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
Chemotherapy-induced peripheral neurotoxicity (CIPN) is one common side effect associated with antineoplastic agents. Despite its relevance, the underlying mechanisms remain poorly understood. In this study, we explored cytokines and macrophages that contribute to two chronic models of CIPN comparing paclitaxel (PTX)- and oxaliplatin (OHP)-induced CIPN in rats. To detect chemotherapy-induced sensory or neuronal abnormalities behavioral tests, pathological and morphometric analysis were used. To investigate systemic inflammation, a panel including IL-6, IL-1β, IL-2, IL-10, GRO/KC(CXCL1), TNFα, IFNγ were tested in serum. Besides, we analyzed dorsal root ganglia (DRG), caudal nerves and spinal cord mRNA expression of a panel of pro-inflammatory markers IL-6, CCL2 and NLRP3, as well as caudal macrophage infiltration. We evidenced a remarkable difference in caudal macrophage infiltration in PTX- vs. OHP-treated rats, which was associated with serum CXCL1 and to a different IL-6 expression pattern in serum, DRG, spinal cord and caudal nerve. Moreover, CCL2, NLRP3 upregulation was also increased in the caudal nerves in PTX-treated animals. On the contrary, OHP induced IL-6 and CCL2 expression in DRG. Since our results suggest that CXCL1 or IL-6 could be considered as critical lynchpins between inflammation pain and CIPN, targeting early inflammatory events could be a promising therapeutic approach.
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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