인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
개인구독
소속 기관이 없으신 경우, 개인 정기구독을 하시면 저렴하게
논문을 무제한 열람 이용할 수 있어요.
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
Abstract Purpose Sepsis is a life-threatening disorder marked by organ dysfunction due to infection. Transient receptor potential vanilloid 1 (TRPV1) is a non-selective, ligand-gated cation channel activated by multiple stimuli. This study investigates the role of TRPV1 in sepsis-associated encephalopathy (SAE). Methods The SAE models of wild-type and TRPV1 knockout (TRPV1 -/- ) mice were established through intraperitoneal injection of 10 mg/kg lipopolysaccharide. Brain tissues and serum were collected 24 h post-injection for analysis. Rectal temperature was monitored at 12 and 24 h, and the 7-day survival rate was recorded. Mice were pretreated with capsaicin (CAP), and brain tissue and serum were collected for detection. Results TRPV1 expression was significantly elevated in the brain tissues of mice with sepsis. TRPV1 -/- aggravated SAE symptoms, as evidenced by a significant decrease in rectal temperature, a reduced 7-day survival rate, an elevated Murine Sepsis Score, and greater impairment in learning and memory. Mechanistically, TRPV1 deficiency increased NF-κB, pyroptosis-related proteins, and levels of IL-6 and TNF-α in SAE mice. CAP pretreatment significantly reduced abnormal neurons in the CA1 region, decreased NF-κB, Pro-caspase1, and Cleaved-caspase1 in brain tissues, and lowered IL-1β and IL-18 serum levels, with this effect being TRPV1-dependent. Conclusion In summary, TRPV1 deficiency worsens SAE-induced damage in mice, associated with activation of NF-κB and pyroptosis pathways. CAP pretreatment improved the damage caused by SAE by activating TRPV1.
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.
최근 본 자료 전체보기
