Уважаемые коллеги, доброго времени суток! Представляем вам греческое научное издание Molecular Medicine Reports. Журнал имеет третий квартиль, издается в Spandidos Publications, его SJR за 2019 г. равен 0,63, импакт-фактор - 2,1, печатный ISSN - 1791-2997, электронный - 1791-3004, предметные области - Биохимия, Онкология, Молекулярная биология, Молекулярная медицина, Исследования рака, Генетика. Вот так выглядит обложка:
Редактором является Деметриос Спандидос, контактные данные - spandidos@spandidos.gr, subscriptions@spandidos-publications.com.
Это ежемесячный рецензируемый журнал, доступный как в печатном, так и в электронном виде, который включает в себя исследования, посвященные молекулярной медицине, при этом подчеркивая такие аспекты, как фармакология, патология, генетика, неврология, инфекционные заболевания, молекулярная кардиология и молекулярная хирургия. Исследования In vitro и in vivo экспериментальных модельных систем, относящихся к механизмам различных заболеваний, предлагают ученым необходимые инструменты и знания, с помощью которых можно помочь в диагностике и лечении заболеваний человека.
Пример статьи, название - IL-32 exacerbates adenoid hypertrophy via activating NLRP3-mediated cell pyroptosis, which promotes inflammation. Заголовок (Abstract) - Adenoid hypertrophy (AH) is a common pediatric disease caused by inflammatory stimulation. The pro-inflammatory cytokine IL-32 has been reported to promote airway inflammation and also be involved in the pyroptosis pathway. However, whether IL-32 can contribute to AH by mediating pyroptosis remains to be elucidated. The present study aimed to investigate the role of IL-32 in AH and determine the potential underlying mechanisms. Adenoid tissues were collected from healthy children and children with AH, and the expression of IL-32, NACHT LRR and PYD domains-containing protein 3 (NLRP3) and IL-1β in normal and hypertrophic tissues were measured. Human nasal epithelial cells (HNEpCs) were exposed to a series of IL-32 concentrations. HNEpCs with or without IL-32 silencing were stimulated with lipopolysaccharide (LPS), and cell proliferation, cell apoptosis, gasdermin D (GSDMD) activation, production of inflammatory cytokines and the expression levels of proteins related to the potential mechanisms were evaluated by Cell Counting Kit-8, flow cytometry, immunofluorescence staining, ELISA and western blot assays, respectively. The results showed that IL-32, NLRP3 and IL-1β exhibited higher expression in adenoid tissues with AH compared with normal tissues. In HNEpC cells, treatment with IL-32 (2 and 10 ng/ml) promoted cell proliferation, while 50 ng/ml IL-32 inhibited cell proliferation at 12, 24 and 48 h post-treatment. IL-32 (2, 10 and 50 ng/ml) also resulted in differing degrees of apoptosis, GSDMD activation, release of IL-1β, IL-6 and TNF-α, and increased protein expression levels of NLRP3, cleaved-caspase-1, activated GSDMD, nucleotide-binding oligomerization domain-containing protein (NOD) 1/2 and Toll-like receptor (TLR)4 in a concentration-dependent manner. In addition, compared with the LPS group, IL-32 knockdown significantly inhibited LPS-induced enhancement of cell proliferation, cell apoptosis, GSDMD activation and production of inflammatory cytokines, and reversed the increased protein expression of NLRP3, cleaved-caspase-1, activated GSDMD, NOD1/2 and TLR4. In conclusion, IL-32 may play a role in the progression of AH via promoting inflammation, and the potential mechanism may involve the activation of NLRP3-mediated pyroptosis.
