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Inhibition of platelet activation suppresses reactive enteric glia and mitigates intestinal barrier dysfunction during sepsis
CONCLUSIONS: The inhibition of platelet activation is related to the suppression of CD40L-CD40-TRAF6 signaling pathway and the reduction of EGCs activation, which promotes intestinal barrier function and survival in sepsis mice. These results might provide a potential therapeutic strategy and a promising target for sepsis.PMID:36401163 | PMC:PMC9673322 | DOI:10.1186/s10020-022-00562-w
Source: Molecular Medicine - November 19, 2022 Category: Molecular Biology Authors: Bo Cheng Mengyu Du Shuxuan He Lan Yang Xi Wang Hui Gao Haiqing Chang Wei Gao Yan Li Qiang Wang Yansong Li Source Type: research

Induction of heme oxygenase‑1 expression protects articular chondrocytes against cilostazol‑induced cellular senescence.
Abstract Chondrocyte senescence is associated with the aging and degeneration of cartilage, and eventually leads to joint destruction. The aim of this study was to elucidate the mechanisms responsible for the cytoprotective effects of heme oxygenase‑1 (HO‑1) on chondrocytes in cartilage. Chondrocyte senescence was induced using cilostazol and measured using a specific senescence‑associated β‑galactosidase (SA‑β‑gal) staining assay. Cilostazol altered the expression of type Ⅱ collagen and β‑catenin, which are phenotypic markers of the differentiation and dedifferentiation of chondrocytes. Cilo...
Source: International Journal of Molecular Medicine - August 29, 2014 Category: Molecular Biology Authors: Kim KM, Park SE, Lee MS, Kim K, Park YC Tags: Int J Mol Med Source Type: research

Cilostazol induces mitochondrial fatty acid β-oxidation in C2C12 myotubes.
In this study, we report that cilostazol can elevate complete FAO and decrease both triacylglycerol (TAG) accumulation and TAG secretion. This use of cilostazol treatment increases expression of PGC-1α and, subsequently, its target genes, such as ERRα, NOR1, CD36, CPT1, MCAD, and ACO. Expression of these factors is linked to fatty acid β-oxidation but this effect is inhibited by H-89, a specific inhibitor of the PKA/CREB pathway. Importantly, knockdown of PGC-1α using siRNA abolished the effects of cilostazol in fatty acid oxidation (FAO) and TAG metabolism. These findings suggested that the PKA/CREB/PGC-1α pathway pl...
Source: Biochemical and Biophysical Research communications - April 11, 2014 Category: Biochemistry Authors: Wang B, Zhu L, Sui S, Sun C, Jiang H, Ren D Tags: Biochem Biophys Res Commun Source Type: research