[논문]염분 섭취에 의한 시스플라틴 유도 급성 신장 손상의 촉진과 염증 반응과의 연관성

지선영; 황보현; 김민영; 김다혜; 박범수; 박정현; 이배진; 이혜숙; 최영현

doi:10.15433/ksmb.2021.13.2.086

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 원문보기

한국해양바이오학회지 = Journal of marine bioscience and biotechnology, v.13 no.2, 2021년, pp.86 - 93

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)

Abstract ▼ AI-Helper

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.

주제어

표/그림 (6)

그림 Figure 1. Effects of high salt on cisplatin-induced AKT mice. C57BL/6 mice were orally treated with high salt containing 4% NaCl and administered 20 mg/kg cisplatin or vehicle 1 h later via intraperitoneal injection. High salt was administered 24 and 48 h after injection, and the mice were sacrificed 24 h after the last dose of high salt. (A) Representative images of kidney morphological changes in each group are presented. (B and C) Kidney tissues and injured-tubules of each group were stained with H&E (B) and PAS (C), respectively, and then observed under a fluorescence microscope. Representative images are presented (scale bar = 50 μm).
표 Table 1. Effect of high salt intake on the body and organ weight of cisplatin-induced nephrotoxicity. The organ weight of all animals was measured after 72 h salt feeding. All data are expressed as mean ± S.D (n = 6, **p<0.01 and ***p<0.001 vs normal group)
표 Table 2. Effect of high salt intake on the serum biochemical parameters of cisplatin-induced nephrotoxicity. The levels of major biochemical biomarkers in serum were measured after 72 h salt feeding. The data are expressed as mean ± S.D. (n = 6, *p<0.05, **p<0.01 and ***p<0.001 vs normal group; ##p<0.01 vs cisplatin group)
표 Table 3. Effect of high salt intake on the hematological parameters of cisplatin-induced nephrotoxicity. The hematological parameters of each group were measured after 72 h salt feeding. All data are expressed as mean ± S.D. (n = 6, *p<0.05 and ***p<0.001 vs normal group; #p<0.05 vs cisplatin group)
그림 Figure 2. Effect of high salt intake on renal tubular cell proliferation and death in cisplatin-induced AKT mice. After treatment in the same condition as in the Figure 1, renal tubule cells were stained with antibodies against PCNA (A), TIM-1 (B) and Bax (C), respectively, and then observed under a fluorescence microscope. Representative images are presented (scale bar = 50 μm). (D-F) PCNA TIM-1 and Bax-positive areas were quantitatively measured. All data are expressed as mean ± S.D. (n = 6, ***p<0.001 vs normal group; #p<0.05 and ###p<0.001 vs cisplatin group).
그림 Figure 3. Effect of high salt intake on kidney inflammation in cisplatin-induced AKT mice. After treatment in the same condition as in the Figure 1, renal tubule cells were stained with antibodies against HMGB-1 (A) TNF-α (B) and COX-2 (C), respectively, and then observed under a fluorescence microscope. Representative images are presented (scale bar = 50 μm). (D-F) HMGB-1, TNF-α and COX-2-positive areas were quantitatively measured. All data are expressed as mean ± S.D. (n = 6, *p<0.05 and ***p<0.001 vs normal group; #p<0.05 vs cisplatin group).

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