Arch Med Sci
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Vascular smooth muscle cell (VSMC) proliferation plays a major role in the progression of vascular diseases. In the present study, we established the efficacy and the mechanisms of action of hinokitiol, a tropolone derivative found in Chamaecyparis taiwanensis, Cupressaceae, in relation to platelet-derived growth factor-BB (PDGF-BB) and serum-dependent VSMC proliferation. ⋯ These data suggest that the anti-proliferative effects of hinokitiol in VSMCs may be mediated by activation of p21 and p53 signaling pathways, and it may contribute to the prevention of vascular diseases associated with VSMC proliferation.
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We compared the side effects of ketamine and thiopental used alone and of a ketamine/thiopental combination dose on the brain,heart, and bronchial tissues of rats. ⋯ The studied doses of ketamine led to oxidative stress by increasing the amount of adrenaline. Thiopental increased oxidative stress with decreases in adrenaline. A longer anesthetic effect with minimal adverse events may be achieved by ketamine and thiopental in combination.
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Osteoarthritis is an inflammatory disorder associated with oxidative stress and apoptosis leading to cartilage destruction and impairment of cartilage formation. In the present study, we studied the protective effect of lutein against monosodium iodoacetate (MIA)-induced osteoarthritis in primary chondrocyte cells. ⋯ The present study shows significant cytoprotection offered by lutein against MIA-induced oxidative stress, inflammation and apoptosis by the modulatory effect of NF-κB and Nrf2 activation.
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Patients with sickle cell disease have increased left ventricular size, which is not usually accompanied by changes in systolic function indexes. We assessed echocardiographic abnormalities present in patients with sickle cell anemia (SCA) and compared echocardiographic parameters to other sickle cell diseases (OSCD). ⋯ There was an increase of left ventricular and left atrial sizes in patients with SCA, compared to patients with OSCD, without changes in systolic or diastolic function in both groups. This could be due to the hyperkinetic state due to the more severe anemia in the SCA subjects.
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Inadequate trophoblast invasion and placentation are widely believed to contribute to preeclampsia, and multiple lines of evidence indicate the involvement of hypoxia in preeclampsia. However, the molecular mechanisms underlying the association of placental hypoxia with preeclampsia are not clear. ⋯ HO-1 was overexpressed in PE placenta, in association with reduced STAT3 phosphorylation (Tyr 705). HO-1 inhibits the STAT3 phosphorylation in placental JEG-3 cells under hypoxia. Thus, we speculate that overexpressed HO-1 might contribute to the reduced STAT3 phosphorylation (Tyr 705) and the pathogenesis of preeclampsia.