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Drug: Cilostazol
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Total 9 results found since Jan 2013.
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
Cilostazol inhibits interleukin-1-induced ADAM17 expression through cAMP independent signaling in vascular smooth muscle cells.
Abstract
Increased a disintegrin and metalloprotease 17 (ADAM17) expression in vascular smooth muscle cells (VSMC) is implicated in the development of cardiovascular diseases including atherosclerosis and hypertension. Although cilostazol, type phosphodiesterase (PDE?) inhibitor, has recently been found to inhibit VSMC proliferation, the mechanisms remain largely unclear. Here we hypothesized that cilostazol regulates the ADAM17 expression in VSMC. In cultured VSMC, interleukin (IL)-1α and IL-1β significantly increased ADAM17 expression. MEK inhibitor U0126, NF-κB inhibitor BAY-11-7085 and siRNA targeting p65/R...
Source: Cell Biology International - October 30, 2015 Category: Cytology Authors: Takaguri A, Morimoto M, Imai SI, Satoh K Tags: Cell Biol Int Source Type: research
Cilostazol attenuates murine hepatic ischemia and reperfusion injury via heme oxygenase-dependent activation of mitochondrial biogenesis
Hepatic ischemia-reperfusion (I/R) can cause hepatocellular injury associated with the inflammatory response and mitochondrial dysfunction. We studied the protective effects of the phosphodiesterase inhibitor cilostazol in hepatic I/R and the roles of mitochondria and the Nrf2/heme oxygenase-1 (HO-1) system. Wild-type, Hmox1–/–, or Nrf2–/– mice were subjected to hepatic I/R in the absence or presence of cilostazol followed by measurements of liver injury. Primary hepatocytes were subjected to cilostazol with the HO-1 inhibitor ZnPP, or Nrf2-specific siRNA, followed by assessment of mitochondrial bio...
Source: AJP: Gastrointestinal and Liver Physiology - July 1, 2015 Category: Gastroenterology Authors: Joe, Y., Zheng, M., Kim, H. J., Uddin, M. J., Kim, S.-K., Chen, Y., Park, J., Cho, G. J., Ryter, S. W., Chung, H. T. Tags: LIVER AND BILIARY TRACT Source Type: research
Cilostazol Attenuates Murine Hepatic Ischemia and Reperfusion Injury via Heme Oxygenase-Dependent Activation of Mitochondrial Biogenesis.
Abstract
Hepatic ischemia/reperfusion (I/R) can cause hepatocellular injury associated with the inflammatory response and mitochondrial dysfunction. We studied the protective effects of the phosphodiesterase inhibitor cilostazol in hepatic I/R, and the roles of mitochondria, and the Nrf2/ heme oxygenase-1 (HO-1) system. Wild type, Hmox1(-/-) or Nrf2(-/-) mice were subjected to hepatic I/R in the absence or presence of cilostazol followed by measurements of liver injury. HepG2 cells were subjected to cilostazol with the HO-1 inhibitor ZnPP, or Nrf2 specific siRNA, followed by assessment of mitochondrial biogenesis....
Source: Am J Physiol Gastroi... - May 7, 2015 Category: Gastroenterology Authors: Joe Y, Zheng M, Kim HJ, Uddin MJ, Kim SK, Chen Y, Park J, Cho GJ, Ryter SW, Chung HT Tags: Am J Physiol Gastrointest Liver Physiol 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
The hypolipidemic effect of cilostazol can be mediated by regulation of hepatic low-density lipoprotein receptor-related protein 1 (LRP1) expression
Conclusion: Taken together, our results demonstrated that cilostazol enhances LRP1 expression in liver by activating PPARγ through the PPRE in the LRP1 promoter. Increased hepatic LRP1 may be essential for the reduction of circulating triglycerides brought about by cilostazol.
Source: Metabolism - Clinical and Experimental - October 21, 2013 Category: Biomedical Science Authors: Hyung Jun Kim, Jae Hoon Moon, Hyun Min Kim, Mi Ra Yun, Byung Hun Jeon, ByungWan Lee, Eun Seok Kang, Hyun Chul Lee, Bong Soo Cha Tags: Basic Science Source Type: research
