인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Many plant-derived bioactive molecules with low solubility and permeability can cause hepatocyte injury. However, the mechanism by which they induce hepatic damage without passive diffusion into the hepatic circulatory system remains unclear. This study demonstrate that indirubin, the main component of indigo naturalis with poor aqueous solubility, predisposes mice with chronic colitis to hepatic injury. This closely mimics the hepatic damage commonly observed in ulcerative colitis patients treated with indigo naturalis. Upon administration, indirubin is detected in the plasma, Peyer's patches, and hepatic tissue, with its distribution linked to macrophage infiltration into the liver. Ablation of macrophages significantly reduces indirubin accumulation and attenuates elevated hepatic transaminases in mice with chronic colitis. Mechanistically, macrophages internalize and transport indirubin aggregates from Peyer's patches through the circulatory system to the livers. This internalization activates the NLRP3 inflammasome, leading to the formation of macrophage extracellular traps (METs), which contribute to oxidative stress-induced liver injury. The study identifies indirubin as a potentially toxic component of indigo naturalis that provokes METs-mediated oxidative damage. Additionally, the findings reveal a novel transport pathway for poorly soluble molecules to reach the liver via uptake by macrophages within Peyer's patches.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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