Inhibitory effect of caffeic acid phenethyl ester (CAPE) on LPS-induced inflammation of human middle ear epithelial cells

2008 ◽  
Vol 128 (12) ◽  
pp. 1303-1307 ◽  
Author(s):  
Jae-Jun Song ◽  
Jae Gu Cho ◽  
Soon-Jae Hwang ◽  
Chang Gun Cho ◽  
Seok-Won Park ◽  
...  
2003 ◽  
Vol 123 (3) ◽  
pp. 362-366 ◽  
Author(s):  
Jae Young Choi ◽  
Kyou-nam Cho ◽  
Joo-heon Yoon

2018 ◽  
Vol 2018 ◽  
pp. 1-1 ◽  
Author(s):  
Shin Hye Kim ◽  
Sun Hwa Shin ◽  
Yoon Young Go ◽  
Sung-Won Chae ◽  
Jae-Jun Song

2019 ◽  
Vol 20 (12) ◽  
pp. 3055 ◽  
Author(s):  
Eun Ju Shin ◽  
Seongin Jo ◽  
Hyo-kyoung Choi ◽  
Sungbin Choi ◽  
Sanguine Byun ◽  
...  

Caffeic acid phenethyl ester (CAPE), a naturally occurring bioactive compound, displays anti-inflammatory, anti-carcinogenic, and anti-microbial effects. However, the effect of CAPE on skin photoaging is unknown. Herein, we investigated the inhibitory effect of CAPE against ultraviolet (UV) irradiation-mediated matrix metalloproteinase (MMP)-1 expression and its underlying molecular mechanism. CAPE treatment suppressed UV-induced MMP-1 levels in both human dermal fibroblasts (HDF) and human skin tissues. While CAPE did not display any significant effects against the upstream regulatory pathways of MMP-1, CAPE was capable of reversing UV-mediated epigenetic modifications. CAPE suppressed UV-induced acetyl-histone H3 (Lys9) as well as total lysine acetylation in HDF cells. Similarly, CAPE also attenuated UV-induced lysine acetylations in human skin tissues, suggesting that the CAPE-mediated epigenetic alterations can be recapitulated in ex vivo conditions. CAPE was found to attenuate UV-induced histone acetyltransferase (HAT) activity in HDF. Notably, CAPE was able to directly inhibit the activity of several HATs including p300, CREP-binding protein (CBP), and p300/CBP-associated factor (PCAF), further confirming that CAPE can function as an epigenetic modulator. Thus, our study suggests that CAPE maybe a promising agent for the prevention of skin photoaging via targeting HATs.


2002 ◽  
Vol 122 (3) ◽  
pp. 270-275 ◽  
Author(s):  
Jae Young Choi ◽  
Chang-Hoon Kim ◽  
Won-Sang Lee ◽  
Hee-Nam Kim ◽  
Kyoung-Seob Song ◽  
...  

1983 ◽  
Vol 91 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Timothy T.K. Jung ◽  
S.K. Juhn ◽  
Alfred F. Michael

Prostaglandins were found in the middle ear effusion and may play an important role in inflammation and bone resorption occurring in otitis media. With the use of an immunohistochemical technique, prostaglandin cyclooxygenase was localized in epithelial cells of human skin, endothelial cells of arterioles, mononuclear leukocytes and fibroblasts of human middle ear mucosa and granulation tissue, epithelial cells of chinchilla middle ear mucosa, and the external auditory canal skin.


2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Shin Hye Kim ◽  
Sun Hwa Shin ◽  
Yoon Young Go ◽  
Sung-Won Chae ◽  
Jae-Jun Song

Lead is a ubiquitous metal in the environment, but no studies have examined lead toxicity on the middle ear. Here, we investigated lead toxicity and its mechanism in human middle ear epithelial cells (HMEECs). Moreover, we investigated the protective effects of amniotic membrane extract (AME) and chorionic membrane extract (CME) against lead toxicity in HMEECs. Cell viability was analyzed using the cell counting kit, and reactive oxygen species (ROS) activity was measured using a cellular ROS detection kit. After lead(II) acetate trihydrate treatment, mRNA levels of various genes were assessed by semiquantitative real-time polymerase chain reaction. Following treatment with AME or CME after lead exposure, the changes in cell viability, ROS activity, and gene expression were analyzed. Exposure to >100 μg/mL of lead(II) acetate trihydrate caused a significant decrease in cell viability and increased ROS production in HMEECs. Lead exposure significantly increased the mRNA expression of genes encoding inflammatory cytokines and mucins. Administration of AME or CME restored cell viability, reduced ROS activity, and ameliorated mRNA levels. Our findings suggest that environmental lead exposure is related to the development of otitis media, and AME and CME may have antioxidative and anti-inflammatory effects against lead toxicity.


2014 ◽  
Vol 78 (5) ◽  
pp. 777-781 ◽  
Author(s):  
Gi Jung Im ◽  
Moo Kyun Park ◽  
Jae-Jun Song

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