RESUMEN
Myxosarcoma only accounts for a very small proportion of primary malignant tumors of the heart. The disease has no specificity in clinical manifestations or features on medical images. In this case study, we report about a middle-aged female patient afflicted with cardiac myxosarcoma. The initial transthoracic echocardiography of the patient revealed a cardiac myxoma. However, the postoperative histopathology confirmed the presence of a malignant cardiac myxosarcoma. Post-surgery follow-up imaging examinations revealed local recurrence in the left atrium as well as soft-tissue and bone metastases. The recurrent tumor and metastases were subsequently treated with chemotherapy and radiotherapy. However, the tumor did not respond to treatment and the disease progressed.
Asunto(s)
Neoplasias Cardíacas , Neoplasias del Mediastino , Mixoma , Mixosarcoma , Neoplasias del Timo , Persona de Mediana Edad , Femenino , Humanos , Mixosarcoma/diagnóstico por imagen , Mixosarcoma/patología , Mixosarcoma/secundario , Neoplasias Cardíacas/patología , Mixoma/diagnóstico por imagen , Atrios Cardíacos/diagnóstico por imagen , Atrios Cardíacos/patología , EcocardiografíaRESUMEN
Ginkgolide A (GA) is a one of the active components of Ginkgo biloba. We aimed to detect the effects GA on the lipopolysaccharide (LPS)-induced inflammatory response in human coronary artery endothelial cells (HCAECs) and whether the effects are associated with the inhibition of toll-like receptor 4 (TLR4)-NF-κB signaling through PI3K/Akt pathway. HCAECs were stimulated with LPS and treated with GA or TLR4 inhibitor CLI-095. A PI3K/Akt inhibitor LY294002 was used to block the PI3K/Akt pathway. The toxic effects of GA, LPS and LY294002 on HCAEC were evaluated using MTT assay. Levels inflammatory mediators, TLR4 mRNA, NF-κB signaling activity were valuated. We found LPS stimulation significantly increased the release of IL-6, IL-8, MCP-1 and TNF-α from HCAECs, elevated the TLR4 mRNA expression and activated the NF-κB signaling. GA and CLI-095 abolished the LPS-induced inflammatory mediator release and NF-κB signaling activation, and GA reduced the TLR4 mRNA expression without affecting cell viability. However, PI3K/Akt blocking abolished the effects of GA on HCAECs. We conclude that GA could attenuate the LPS-induced inflammatory response in HCAECs and the anti-inflammatory activity might be associated with the inhibition of TLR4-NF-κB signaling through PI3K/AKT pathway. These findings suggest a therapeutic potential of GA in endothelial inflammation.
