Inflammaging is a potential risk factor for cardiovascular diseases. It results in the development of thrombosis and atherosclerosis. The accumulation of senescent cells in vessels causes vascular inflammaging and contributes to plaque formation and rupture. In addition to being an acquired risk factor for cardiovascular diseases, ethanol can induce inflammation and senescence, both of which have been implicated in cardiovascular diseases. In the current study, we used colchicine to abate the cellular damaging effects of ethanol on endothelial cells. Colchicine prevented senescence and averted oxidative stress in endothelial cells exposed to ethanol. It lowered the relative protein expression of aging and senescence marker P21 and restored expression of the DNA repair proteins KU70/KU80. Colchicine inhibited the activation of nuclear factor kappa B (NFκ-B) and mitogen activated protein kinases (MAPKs) in ethanol-treated endothelial cells. It reduced ethanol-induced senescence-associated secretory phenotype. In summary, we show that colchicine ameliorated the ethanol-caused molecular events, resulting in attenuated senescence and senescence-associated secretory phenotype in endothelial cells.

The cardiovascular risk factors, including smoking, ethanol, and oxidative stress, can induce cellular senescence. The senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase (MMPs). These pro-inflammatory molecules and MMPs promote the infiltration and accumulation of inflammatory cells in the vascular tissue, exacerbating vascular tissue inflammation. MMPs damage vascular tissue by degenerating the extracellular matrix. Consequently, these cellular and molecular events promote the initiation and progression of cardiovascular diseases. We used Rapalink-1, an mTOR inhibitor, to block ethanol-induced senescence. Rapalink-1 inhibited oxidative-stress-induced DNA damage and senescence in endothelial cells exposed to ethanol. It attenuated the relative protein expression of senescence marker P21 and improved the relative protein expression of DNA repair protein KU70 and aging marker Lamin B1. It inhibited the activation of NF-κB, MAPKs (P38 and ERK), and mTOR pathway proteins (mTOR, 4EBP-1, and S6). Moreover, Rapalink-1 suppressed ethanol-induced mRNA expression of ICAM-1, E-selectin, MCP-1, IL-8, MMP-2, and TIMP-2. Rapalink-1 also reduced the relative protein expression of MMP-2. In summary, Rapalink-1 prevented senescence, inhibited pro-inflammatory pathway activation, and ameliorated pro-inflammatory molecule expression and MMP-2.

Background: Angiocentric glioma (AG) is an extremely rare intracranial tumor that was first described in 2005 and identified as a special type of intracranial tumor in 2007 by the WHO, which mainly affects children and young adolescents. Epilepsy is the main presentation; therefore, it was recognized as a seizure-related tumor in the past. Here, we report a case of AG with acute intracerebral hemorrhage (ICH) as the first symptom who never had a seizure onset. Case Description: A 3-year-old girl with the right limb weakness was admitted to our hospital 4 h after onset in 2018. Computed tomography showed a hematoma of about 20 ml accompanied by a hyper/iso-dense spheroid lesion located in the sub-cortex of the left parietal lobe. Magnetic resonance image (MRI) showed signs of hypointense signal in T1, T2, and fluid-attenuated inversion recovery sequence, distinct enhancement of this tumefactive lesion in the contrast-enhanced sequence. Thus, the admission diagnosis was neoplasm with acute ICH. A gross total resection of the tumor was achieved by parietal craniotomy. The histopathological diagnosis was AG. No signs showed tumor recurrence after 36 months of follow-up. Conclusion: This is the sole case of AGs with acute intracranial hemorrhage as the first symptom without any kind of epilepsy by far. This case had unique MRI signs that were different from the previous description. This case enriches the clinical and radiological manifestations of AG and reveals that further investigations are needed to further understand AG.