YOU YEON CHUNG,
BYOUNGJAE KIM, KWANG-YOON JUNG, KYUNG HO OH, SOON-YOUNG KWON, JEONG-SOO WOO, JAE-GU CHO, SEUNG-KUK BAEK
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¸ñÀû: Despite the increasing prevalence of laryngopharyngeal reflux
disease (LPRD), its research has faced challenges due to the
absence of objective diagnosis, controversies surrounding its
molecular-biological etiology, and poorly understood mechanisms,
compounded by the lack of suitable disease research models.
Previous in-vitro models have simulated LPR through acid
exposure, elucidating that the escalation of MMP-7 is triggered
by reactive oxygen species (ROS), involving ERK and c-Jun in the
pathogenesis. This study aims to establish in-vivo mouse models
of LPRD by feeding acid and N-acetyl cysteine (NAC). ¹æ¹ý:Daily doses of acidic water, with/without concurrent NAC exposure,
were formulated to induce LPRD symptoms in mice. Pharyngeal
tissues were histologically evaluated and compared through
immunohistochemistry (IHC) with E-cadherin, MMP-7, and its
regulatory factors (ROS and its downstream mediators, including
ERK and c-Jun) to confirm the establishment of an LPRD animal
model. Additionally, the expressions of E-cad and MMP-7 in the
pharyngeal mucosa of the mice were analyzed by immunoblotting. °á°ú:In the acid treatment group, a significant decrease in E-cadherin and a marked increase in MMP-7 expression were observed. MMP-7 regulatory factors were also elevated. In contrast, in the NAC treatment group, these effects were reversed. The immunoblotting results corresponded to these findings. °á·Ð:Comparison of in-vivo research results with previous in-vitro
studies verified MMP-7 regulatory factors as therapeutic targets
for LPRD. The administration of acidic water effectively induced
LPRD, and NAC demonstrated practical efficacy as an MMP-7
inhibitor, potentially serving as an LPRD treatment. |