| アイテムタイプ |
紀要論文 / departmental bulletin paper(1) |
| 公開日 |
2025-05-16 |
| タイトル |
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|
タイトル |
The relationship between Tacrolimus-induced nephrotoxicity and Endothelin 1 on renal ischemic reperfusion injury model in spontaneously hypertensive rats |
|
言語 |
en |
| 作成者 |
Nose, Kazuhiro
Matsuura, Takeshi
Kurita, Takashi
|
| 言語 |
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|
言語 |
eng |
| キーワード |
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主題 |
tacrolimus-induced nephrotoxicity, endothelin 1, renal ischemic reperfusion injury, spontaneously hypertensive rats |
| 内容記述 |
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内容記述タイプ |
Abstract |
|
内容記述 |
Objective : With regard to the mechanism of tacrolimus (Tac)-induced nephrotoxicity in a rat model of renal ischemic reperfusion injury, we hypothesized that examining the phenomenon and its response to Endothelin 1 may lead to improved prognosis in transplanted kidneys in humans. Materials and Method : Two experiments were conducted. Both experiments used 10-week-old male spontaneously hypertensive rats (SHR). Tacrolimus was administered (dosage 1 mg/kg or 2 mg/kg) daily for 2 weeks. In experiment 1, the SHR were divided into a nephrectomy group and a non-nephrectomy group. In experiment 2, the SHR were divided into an ischemic group and a non-ischemic group. The hematobio-chemical and pathological indices and the cytokines of these model rats were studied. Results : In experiment 1, the nephrectomy group showed significantly decreased creatinine clearance (CCr) levels, depending upon the Tac dosage. Histologically, severity of vacuolized deformity of the renal tubule varied with the Tac dosage. In experiment 2, the renal function in the ischemic group showed prompt improvement, using the BUN, Cr, and CCr levels as indices. Administering Tac to SHR with impaired reperfusion due to ischemia resulted in increased nephrotoxicity. Examination of the cytokines revealed that, although the expression of Endothelin 1 was induced by impaired reperfusion after ischemia, the expression of the endothelin-A receptor was suppressed. Discussion : Nephrotoxicity was markedly more severe in the rats with renal dysfunction than in the rats with normal renal function that had received the same dosage of Tac. Nephrotoxicity was potentiated by renal ischemic reperfusion injury, which suggests that Endothelin 1 was involved. |
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言語 |
en |
| 出版者 |
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|
出版者 |
The Kinki University Medical Association |
|
言語 |
en |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
departmental bulletin paper |
| 出版タイプ |
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|
出版タイプ |
AM |
|
出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
| 収録物識別子 |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
03866092 |
| 開始ページ |
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|
開始ページ |
39 |
| 終了ページ |
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|
終了ページ |
46 |
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY
巻 28,
号 2,
p. 39-46,
発行日 2003-12
|
AA0050842X-20031200-0039.pdf (658.6 KB)
