted a potential anti-inflammatory and antioxidant effect against hepato-renal damage induced by PAR or DF overconsumption.

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