Cilostazol attenuates cardiac oxidative stress and inflammation in hypercholesterolemic rats

Cilostazol may be a better therapeutic agent for acute ischemic stroke because of its efficacy in preventing post-stroke depression

“…In addition to the anti-platelet aggregation and vasodilator effects of clinical application, cilostazol has been proved to have anti-inflammatory effects in major depressive disorder related clinical experiments and model rats with hypercholesterolemia, diabetes, and colitis. It has good inhibitory effect on NF-κB, TNF-α, IL-6 and IL-1β[8, 18, 48, 49]. We speculate that cilostazol can effectively inhibit thrombosis and block blood vessels in patients with AIS through anti-platelet aggregation and vasodilation, and then further inhibit the inflammatory response in the focal area caused by stroke, inhibit the progression of AIS, and effectively prevent the recurrence of AIS.…”

“…Both depression and PSD are related to the level of inflammation [1,[11][12][13]31], and cilostazol has been proven to improve the level of inflammation [8][9][10]32]. Therefore, we further examined the plasma levels of TNF-α, IL-1β and NLR in the two groups of patients at admission and at the end of follow-up, respectively, to verify whether the preventive effect of cilostazol on PSD is related to its inflammatory regulation.…”

“…Cilostazol, a specific phosphodiesterase (PDE)-3 inhibitor, which can block cAMP degradation, inhibit adenosine uptake, platelet aggregation and dilate blood vessels, has been used in the treatment of atherosclerosis, intermittent claudication, IS and other vascular embolic diseases [5][6][7]. With the continuous in-depth study on the efficacy of cilostazol, it has also been found to regulate the level of inflammation in the body, for example, by inhibiting the activation of nuclear factor-κB (NF-κB) to protect the heart injury caused by hypercholesterolemia [8]. Studies on mouse models of atherosclerosis have also shown that cilostazol can significantly improve the proinflammatory state of vascular endothelial cells and slow down the progression of atherosclerosis by down-regulating intercellular adhesion molecule-1 (ICAM-1), monocyte/macrophage-2 (MOMA-2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and other inflammation-related factors [9].…”

“…Cilostazol, a specific phosphodiesterase (PDE)-3 inhibitor, which can block cAMP degradation, inhibit adenosine uptake, platelet aggregation and dilate blood vessels, has been used in the treatment of atherosclerosis, intermittent claudication, IS and other vascular embolic diseases [5][6][7]. With the continuous in-depth study on the efficacy of cilostazol, it has also been found to regulate the level of inflammation in the body, for example, by inhibiting the activation of nuclear factor-κB (NF-κB) to protect the heart injury caused by hypercholesterolemia [8]. Studies on mouse models .…”

The Role of Cilostazol, a Phosphodiesterase-3 Inhibitor, in the Development of Atherosclerosis and Vascular Biology: A Review with Meta-Analysis

“…This anti-inflammatory potential was mediated by the downregulation of p65 NF-κB and the enhancement of sirtuin-1, leading to the downregulation of NLRP3, an apoptosis-associated speck-like protein, active caspase-1, and interleukin-1β [ 74 ]. In an animal study of hypercholesterolemic rats, cilostazol treatment protected against hypercholesterolemia-induced cardiac damage via molecular mechanisms targeting the crosstalk between Nrf2 induction and NF-κB inhibition in the heart [ 77 ]. Another study using the mouse models of myocardial ischemia–reperfusion showed that cilostazol treatment attenuated multiple inflammatory markers through the activation of the peroxisome proliferator-activated receptor-γ (PPARγ), Janus kinase 2 (JAK2), and the signal transducer and activator of transcription 3 (STAT3) pathways [ 78 ].…”