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  • Open Access

    REVIEW

    Ketone bodies and inflammation modulation: A mini-review on ketogenic diet’s potential mechanisms in mood disorders

    YAN ZHENG1,2, SIHUI MA3,4,*, KATSUHIKO SUZUKI4, HISANORI KATO3, HUIJUAN JIA3,*

    BIOCELL, Vol.47, No.8, pp. 1897-1906, 2023, DOI:10.32604/biocell.2023.027632 - 28 August 2023

    Abstract Mental disorders such as depression and anxiety inflict significant burdens on individuals and society. Commonly prescribed treatments often involve cognitive therapy and medications. However, for patients resistant to these conventional methods, alternative therapies like the Ketogenic Diet (KD) offer a promising avenue. KD and its key metabolite, β-hydroxybutyrate (BHB), have been hypothesized to alleviate mental disorders through anti-inflammatory actions, a crucial pathway in the pathophysiology of depression. This mini-review examines 15 clinical trials exploring the influence of KD and BHB on inflammation and their potential roles in managing mental disorders. Both human and animal studies More >

  • Open Access

    ARTICLE

    Allicin neuroprotective effect during oxidative/inflammatory injury involves AT1-Hsp70-iNOS counterbalance axis

    LUCIANA MAZZEI1,2, MARÍA BELÉN RUIZ-ROSO3, NATALIA DE LAS HERAS3, SANDRA BALLESTEROS3, CAROLINA TORRESPALAZZOLO4, LEÓN FERDER5, ALEJANDRA BEATRIZ CAMARGO4, WALTER MANUCHA1,2,*

    BIOCELL, Vol.44, No.4, pp. 671-681, 2020, DOI:10.32604/biocell.2020.014175 - 24 December 2020

    Abstract The ancestral cultures have described many therapeutic properties of garlic; therefore, it is of central interest to elucidate the molecular basis explaining this millenary empirical knowledge. Indeed, it has been demonstrated a neuroprotective effect of allicin–a phytochemical present in garlic- linked to oxidative-inflammatory modulation. Allicin improved neuronal injury by heat shock protein 70 (Hsp70) and inducible nitric oxide synthase (iNOS) regulation. Also, allicin exerts renal protection involving a possible angiotensin type 1 receptor (AT1) interaction. In connection, AT1 overexpression has been recognized as a central deleterious factor in many brain diseases. However, there are no… More >

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