Traded along spice routes separating ancient cultures by vast distances, spices like cumin were once worth their weight in gold. Has modern science now revealed why, beyond their remarkable aesthetic value, they were so highly prized?

Many spices are perfectly happy living a charmed life as seasonings, peppering things generously with flavor, and without ever arousing the suspicion that they may be capable of profound acts of healing as well.  

Meet cumin, a member of the parsley family, which is to say from a well-known family of healers native to the central Mediterranean region (southern Italy, Algeria and Tunisia).

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PMID: 

J Clin Endocrinol Metab. 2019 Sep 19. Epub 2019 Sep 19. PMID: 31536135

Abstract Title: 

In utero bisphenol A exposure is linked with sex specific changes in the transcriptome and methylome of human amniocytes.

Abstract: 

CONTEXT: Prenatal exposure to bisphenol A (BPA) is linked to obesity and diabetes, but the molecular mechanisms driving these phenomena are not known. Alterations in DNA methylation in amniocytes exposed to BPA in utero represent a potential mechanism leading to metabolic dysfunction later in life.OBJECTIVE: To profile changes in genome-wide DNA methylation and expression in second trimester human amniocytes exposed to BPA in utero.DESIGN: A nested case-control study was performed in amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis and gestational age at birth. Cases had amniotic fluid BPA measuring 0.251-23.74 ng/mL. Sex-specific genome-wide DNA methylation analysis and RNA-sequencing were performed to determine differentially methylation regions (DMRs) and gene expression changes associated with BPA exposure. Ingenuity pathway analysis was performed to identify biologically relevant pathways enriched after BPA exposure. In silico Hi-C analysis identified potential chromatin interactions with DMRs.RESULTS: There were 101 genes with altered expression in male amniocytes exposed to BPA (q

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PMID: 

Ecotoxicol Environ Saf. 2019 Sep 18 ;185:109684. Epub 2019 Sep 18. PMID: 31541948

Abstract Title: 

Bisphenol A analogs in patients with chronic kidney disease and dialysis therapy.

Abstract: 

Bisphenol A (BPA) accumulates in patients with chronic kidney disease (CKD), and hemodialysis filters may contribute to bisphenol burden in patients on hemodialysis (HD). The serum levels of BPA and three BPA analogs, namely, bisphenol B (BPB), bisphenol S (BPS), and bisphenol F (BPF), in 58 patients with CKD, 66 patients on dialysis therapy and 30 healthy control were investigated. The content of four bisphenols (BPs) was also examined in three types of dialysis filters, followed by an in vitro elution experiment to test the release of BPs from the dialysis filters. The serum levels of BPA (r = -0.746, p 

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PMID: 

Int J Mol Sci. 2019 Sep 1 ;20(17). Epub 2019 Sep 1. PMID: 31480534

Abstract Title: 

Ginsenoside Compound K Induces Ros-Mediated Apoptosis and Autophagic Inhibition in Human Neuroblastoma Cells In Vitro and In Vivo.

Abstract: 

Autophagy can result in cellular adaptation, as well as cell survival or cell death. Modulation of autophagy is increasingly regarded as a promising cancer therapeutic approach. Ginsenoside compound K (CK), an active metabolite of ginsenosides isolated fromC.A. Meyer, has been identified to inhibit growth of cancer cell lines. However, the molecular mechanisms of CK effects on autophagy and neuroblastoma cell death have not yet been investigated. In the present study, CK inhibited neuroblastoma cell proliferation in vitro and in vivo. Treatment by CK also induced the accumulation of sub-G1 population, and caspase-dependent apoptosis in neuroblastoma cells. In addition, CK promotes autophagosome accumulation by inducing early-stage autophagy but inhibits autophagic flux by blocking of autophagosome and lysosome fusion, the step of late-stage autophagy. This effect of CK appears to be mediated through the induction of intracellular reactive oxygen species (ROS) and mitochondria membrane potential loss. Moreover, chloroquine, an autophagy flux inhibitor, further promoted CK-induced apoptosis, mitochondrial ROS induction, and mitochondria damage. Interestingly, those promoted phenomena were rescued by co-treatment with a ROS scavenging agent and an autophagy inducer. Taken together, our findings suggest that ginsenoside CK induced ROS-mediated apoptosis and autophagic flux inhibition, and the combination of CK with chloroquine, a pharmacological inhibitor of autophagy, may be a novel therapeutic potential for the treatment of neuroblastoma.

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PMID: 

Mol Brain. 2019 Sep 5 ;12(1):77. Epub 2019 Sep 5. PMID: 31488185

Abstract Title: 

Minor ginsenoside F1 improves memory in APP/PS1 mice.

Abstract: 

Ginseng has been shown to produce a cognitive improvement effect. The key molecular components in ginseng that produce pharmacological effects are ginsenosides. Previous studies reported a memory improvement effect of a few major ginsenosides. However, the identity of specific minor ginsenosides mediating such function remains unknown. Here, we report that a minor ginsenoside F1 improves memory function in APPswe/PSEN1dE9 (APP/PS1) double-transgenic Alzheimer's disease (AD) model mice. After 8-wk oral administration of F1 jelly, we observed that spatial working memory, but not context-dependent fear memory, was restored in AD mice. To search for a possible underlying molecular and cellular mechanism, we investigated the effect of F1 on Aβ plaque. We observed F1 administration reduced the Aβ plaque area and density in the cortex, but not in the hippocampus of AD mice. Next, we tested for the effect of F1 on the expression level of key molecules involved in learning and memory. Results from Western blot assay revealed that an abnormally reduced level of a phosphorylated form of CREB in the hippocampus of AD mice was restored to a normal level by F1 administration. Moreover, in the same animals, BDNF level was augmented in the cortex. Our results, therefore, suggest that minor ginsenoside F1 constitutes a promising target to develop therapeutic agents for AD.

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PMID: 

J Food Biochem. 2019 Sep 9:e13032. Epub 2019 Sep 9. PMID: 31502279

Abstract Title: 

Ginsenoside Rg1 abolish imiquimod-induced psoriasis-like dermatitis in BALB/c mice via downregulating NF-κB signaling pathway.

Abstract: 

This animal experiment was framed to evaluate the beneficial effect of ginsenoside Rg1 (GRg1) against imiquimod (IMQ)-induced psoriasis-like dermatitis model to reveal the underpinning mechanism. Fifty healthy BALB/c mice were divided into five groups as control, GRg1, IMQ induced, oral treatment of GRg1 (50 mg/kg), or dexamethasone (DXM; 10 mg/kg) in IMQ-induced mice. Treatment with GRg1 or DXM significantly mitigates (p 

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PMID: 

Anal Cell Pathol (Amst). 2019 ;2019:3815786. Epub 2019 Aug 26. PMID: 31534898

Abstract Title: 

Ginsenoside Rg3 Prolongs Survival of the Orthotopic Hepatocellular Carcinoma Model by Inducing Apoptosis and Inhibiting Angiogenesis.

Abstract: 

Aim: Microvessel density is a marker of tumor angiogenesis activity for development and metastasis. Our preliminary study showed that ginsenoside Rg3 (Rg3) induces apoptosis in hepatocellular carcinoma (HCC). The aim of this study was to investigate the cross-link for apoptosis induction and antiangiogenesis effect of Rg3 on orthotopic HCC.Methods: The murine HCC cells Hep1-6 were implanted in the liver of mouse. With oral feeding of Rg3 (10 mg/kg once a day for 30 days), the quantitative analysis of apoptosis was performed by using pathology and a transmission electron microscope and microvessel density was quantitatively measured by immunohistochemical staining of the CD105 antibody. The mice treated with Rg3 (= 10) were compared with the control (= 10) using Kaplan-Meier analysis. Animal weight and tumor weight were measured to determine the toxicity of Rg3 and antitumor effect on an orthotopic HCC tumor model.Results: With oral feeding of Rg3 daily in the first 30 days on tumor implantation, Rg3 significantly decreased the orthotopic tumor growth and increased the survival of animals (

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PMID: 

Oncol Lett. 2019 Oct ;18(4):3880-3886. Epub 2019 Jul 29. PMID: 31516599

Abstract Title: 

Vitamin C induces human melanoma A375 cell apoptosis via Bax- and Bcl-2-mediated mitochondrial pathways.

Abstract: 

Melanoma is the most malignant type of skin cancer and is resistant to numerous chemotherapeutic and radiotherapy-based treatment approaches due to the activation of rapid and reversible pro-survival signaling pathways. As a result, patients will often present with a poor prognosis. Therefore, novel preventive methods and treatments are urgently required for patients with melanoma. Vitamin C (also known as L-ascorbic acid) is a water-soluble vitamin that is widely used as a dietary additive and has been demonstrated to exhibit anti-cancer properties. In the present study, the effects of vitamin C in human melanoma A375 cells, and the mechanisms underlying these effects were investigated. Vitamin C potently suppressed human melanoma A375 cell proliferation by inducing apoptosis in A375 cells. Induction of apoptosis was related to caspase-9 and caspase-3 activation and the mitochondrial membrane potential of A375 cells significantly decreased in the presence of vitamin C. Furthermore, vitamin C induced apoptosis in A375 cells by activating the Bax- and Bcl-2-mediated mitochondrial pathway. These results indicate that vitamin C may be a potentially useful clinical anti-tumor drug for treating patients with melanoma.

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PMID: 

Molecules. 2019 May 28 ;24(11). Epub 2019 May 28. PMID: 31141940

Abstract Title: 

Antidepressant-Like Effect and Mechanism of Action of Honokiol on the Mouse Lipopolysaccharide (LPS) Depression Model.

Abstract: 

There is growing evidence that neuroinflammation is closely linked to depression. Honokiol, a biologically active substance extracted from, which is widely used in traditional Chinese medicine, has been shown to exert significant anti-inflammatory effects and improve depression-like behavior caused by inflammation. However, the specific mechanism of action of this activity is still unclear. In this study, the lipopolysaccharide (LPS) mouse model was used to study the effect of honokiol on depression-like behavior induced by LPS in mice and its potential mechanism. A single administration of LPS (1 mg/kg, intraperitoneal injection) increased the immobility time in the forced swimming test (FST) and tail suspension test (TST), without affecting autonomous activity. Pretreatment with honokiol (10 mg/kg, oral administration) for 11 consecutive days significantly improved the immobility time of depressed mice in the FST and TST experiments. Moreover, honokiol ameliorated LPS-induced NF-κB activation in the hippocampus and significantly reduced the levels of the pro-inflammatory cytokines; tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interferon γ (IFN-γ). In addition, honokiol inhibited LPS-induced indoleamine 2,3-dioxygenase (IDO) activation and quinolinic acid (a toxic product) increase and reduced the level of free calcium in brain tissue, thereby inhibiting calcium overload. In summary, our results indicate that the anti-depressant-like effects of honokiol are mediated by its anti-inflammatory effects. Honokiol may inhibit the LPS-induced neuroinflammatory response through the NF-κB signaling pathway, reducing the levels of related pro-inflammatory cytokines, and furthermore, this may affect tryptophan metabolism and increase neuroprotective metabolites.

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PMID: 

Neurotoxicology. 2019 Sep 16. Epub 2019 Sep 16. PMID: 31536738

Abstract Title: 

Monoamine oxidase inhibitory activity of flavoured e-cigarette liquids.

Abstract: 

BACKGROUND AND AIMS: Monoamine oxidase inhibitors have been hypothesised to be important in tobacco dependence, reinforcing the brain's response to nicotine by delaying the degradation of neurotransmitters by monoamine oxidases. The development of electronic cigarettes has provided an alternative nicotine delivery system, which is widely viewed as less toxic than tobacco smoke. However, significant data gaps remain. This paper reports the results of measurements of monoamine oxidase inhibitory activity in a small sample of commercially available, flavoured e-liquids.METHODS: Twelve e-liquids were tested for monoamine oxidase inhibitory activity, using the kynuramine assay and monoamine oxidase enzymes (human, recombinant). Control samples of carrier liquids, propylene glycol and glycerol, and nicotine were also tested.RESULTS: Four e-liquids contained high levels of inhibitory activity, four more were moderately inhibitory. The remaining four e-liquids were mildly inhibitory, while the carrier liquids, and nicotine were inactive at relevant concentrations. The active compounds in the e-liquids were subsequently identified as vanillin and ethyl vanillin. Under some conditions of use, the sampled e-liquids with the highest concentrations of monoamine oxidase inhibitory activity have the potential to expose consumers to physiologically significant levels of MAO inhibitory activity.CONCLUSIONS: While only a small sample of e-liquids was tested, the findings suggest that some flavours have pharmacological actions, with potential to enhance the response to nicotine or to other drugs. The public health implications of these preliminary findings on addiction and smoking cessation warrant exploration and further research.

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