PMID: 

Br J Nutr. 2020 Jan 29:1-24. Epub 2020 Jan 29. PMID: 31992372

Abstract Title: 

Flaxseed oil in the context of a weight loss program ameliorates fatty liver grade in patients with non-alcoholic fatty liver disease: a randomized double-blind controlled trial.

Abstract: 

Long-chain omega-3 fatty acids have shown to regulate lipid metabolism and reduce fat accumulation in the liver. This trial investigated the effect of flaxseed oil, as a rich source of alpha-linolenic acid, on fatty liver and cardiometabolic risk factors in patients with non-alcoholic fatty liver disease (NAFLD). The randomized, double-blind, controlled trial was performed on 68 NAFLD patients who divided into flaxseed (n=34) and sunflower (n=34) oil groups. Patients were given a hypocaloric diet (-500 kcal/d) and 20 g/d of the corresponding oil for 12 weeks. Fatty liver grade, liver enzymes, and cardiometabolic parameters were determined. The intention-to-treat approach was used for data analysis. Fatty liver grade significantly decreased in both groups (-0.68 in flaxseed vs. -0.29 in sunflower, P=0.002). ALT and AST decreased in both groups (P

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PMID: 

Lipids Health Dis. 2020 Feb 7 ;19(1):20. Epub 2020 Feb 7. PMID: 32028957

Abstract Title: 

Dietary flaxseed oil rich in omega-3 suppresses severity of type 2 diabetes mellitus via anti-inflammation and modulating gut microbiota in rats.

Abstract: 

BACKGROUND: Type 2 diabetes mellitus (T2DM) is closely associated with hyperglycemia, abnormal lipid profiles, chronic low-grade inflammation and gut dysbiosis. Dietary intervention plays a crucial role in the control of diabetes. Flaxseed oil (FO), a plant-derived omega-3 (ω-3) polyunsaturated fatty acids (PUFAs), is rich in α-linolenic acid (ALA) which has been proved to benefit for chronic metabolic disease. However, the exact effects of dietary FO on T2DM remains largely unclear.METHODS: In the present study, SD rats were randomly allocated into four groups: pair-fed (PF) with corn oil (CO) group (PF/CO); DM with CO group (DM/CO); PF with FO group (PF/FO); DM with FO group (DM/FO). A diabetic rat model was generated by a single intraperitoneal injection of streptozotocin-nicotinamide (STZ-NA). After 5 weeks of intervention, rats were euthanized and associated indications were investigated.RESULTS: Dietary FO significantly reduced fasting blood glucose (FBG), glycated hemoglobin (GHb), blood lipid, plasma lipopolysaccharide (LPS), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, IL-17A and malondialdehyde (MDA), compared to control group, respectively. Moreover, body mass (BM) and superoxide dismutase (SOD) in DM/FO group were dramatically increased respectively, compared with those in DM/CO group. But insulin (INS) and homeostasismodel assessment of insulin resistance (HOMA-IR) remained no significant difference between DM/CO group and DM/FO group. Sequencing analysis of gut microbiota showed a reduction in the relative abundance of Firmicutes and Blautia, as well as a reduction in the ratio of Bacteroidetes-Firmicutes in DM/FO group compared to DM/CO group. An elevation in the relative abundance of Bacteroidetes and Alistipes were detected in DM/FO group. Acetic acid, propionic acid and butyric acid belonging to short chain fatty acids (SCFAs) as gut microbiota metabolites, were dramatically increased after FO intervention. Correlation analysis revealed that the relative abundance of Firmicutes and Blautia were positively correlated with IL-1β, TNF-α, IL-6, IL-17A or LPS, respectively. Additionally, Bacteroidetes and Alistipes were negatively correlated with LPS.CONCLUSIONS: Taken together, dietary FO ameliorated T2DM via suppressing inflammation and modulating gut microbiota, which may potentially contribute to dietary control of diabetes.

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PMID: 

Complement Ther Med. 2020 Jan ;48:102267. Epub 2019 Nov 26. PMID: 31987231

Abstract Title: 

The effect of oral capsule of curcumin and vitamin E on the hot flashes and anxiety in postmenopausal women: A triple blind randomised controlled trial.

Abstract: 

OBJECTIVE: The decline and eventual cessation of estrogen production cause a variety of symptoms during menopause, affecting each woman differently. Most women reported severe hot flashes and night sweats during menopause. The present study aimed to determine and compare the efficacy of curcumin and vitamin E on hot flashes and anxiety (primary objectives), sexual function, menopausal symptoms and adverse effects (secondary objectives).MATERIALS AND METHODS: This was a triple-blind randomized controlled clinical trial. The participants consisted of 93 postmenopausal women in Ahar city-Iran. They were assigned into three groups (two intervention groups and one control group). The first intervention group received oral capsule of curcumin (500 mg), the second intervention group was given oral tablets of vitamin E (200 IU/day), and the third group (control) received placebo twice a day for eight weeks. The participants completed the hot flash checklist one week before the intervention, and 4 weeks and 8 weeks after the intervention. They also filled out the Anxiety Scale, the Female Sexual Function Index (FSFI), the Greene Climacteric Scale before the intervention, and 4 weeks and 8 weeks after the intervention. One-way ANOVA, repeated measures ANOVA and ANCOVA tests were used for data analysis.RESULTS: There was no statistically significant difference between groups in terms of demographic characteristics, mean number of hot flashes, mean score of anxiety, sexual function index and menopausal symptoms before the intervention (p > 0.05). The mean age of participants was 51.7 years. Mean number of hot flashes in the curcumin group (adjusted mean difference = -10.7, 95%confidence interval = -3.6 to -17.9, P = 0.001) and in the vitamin E group (-8.7, -0.6 to -15.0, P = 0.029) was significantly lower than the placebo group after the intervention. The first significant effect of curcumin on hot flashes was observed after four weeks (P = 0.027). However, there was no significant difference between vitamin E group and placebo four weeks after intervention (P = 0.052) and the first significant effectof vitamin E on hot flashes was observed after eight weeks (P = 0.025). There was no statistically significant difference between the groups in terms of sexual function index, anxiety and menopausal symptoms (P > 0.05).CONCLUSION: The results of this study showed that oral intake of curcumin and vitamin E significantly reduced hot flashes in postmenopausal women but had no significant effect on anxiety, sexual function and menopausal symptoms.

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PMID: 

Saudi Pharm J. 2020 Jan ;28(1):116-126. Epub 2019 Dec 7. PMID: 31920438

Abstract Title: 

Propolis ameliorates cerebral injury in focal cerebral ischemia/reperfusion (I/R) rat model via upregulation of TGF-β1.

Abstract: 

Neuroprotective impact of transforming growth factorβ1 (TGF-β1) is increasingly recognized in different brain injuries. Propolis exhibits a broad spectrum of biological and pharmacological properties including neuroprotective action. The objective of the investigation was to explore the involvement of TGF-β1 signaling in the neuroprotective mechanism of propolis in I/R rats. In this study, focal cerebral ischemia model was built by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. The investigation was carried out on 48 rats that were arranged into four groups (n = 12): the sham group, I/R control group, I/R + propolis (50 mg/kg) group and I/R + propolis (100 mg/kg) group. The results revealed that propolis preserved rats against neuronal injury induced by cerebral I/R. It significantly reduced neurological deficit scores and improved motor coordination and locomotor activity in I/R rats. Propolis antagonized the damage induced by cerebral I/R through suppression of malondialdehyde (MDA) and elevation of reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), brain-derived neurotropic factor (BDNF) and dopamine levels in the brain homogenates of I/R rats. Other ameliorations were also observed based on reduction of neurodegeneration and histological alterations in the brain tissues. These results also proposed that the neuroprotective effect of propolis might be related to upregulation of TGF-β1 and suppressed matrix metallopeptidase-9 (MMP9) mRNAexpression.

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PMID: 

J Ethnopharmacol. 2019 Dec 21 ;252:112496. Epub 2019 Dec 21. PMID: 31870795

Abstract Title: 

Green propolis increases myeloid suppressor cells and CD4Foxp3cells and reduces Th2 inflammation in the lungs after allergen exposure.

Abstract: 

ETHNOPHARMACOLOGICAL RELEVANCE: Propolis is a natural product produced by honeybees used as a medicine at least to 300 BC. In the last decades, several studies showed biological and pharmacological properties of propolis, witch scientifically explains the empirical use for centuries. The anti-inflammatory activity of propolis with the purpose to reduce Th2 inflammation has been evaluated in allergic asthma. However, it remains to be determined how propolis negatively regulates the immune response after allergen re-exposure.AIM OF THE STUDY: We hypothesized that the anti-inflammatory activity of propolis is dependent on the induction of myeloid derived suppressor cells (MDSC) and regulatory T cells.MATERIALS AND METHODS: To assess this hypothesis, we used an ovalbumin-induced asthma model to evaluate the effect of EPP-AF® dry extract from Brazilian green propolis.RESULTS: Propolis treatment decreased pulmonary inflammation and mucus production as well as eosinophils and IL-5 in the broncoalveolar lavage. Propolis enhanced also in vitro differentiation and in vivo frequency of lung MDSC and CD4Foxp3regulatory T cells.CONCLUSIONS: Together these results confirm the immunomodulatory potential of propolis during sensitization and challenge with allergen. In addition, the collecting findings show, for the first time, that propolis increases the frequency of MDSC and CD4Foxp3regulatory T cells in the lungs, and suggest that it could be use as target for development of new immunotherapy or adjuvant immunotherapy for asthma.

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PMID: 

Am J Chin Med. 2019 ;47(8):1869-1883. Epub 2019 Dec 2. PMID: 31786944

Abstract Title: 

Bee Venom Suppresses EGF-Induced Epithelial-Mesenchymal Transition and Tumor Invasion in Lung Cancer Cells.

Abstract: 

Bee venom ofis a traditional medicine in Asia. It has been used with promoting results for the treatment of pain, rheumatoid, and cancer disease. The purpose of this study was to investigate the effects of bee venom on epidermal growth factor (EGF)-induced epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) and determine possible signaling pathway affected in EGF-induced EMT in A549 cells. Bee venom inhibited EGF-induced F-actin reorganization and cell invasion, and suppressed EGF-induced EMT, processes associated with tumor metastasis in NSCLC. Bee venom enhanced the upregulation of E-cadherin and the downregulation of vimentin and inhibited EGF-induced ERK, JNK, FAK, and mTOR phosphorylation in A549 cells. However, the inhibition of JNK phosphorylation by bee venom was not related to the inhibitory effects of EMT. Furthermore, we found that bee venom suppressed the EMT-related transcription factors ZEB2 and Slug by blocking EGF-induced ERK, FAK and mTOR phosphorylation. Bee venom inhibits EGF-induced EMT by blocking the phosphorylation of ERK, FAK, and mTOR, resulting in the suppression of ZEB2 and Slug. These data suggest bee venom as a potential antimetastatic agent for NSCLC.

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PMID: 

Toxicology. 2020 Feb 3:152393. Epub 2020 Feb 3. PMID: 32027964

Abstract Title: 

Maternal exposure to environmental bisphenol A impairs the neurons in hippocampus across generations.

Abstract: 

Humans from fetal to adult stages are chronically and passively exposed to bisphenol A (BPA, an endocrine disruptor) due to its ubiquitous existence in daily life. To investigate the long-term neurotoxicity of maternal exposure to BPA for offspring, mice were used as the animal model. In this study, pregnant mice (F0) were orally dosed with BPA (i.e. mice from low-, medium- and high-exposed groups were treated with 0.5, 50, 5000 μg/kg·bw of BPA per day) until weaning. Then, the first generation (F1) mice were used to generate the F2 ones. The offspring of mice not exposed to BPA served as the control groups. The Y-maze test, comet assay, hematoxylin-eosin (HE) staining method, Golgi-Cox assay and liquid chromatography-tandem mass spectrometry (LC/MS/MS) were conducted to study any alterations to learning and memory abilities, the morphological variations in hippocampal neurons and transmitter levels of F1 and F2 mice induced by BPA exposure. Results showed that even a low-dose of maternal BPA exposure could sex-dependently and significantly impair the learning and memory ability of F1 male mice, but not of generation F2. Furthermore, decreased neuron quantities and spine densities in hippocampi were observed in both F1 and F2 generations after maternal BPA exposure. However, DNA damage of brain cells were only limited to F1 offspring, in which DNA damage was only observed in the low-exposed male mice and medium-exposed female mice. Additionally, maternal BPA exposure leads to variations in hippocampal neurotransmitter levels, indicated by the decreased ratio of Glu/GABA in F1 offspring. In conclusion,maternal exposure to an environmental dose of BPA resulted in lasting adverse effects on neurological development for offspring mice.

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PMID: 

Curr Genomics. 2019 May ;20(4):260-274. PMID: 32030086

Abstract Title: 

Genome-Wide Analysis of Low Dose Bisphenol-A (BPA) Exposure in Human Prostate Cells.

Abstract: 

: Endocrine disrupting compounds (EDCs) have the potential to cause adverse effects on wild-life and human health. Two important EDCs are the synthetic estrogen 17α-ethynylestradiol (EE2) and bisphenol-A (BPA) both of which are xenoestrogens (XEs) as they bind the estrogen receptor and dis-rupt estrogen physiology in mammals and other vertebrates. In the recent years the influence of XEs on oncogenes, specifically in relation to breast and prostate cancer has been the subject of considerable study.Methodology: In this study, healthy primary human prostate epithelial cells (PrECs) were exposed to environmentally relevant concentrations of BPA (5nM and 25nM BPA) and interrogated using a whole genome microarray.Results: Exposure to 5 and 25nM BPA resulted in 7,182 and 7,650 differentially expressed (DE) genes, respectively in treated PrECs. Exposure to EE2 had the greatest effect on the PrEC transcriptome (8,891 DE genes).Conclusion: We dissected and investigated the nature of the non-estrogenic gene signature associated with BPA with a focus on transcripts relevant to epigenetic modifications. The expression of transcripts encoding nuclear hormone receptors as well as histone and DNA methylation, modifying enzymes were significantly perturbed by exposure to BPA.

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PMID: 

Andrologia. 2020 Feb 5:e13524. Epub 2020 Feb 5. PMID: 32022330

Abstract Title: 

Protective effect of rutin on mercuric chloride-induced reproductive damage in male rats.

Abstract: 

This study investigated the effects of rutin against reproductive damage caused by toxic mercury in male rats. Thirty-five Sprague Dawley rats were used. Control group was injected with saline for 7 days. The rutin-100 group received 100 mg/kg/b.w. rutin for 7 days. Mercuric chloride (HgCl) group received 1.23 mg/kg/b.w. of HgClfor 7 days. Mercury chloride + rutin-50 group received 50 mg/kg/b.w. rutin and HgCl1.23 mg/kg/b.w. for 7 days. HgCl + rutin-100 group received 100 mg/kg/b.w. rutin and HgCl1.23 mg/kg/b.w. for 7 days. It was detected that HgCltreatment increased malondialdehyde (MDA) levels, tumour necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) expressions, necrosis and degeneration of spermatogonium, dead and abnormal sperm percentages; tubular walls thinning; and decreased antioxidant enzyme activities and sperm motility. It was determined that rutin application reduced testicular damage caused byHgCl. In conclusion, rutin administration may treat HgCltoxicity in testes.

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PMID: 

Cell Physiol Biochem. 2018 ;49(5):2012-2021. Epub 2018 Sep 21. PMID: 30244244

Abstract Title: 

Ligustrazine Inhibits Growth, Migration and Invasion of Medulloblastoma Daoy Cells by Up-Regulation of miR-211.

Abstract: 

BACKGROUND/AIMS: Ligustrazine (LSZ) has been identified as an antitumor agent against some types of cancers. Nevertheless, its ability to inhibit growth, migration and invasion of medulloblastoma cells is still unclear. This study aimed to explore the effect of LSZ on Daoy cells.METHODS: The effects of LSZ on viability, proliferation, apoptosis, migration, and invasion of Daoy cells were analyzed by CCK-8, BrdU, flow cytometry and Transwell assays, respectively. The effect of LSZ on miR-211 expression was analyzed by qRT-PCR. miR-211 inhibitor transfection was performed to suppress miR-211 expression. The effects of LSZ on apoptosis-related factors, MMP-2, MMP-9, and Vimentin (Vim), as well as main factors of PI3K/AKT and mTOR pathways were analyzed by Western blot.RESULTS: LSZ inhibited viability but promoted apoptosis of Daoy cells. Additionally, the proliferative, migratory and invasive abilities of Daoy cells were decreased by LSZ. Meanwhile, LSZ promoted the activations of Caspase-3 and Caspase-9, increased Bax level, decreased Bcl-2 level, as well as inhibited the expressions of MMP-2, MMP-9 and Vim. Additionally, we found that LSZ enhanced miR-211 expression and exerted its anti-medulloblastoma effect by up-regulation of miR-211. Furthermore, LSZ inhibited PI3K/AKT and mTOR signaling pathways by up-regulating miR-211.CONCLUSION: LSZ suppressed medulloblastoma Daoy cells by up-regulating miR-211 and further modulating the activations of PI3K/AKT and mTOR signaling pathways.

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