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  1. Article: Anti-Tumor Activity of

    Menegazzi, Marta / Masiello, Pellegrino / Novelli, Michela

    Antioxidants (Basel, Switzerland)

    2020  Volume 10, Issue 1

    Abstract: In this paper we review the mechanisms of the antitumor effects ... ...

    Abstract In this paper we review the mechanisms of the antitumor effects of
    Language English
    Publishing date 2020-12-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10010018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Can Hypericum perforatum (SJW) prevent cytokine storm in COVID-19 patients?

    Masiello, Pellegrino / Novelli, Michela / Beffy, Pascale / Menegazzi, Marta

    Phytotherapy research : PTR

    2020  Volume 34, Issue 7, Page(s) 1471–1473

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus Infections ; Cytokines ; Humans ; Hypericum ; Pandemics ; Phytotherapy ; Pneumonia, Viral ; SARS-CoV-2
    Chemical Substances Cytokines
    Keywords covid19
    Language English
    Publishing date 2020-06-05
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 639136-9
    ISSN 1099-1573 ; 0951-418X
    ISSN (online) 1099-1573
    ISSN 0951-418X
    DOI 10.1002/ptr.6764
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  3. Article ; Online: Protective Role of St. John's Wort and Its Components Hyperforin and Hypericin against Diabetes through Inhibition of Inflammatory Signaling: Evidence from In Vitro and In Vivo Studies.

    Novelli, Michela / Masiello, Pellegrino / Beffy, Pascale / Menegazzi, Marta

    International journal of molecular sciences

    2020  Volume 21, Issue 21

    Abstract: Diabetes mellitus is a very common chronic disease with progressively increasing prevalence. Besides the well-known autoimmune and inflammatory pathogenesis of type 1 diabetes, in many people, metabolic changes and inappropriate lifestyle favor a subtle ... ...

    Abstract Diabetes mellitus is a very common chronic disease with progressively increasing prevalence. Besides the well-known autoimmune and inflammatory pathogenesis of type 1 diabetes, in many people, metabolic changes and inappropriate lifestyle favor a subtle chronic inflammatory state that contributes to development of insulin resistance and progressive loss of β-cell function and mass, eventually resulting in metabolic syndrome or overt type 2 diabetes. In this paper, we review the anti-inflammatory effects of the extract of
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/prevention & control ; Humans ; Hypericum/chemistry ; Inflammation/drug therapy ; Phloroglucinol/analogs & derivatives ; Phloroglucinol/pharmacology ; Phytotherapy ; Plant Extracts/pharmacology ; Terpenes/pharmacology
    Chemical Substances Plant Extracts ; Terpenes ; Phloroglucinol (DHD7FFG6YS) ; hyperforin (RM741E34FP)
    Keywords covid19
    Language English
    Publishing date 2020-10-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21218108
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  5. Article ; Online: Can Hypericum perforatum (SJW) prevent cytokine storm in COVID-19 patients?

    Masiello, Pellegrino / Novelli, Michela / Beffy, Pascale / Menegazzi, Marta

    2020  

    Abstract: no abstract available] ...

    Abstract [no abstract available]
    Keywords hyperforin ; covid19
    Language English
    Publishing country it
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Can Hypericum perforatum ( SJW ) prevent cytokine storm in COVID ‐19 patients?

    Masiello, Pellegrino / Novelli, Michela / Beffy, Pascale / Menegazzi, Marta

    Phytotherapy Research

    2020  Volume 34, Issue 7, Page(s) 1471–1473

    Keywords Pharmacology ; covid19
    Language English
    Publisher Wiley
    Publishing country us
    Document type Article ; Online
    ZDB-ID 639136-9
    ISSN 1099-1573 ; 0951-418X
    ISSN (online) 1099-1573
    ISSN 0951-418X
    DOI 10.1002/ptr.6764
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Protective Role of St. John’s Wort and Its Components Hyperforin and Hypericin against Diabetes through Inhibition of Inflammatory Signaling

    Michela Novelli / Pellegrino Masiello / Pascale Beffy / Marta Menegazzi

    International Journal of Molecular Sciences, Vol 21, Iss 8108, p

    Evidence from In Vitro and In Vivo Studies

    2020  Volume 8108

    Abstract: Diabetes mellitus is a very common chronic disease with progressively increasing prevalence. Besides the well-known autoimmune and inflammatory pathogenesis of type 1 diabetes, in many people, metabolic changes and inappropriate lifestyle favor a subtle ... ...

    Abstract Diabetes mellitus is a very common chronic disease with progressively increasing prevalence. Besides the well-known autoimmune and inflammatory pathogenesis of type 1 diabetes, in many people, metabolic changes and inappropriate lifestyle favor a subtle chronic inflammatory state that contributes to development of insulin resistance and progressive loss of β-cell function and mass, eventually resulting in metabolic syndrome or overt type 2 diabetes. In this paper, we review the anti-inflammatory effects of the extract of Hypericum perforatum L. (St. John’s wort, SJW) and its main active ingredients firstly in representative pathological situations on inflammatory basis and then in pancreatic β cells and in obese or diabetic animal models. The simultaneous and long-lasting inhibition of signal transducer and activator of transcription (STAT)-1, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinases (MAPKs)/c-jun N-terminal kinase (JNK) signaling pathways involved in pro-inflammatory cytokine-induced β-cell dysfunction/death and insulin resistance make SJW particularly suitable for both preventive and therapeutic use in metabolic diseases. Hindrance of inflammatory cytokine signaling is likely dependent on the hyperforin content of SJW extract, but recent data reveal that hypericin can also exert relevant protective effects, mediated by activation of the cyclic adenosine monophosphate (cAMP)/protein kinase cAMP-dependent (PKA)/adenosine monophosphate activated protein kinase (AMPK) pathway, against high-fat-diet-induced metabolic abnormalities. Actually, the mechanisms of action of the two main components of SJW appear complementary, strengthening the efficacy of the plant extract. Careful quantitative analysis of SJW components and suitable dosage, with monitoring of possible drug–drug interaction in a context of remarkable tolerability, are easily achievable pre-requisites for forthcoming clinical applications.
    Keywords St. John’s wort ; hyperforin ; hypericin ; cytokines ; inflammatory signaling ; pancreatic beta cells ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Nutrient-Induced Metabolic Stress, Adaptation, Detoxification, and Toxicity in the Pancreatic β-Cell.

    Prentki, Marc / Peyot, Marie-Line / Masiello, Pellegrino / Madiraju, S R Murthy

    Diabetes

    2020  Volume 69, Issue 3, Page(s) 279–290

    Abstract: Paraphrasing the Swiss physician and father of toxicology Paracelsus (1493-1541) on chemical agents used as therapeutics, "the dose makes the poison," it is now realized that this aptly applies to the calorigenic nutrients. The case here is the ... ...

    Abstract Paraphrasing the Swiss physician and father of toxicology Paracelsus (1493-1541) on chemical agents used as therapeutics, "the dose makes the poison," it is now realized that this aptly applies to the calorigenic nutrients. The case here is the pancreatic islet β-cell presented with excessive levels of nutrients such as glucose, lipids, and amino acids. The short-term effects these nutrients exert on the β-cell are enhanced insulin biosynthesis and secretion and changes in glucose sensitivity. However, chronic fuel surfeit triggers additional compensatory and adaptive mechanisms by β-cells to cope with the increased insulin demand or to protect itself. When these mechanisms fail, toxicity due to the nutrient surplus ensues, leading to β-cell dysfunction, dedifferentiation, and apoptosis. The terms glucotoxicity, lipotoxicity, and glucolipotoxicity have been widely used, but there is some confusion as to what they mean precisely and which is most appropriate for a given situation. Here we address the gluco-, lipo-, and glucolipo-toxicities in β-cells by assessing the evidence both for and against each of them. We also discuss potential mechanisms and defend the view that many of the identified "toxic" effects of nutrient excess, which may also include amino acids, are in fact beneficial adaptive processes. In addition, candidate fuel-excess detoxification pathways are evaluated. Finally, we propose that a more general term should be used for the in vivo situation of overweight-associated type 2 diabetes reflecting both the adaptive and toxic processes to mixed calorigenic nutrients excess: "nutrient-induced metabolic stress" or, in brief, "nutri-stress."
    MeSH term(s) Diabetes Mellitus, Type 2 ; Glucose ; Humans ; Insulin ; Insulin-Secreting Cells ; Nutrients ; Stress, Physiological
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2020-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi19-0014
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  9. Article: Anti-Tumor Activity of Hypericum perforatum L. and Hyperforin through Modulation of Inflammatory Signaling, ROS Generation and Proton Dynamics

    Menegazzi, Marta / Masiello, Pellegrino / Novelli, Michela

    Antioxidants. 2020 Dec. 28, v. 10, no. 1

    2020  

    Abstract: In this paper we review the mechanisms of the antitumor effects of Hypericum perforatum L. (St. John’s wort, SJW) and its main active component hyperforin (HPF). SJW extract is commonly employed as antidepressant due to its ability to inhibit monoamine ... ...

    Abstract In this paper we review the mechanisms of the antitumor effects of Hypericum perforatum L. (St. John’s wort, SJW) and its main active component hyperforin (HPF). SJW extract is commonly employed as antidepressant due to its ability to inhibit monoamine neurotransmitters re-uptake. Moreover, further biological properties make this vegetal extract very suitable for both prevention and treatment of several diseases, including cancer. Regular use of SJW reduces colorectal cancer risk in humans and prevents genotoxic effects of carcinogens in animal models. In established cancer, SJW and HPF can still exert therapeutic effects by their ability to downregulate inflammatory mediators and inhibit pro-survival kinases, angiogenic factors and extracellular matrix proteases, thereby counteracting tumor growth and spread. Remarkably, the mechanisms of action of SJW and HPF include their ability to decrease ROS production and restore pH imbalance in tumor cells. The SJW component HPF, due to its high lipophilicity and mild acidity, accumulates in membranes and acts as a protonophore that hinders inner mitochondrial membrane hyperpolarization, inhibiting mitochondrial ROS generation and consequently tumor cell proliferation. At the plasma membrane level, HPF prevents cytosol alkalization and extracellular acidification by allowing protons to re-enter the cells. These effects can revert or at least attenuate cancer cell phenotype, contributing to hamper proliferation, neo-angiogenesis and metastatic dissemination. Furthermore, several studies report that in tumor cells SJW and HPF, mainly at high concentrations, induce the mitochondrial apoptosis pathway, likely by collapsing the mitochondrial membrane potential. Based on these mechanisms, we highlight the SJW/HPF remarkable potentiality in cancer prevention and treatment.
    Keywords Hypericum perforatum ; acidification ; acidity ; alkalinization ; angiogenesis ; animal models ; antidepressants ; antineoplastic activity ; antioxidants ; apoptosis ; carcinogens ; cell proliferation ; colorectal neoplasms ; cytosol ; dynamics ; extracellular matrix ; genotoxicity ; humans ; hyperforin ; lipophilicity ; mechanism of action ; membrane potential ; metastasis ; mitochondria ; mitochondrial membrane ; neoplasm cells ; neurotransmitters ; pH ; paper ; phosphotransferases (kinases) ; plasma membrane ; proteinases ; protons ; risk ; therapeutics
    Language English
    Dates of publication 2020-1228
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    Note NAL-light
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10010018
    Database NAL-Catalogue (AGRICOLA)

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  10. Article: Animal models of type 2 diabetes with reduced pancreatic beta-cell mass.

    Masiello, Pellegrino

    The international journal of biochemistry & cell biology

    2006  Volume 38, Issue 5-6, Page(s) 873–893

    Abstract: Type 2 diabetes is increasingly viewed as a disease of insulin deficiency due not only to intrinsic pancreatic beta-cell dysfunction but also to reduction of beta-cell mass. It is likely that, in diabetes-prone subjects, the regulated beta-cell turnover ... ...

    Abstract Type 2 diabetes is increasingly viewed as a disease of insulin deficiency due not only to intrinsic pancreatic beta-cell dysfunction but also to reduction of beta-cell mass. It is likely that, in diabetes-prone subjects, the regulated beta-cell turnover that adapts cell mass to body's insulin requirements is impaired, presumably on a genetic basis. We still have a limited knowledge of how and when this derangement occurs and what might be the most effective therapeutic strategy to preserve beta-cell mass. The animal models of type 2 diabetes with reduced beta-cell mass described in this review can be extremely helpful (a) to have insight into the mechanisms underlying the defective growth or accelerated loss of beta-cells leading to the beta-cell mass reduction; (b) to investigate in prospective studies the mechanisms of compensatory adaptation and subsequent failure of a reduced beta-cell mass. Furthermore, these models are of invaluable importance to test the effectiveness of potential therapeutic agents that either stimulate beta-cell growth or inhibit beta-cell death.
    MeSH term(s) Animals ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclin D2 ; Cyclin-Dependent Kinase 4/deficiency ; Cyclins/deficiency ; Diabetes Mellitus, Experimental/physiopathology ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/physiopathology ; Disease Models, Animal ; Fetal Growth Retardation/physiopathology ; Homeodomain Proteins ; Insulin Receptor Substrate Proteins ; Insulin-Secreting Cells/pathology ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Transgenic ; Peptides/therapeutic use ; Phosphoproteins/deficiency ; Proto-Oncogene Proteins c-akt/deficiency ; Rats ; Receptor, Insulin ; Ribosomal Protein S6 Kinases, 70-kDa/deficiency ; Trans-Activators/deficiency ; Venoms/therapeutic use ; eIF-2 Kinase/deficiency
    Chemical Substances Ccnd2 protein, mouse ; Cyclic AMP Response Element-Binding Protein ; Cyclin D2 ; Cyclins ; Homeodomain Proteins ; Insulin Receptor Substrate Proteins ; Intracellular Signaling Peptides and Proteins ; Irs2 protein, mouse ; Irs2 protein, rat ; Peptides ; Phosphoproteins ; Trans-Activators ; Venoms ; pancreatic and duodenal homeobox 1 protein ; exenatide (9P1872D4OL) ; Receptor, Insulin (EC 2.7.10.1) ; PERK kinase (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22)
    Language English
    Publishing date 2006
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2005.09.007
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