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.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2021.12
- 수록면
- 86 - 93 (8page)
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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.
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References
참고문헌 (39)
참고문헌 신청
Bovée, D. M. / 2020 / Salt-sensitive hypertension in chronic kidney disease:Distal tubular mechanisms / Am. J. Physiol. Renal Physiol 319:F729~F745
Majid, D. S. / 2015 / Salt-sensi-tive hypertension : perspectives on intrarenal mechanisms / Curr. Hypertens. Rev 11:38~48
Ren, J. / 2019 / Role of T-cell activation in salt-sensitive hypertension / Am. J. Physiol. Heart Circ. Physiol :H1345~H1135
Mattson, D. L. / 2014 / Infiltrating immune cells in the kid- ney in salt-sensitive hypertension and renal injury / Am. J. Physiol. Renal Physiol 307:F499~F508
Hirohama, D. / 2019 / Evaluation of the pathophy-siological mechanisms of salt-sensitive hypertension / Hypertens. Res 42:1848~1857
Majid, D. S. / 2015 / Salt-sensi-tive hypertension : perspectives on intrarenal mechanisms / Curr. Hypertens. Rev 11:38~48
Ren, J. / 2019 / Role of T-cell activation in salt-sensitive hypertension / Am. J. Physiol. Heart Circ. Physiol :H1345~H1135
Mattson, D. L. / 2014 / Infiltrating immune cells in the kid- ney in salt-sensitive hypertension and renal injury / Am. J. Physiol. Renal Physiol 307:F499~F508
Hirohama, D. / 2019 / Evaluation of the pathophy-siological mechanisms of salt-sensitive hypertension / Hypertens. Res 42:1848~1857
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