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DBpia AI
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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2025.7
- 수록면
- 426 - 437 (12page)
이용수
초록· 키워드
Background: Hyperuricemia nephropathy (HN) is a form of renal injury caused by hyperuricemia, which can progress to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Ginsenoside Rg5, a major bioactive compound isolated from Panax ginseng, is recognized for its notable effects, including anti-inflammatory, antioxidant, and anticancer activities.
Method: The toxic doses of MSU crystals and Rg5-induced HK-2 cell damage were assessed using the CCK-8 assay and quantifying oxidative stress markers (MDA, GSH, SOD). Intracellular stress was evaluated with JC-1 and DCFH-DA probes. Bioinformatics analysis identified NOX1, TLR4, and Bcl-2 as potential targets. The protein expression associated with stress, inflammation, pyroptosis, and apoptosis in HK-2 cells was evaluated through a combination of Western blotting, ELISA, flow cytometry, immunofluorescence, and overexpression methods. An HN mice model was established through administration of YE and adenine, and the effects of Rg5 were evaluated. The in vivo mechanisms were further verified.
Results: Rg5 reduced serum uric acid, BUN, ADH, and creatinine levels in MSU crystals-stimulated HK-2 cells and hyperuricemic mice, alleviating renal damage. Rg5 inhibited NOX1 and suppressed the TLR4 pathway, reducing oxidative stress, inflammation, pyroptosis, and apoptosis. NOX1 overexpression reversed the effects of Rg5, while TLR4 overexpression had no effect. Rg5’s efficacy was similar to NOX1 inhibitor ML171.
Conclusion: These results indicate that Rg5 can modulate the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating oxidative stress, inflammation, pyroptosis, and apoptosis in HN, highlighting its potential as a therapeutic approach for controlling HN.
상세정보 수정요청해당 페이지 내 제목·저자·목차·페이지Method: The toxic doses of MSU crystals and Rg5-induced HK-2 cell damage were assessed using the CCK-8 assay and quantifying oxidative stress markers (MDA, GSH, SOD). Intracellular stress was evaluated with JC-1 and DCFH-DA probes. Bioinformatics analysis identified NOX1, TLR4, and Bcl-2 as potential targets. The protein expression associated with stress, inflammation, pyroptosis, and apoptosis in HK-2 cells was evaluated through a combination of Western blotting, ELISA, flow cytometry, immunofluorescence, and overexpression methods. An HN mice model was established through administration of YE and adenine, and the effects of Rg5 were evaluated. The in vivo mechanisms were further verified.
Results: Rg5 reduced serum uric acid, BUN, ADH, and creatinine levels in MSU crystals-stimulated HK-2 cells and hyperuricemic mice, alleviating renal damage. Rg5 inhibited NOX1 and suppressed the TLR4 pathway, reducing oxidative stress, inflammation, pyroptosis, and apoptosis. NOX1 overexpression reversed the effects of Rg5, while TLR4 overexpression had no effect. Rg5’s efficacy was similar to NOX1 inhibitor ML171.
Conclusion: These results indicate that Rg5 can modulate the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating oxidative stress, inflammation, pyroptosis, and apoptosis in HN, highlighting its potential as a therapeutic approach for controlling HN.
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목차
- ABSTRACT
- 1. Introduction
- 2. Materials and methods
- 3. Result
- 4. Discussion
- 5. Conclusion
- References
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