M.-G. Lee

Differential inhibition of oxidized LDL-induced apoptosis in human endothelial cells treated with different flavonoids.

High plasma level of cholesterol is a well-known risk factor for atherosclerotic diseases. Oxidized LDL induces cellular and nuclear damage that leads to apoptotic cell death. We tested the hypothesis that flavonoids may function as antioxidants with regard to LDL incubated with 5 microm-Cu(2+) alone or in combination with human umbilical vein endothelial cells (HUVEC). Cytotoxicity and formation of thiobarbituric acid-reactive substances induced by Cu(2+)-oxidized LDL were examined in the presence of various subtypes of flavonoid. Flavanols, flavonols and flavanones at a non-toxic dose of 50 microm markedly inhibited LDL oxidation by inhibiting the formation of peroxidative products. In contrast, the flavones luteolin and apigenin had no such effect, with >30 % of cells killed after exposure to 0.1 mg LDL/ml. Protective flavonoids, especially (-)-epigallocatechin gallate, quercetin, rutin and hesperetin, inhibited HUVEC nuclear condensation and fragmentation induced by Cu(2+)-oxidized LDL. In addition, immunochemical staining and Western blot analysis revealed that anti-apoptotic Bcl-2 expression was enhanced following treatment with these protective flavonoids. However, Bax expression and caspase-3 cleavage stimulated by 18 h incubation with oxidized LDL were reduced following treatment with these protective flavonoids. The down-regulation of Bcl-2 and up-regulation of caspase-3 activation were reversed by the cytoprotective flavonoids, (-)-epigallocatechin gallate, quercetin and hesperetin, at >/=10 microm. These results suggest that flavonoids may differentially prevent Cu(2+)-oxidized LDL-induced apoptosis and promote cell survival as potent antioxidants. Survival potentials of certain flavonoids against cytotoxic oxidized LDL appeared to stem from their disparate chemical structure. Furthermore, dietary flavonoids may have therapeutic potential for protecting the endothelium from oxidative stress and oxidized LDL-triggered atherogenesis.

CT features of abdominal manifestations of primary antiphospholipid syndrome.

PURPOSE The purpose of this work was to evaluate the CT features of the abdominal manifestations of primary antiphospholipid syndrome (PAPS). METHOD Of the 32 patients who were confirmed to have PAPS among 751 patients with elevated antiphospholipid antibodies during a 2 year period, we retrospectively reviewed the 14 patients who underwent abdominal CT. The clinical indications for abdominal CT included abdominal pain, abdominal distension, or lower leg swelling. CT findings were analyzed with regard to the abdominal vascular system and abdominal organ involvement patterns as well as ancillary findings. RESULTS Of the 14 patients with PAPS, 10 had involvement of the venous system (72%), 2 of the arterial system (14%), and 2 of both systems (14%). Of the 12 patients who had venous system involvement, 4 had thrombosis in the inferior vena cava (IVC), 2 in both the IVC and the hepatic vein, 1 in the IVC and splenic and portal veins, 1 in the IVC and hepatic and adrenal veins, 1 in the hepatic, portal, and renal veins, and 3 in the portal and superior mesenteric veins. Budd-Chiari syndrome developed in five of the nine patients who had thrombosis of the IVC or hepatic vein. Arterial thrombosis was noted in four patients, hepatic artery in two, aorta in one, renal artery in one, pancreatic arcade in one, and splenic artery in one, with infarct of multiple organs including the liver, jejunum, colon, kidney, and adrenal gland. Seven of the 14 patients (50%) manifested thrombosis or infarct of multiple extra-abdominal organs. CONCLUSION PAPS should be included in the differential diagnosis when CT demonstrates infarcts in multiple organs or patients have recurrent episodes of venous or arterial thrombosis.