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Jun-Hee Lee

Publications and source records attributed to Jun-Hee Lee.

5 recordsLinked to original sources

Reactive oxygen species augment B-cell-activating factor expression.

B-cell-activating factor (BAFF) plays a role in mature B-cell generation and maintenance. Lipopolysaccharide (LPS) activates toll-like receptor 4 (TLR4)-dependent signal transduction and induces ROS production. Here, we investigated BAFF production regulated by reactive oxygen species (ROS). BAFF expression was augmented by LPS stimulation and by serum deprivation that induced ROS production. BAFF expression was inhibited by treatment with various antioxidants including N-acetyl-L-cysteine (NAC). We also investigated BAFF expression in vivo using peroxiredoxin II (PrxII)-deficient mouse spleen cells. PrxII is a member of the antioxidant enzyme family that protects cells from oxidative damage. Constitutive production of endogenous ROS was detected in spleen cells lacking PrxII. Serum BAFF protein level and BAFF transcript expression in splenocytes were significantly higher in PrxII(-/-) mice than wildtype mice. A higher BAFF level is consistent with the higher total number of splenocytes and B220(+)cells. Results were supported by NF-kappaB activation as judged by reduced IkappaBalpha degradation and increased nuclear translocation of p65/RelA with LPS stimulation, serum deprivation, and PrxII deletion. Data suggest that TLR4-mediated BAFF expression was increased by ROS and it was inhibited by PrxII controlling ROS production.

Animals↗

Delayed occurrence of H-ras12V-induced hepatocellular carcinoma with long-term treatment with cinnamaldehydes.

Cinnamaldehyde from the bark of Cinnamomum cassia has been reported to have antitumor activity mediated by the inhibition of farnesyl transferase. We assessed in vivo the chemo-preventive effect of cinnamaldehydes on H-ras12V-induced hepatocellular carcinoma formation. A mouse model of hepatocellular carcinoma was established by using the transgene of mutated H-ras12V under the regulation of albumin enhancer/promoter. When treated with cinnamaldehyde for 10 weeks, hepatic tumor development was delayed with 2'-benzoyloxycinnamaldehyde (BCA) compared with control hepatocellular carcinoma formation. The effect of 2'-hydroxycinnamaldehyde (HCA) was comparable. The number of lesions and the size of each lesion were significantly reduced by BCA. Cell proliferation in the lesion was detected by incorporation of 5-bromo-2'-deoxyuridine (BrdU). BCA increased the number of splenocytes, concanavalin A-stimulated splenocyte proliferation and the infiltration of lymphocytes into liver. Data suggest that the delayed hepatic tumor development observed with BCA could be mediated by a long-term immunostimulating effect on T cells.

Acrolein↗

Associations among oxidized low-density lipoprotein antibody, C-reactive protein, interleukin-6, and circulating cell adhesion molecules in patients with unstable angina pectoris.

Oxidized low-density lipoprotein (LDL) is believed to play a key role in the development of atherosclerosis. However, the significance of anti-oxidized LDL antibody in atherogenesis is unclear. The purposes of this study were to assess whether anti-oxidized LDL antibody titers are related to other inflammatory markers of possible interest in atherosclerotic development, such as soluble cell adhesion molecules, interleukin-6, and C-reactive protein (CRP), and to determine the prognostic value of anti-oxidized LDL antibody as a predictor of cardiac events in patients with unstable angina pectoris. Sixty patients (35 men and 25 women; mean age 60 years) with unstable angina were included in this study. The levels of CRP and of intercellular adhesion molecule-1 (ICAM-1) at 24 and 72 hours after admission were significantly higher than their baseline levels (p <0.05, respectively). After adjusting for age, gender, body mass index, and statin use, anti-oxidized LDL antibodies were positively correlated with CRP (r = 0.72, p <0.001) and ICAM-1 (r = 0.68, p <0.001). Elevated anti-oxidized LDL antibodies (mean >11.37 U/ml) and CRP levels (median >2.4 mg/L) on admission were correlated with a significantly lower 16-month, event-free survival rate (Kaplan-Meier event-free survival analysis, log-rank p <0.01 and p <0.05, respectively). Multivariate analysis by logistic regression revealed that elevated levels of anti-oxidized LDL antibody (mean >11.3 U/ml) on admission were an independent risk factor for an adverse cardiac event (odds ratio 2.2, 95% confidence interval 1.5 to 10.7, p = 0.001). This study demonstrates that anti-oxidized LDL antibody expression is associated with the expression of CRP and adhesion molecules, especially ICAM-1, and is a predictor of cardiac events in patients with unstable angina pectoris. The observed elevated levels of anti-oxidized LDL antibody suggest plaque instability and may be useful for identifying patients at higher risk of a cardiac event.

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