한국해양바이오학회지 (Journal of Marine Bioscience and Biotechnology)

한국해양바이오학회 (The Korean Society for Marine Biotechnology)
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염분 섭취에 의한 시스플라틴 유도 급성 신장 손상의 촉진과 염증 반응과의 연관성

Facilitation of cisplatin-induced acute kidney injury by high salt intake through increased inflammatory response

  • 지선영 (동의대학교 항노화연구소) ;
  • 황보현 (동의대학교 항노화연구소) ;
  • 김민영 (동의대학교 항노화연구소) ;
  • 김다혜 (동의대학교 항노화연구소) ;
  • 박범수 (동의대학교 한의과대학 생화학교실) ;
  • 박정현 ((주)마린바이프로세스) ;
  • 이배진 ((주)마린바이프로세스) ;
  • 이혜숙 (동의대학교 항노화연구소) ;
  • 최영현 (동의대학교 한의과대학 생화학교실)
  • Ji, Seon Yeong (Anti-Aging Research Center, Dong-eui University) ;
  • Hwangbo, Hyun (Anti-Aging Research Center, Dong-eui University) ;
  • Kim, Min Yeong (Anti-Aging Research Center, Dong-eui University) ;
  • Kim, Da Hye (Anti-Aging Research Center, Dong-eui University) ;
  • Park, Beom Su (Department of Biochemistry, College of Korean Medicine, Dong-eui University) ;
  • Park, Joung-Hyun (Ocean Fisheries & Biology Center, Marine Bioprocess Co., Ltd.) ;
  • Lee, Bae-Jin (Ocean Fisheries & Biology Center, Marine Bioprocess Co., Ltd.) ;
  • Lee, Hyesook (Anti-Aging Research Center, Dong-eui University) ;
  • Choi, Yung Hyun (Department of Biochemistry, College of Korean Medicine, Dong-eui University)
  • 투고 : 2021.11.25
  • 심사 : 2021.12.02
  • 발행 : 2021.12.31
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초록

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

키워드

과제정보

이 논문은 2020년 해양수산부 재원으로 해양수산과학기술진흥원의 지원을 받아 수행된 연구임(유산균이 살아있는 고농도 발효 GABA 소금의 개발 및 상용화 계획, 과제번호 20200073).

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