2022年
シスプラチン誘発急性腎障害に対するバルプロ酸ナトリウムの影響
日本薬理学会年会要旨集
- 巻
- 95
- 号
- 開始ページ
- 1-SS-48
- 終了ページ
- pm19S
- 記述言語
- 日本語
- 掲載種別
- DOI
- 10.1254/jpssuppl.95.0_1-ss-48
- 出版者・発行元
- 公益社団法人 日本薬理学会
OBJECTIVE: Cisplatin-induced acute kidney injury (AKI) is well known, and the nephrotoxicity of cisplatin restricts its clinical application. Currently, there are no drugs are recommended for the prevention of cisplatin-induced AKI. Forced hydration and diuresis may partially prevent nephrotoxicity of cisplatin, but it is still difficult to entirely prevent kidney injury. Thus, establishment of a new preventive method against cisplatin-induced AKI is required. Therefore, in this study, the purpose of this study was to clarify the efficacy of sodium valproate in cisplatin-induced AKI.
METHODS: In order to establish cisplatin‐induced AKI animal model, C57BL/6 mice were administered with either cisplatin (15 mg/kg, i.p.) or saline (control). The degree of renal damage was assessed by various renal function parameters and pathological evaluation. The effect of sodium valproate on cisplatin-induced cytotoxicity was evaluated using HK2 cells, MKN-1 cells and LLC cells.
RESULTS: Cisplatin treatment worsened various renal function parameters and tubular damage scores, which were significantly improved by co-treatment with sodium valproate. The decrease in cell viability of HK2 cells by cisplatin was significantly improved by co-treatment with sodium valproate. On the other hand, sodium valproate had no adverse effect on the reduction of cell viability of various cancer cells by cisplatin.
CONCLUSIONS: The results of this study indicated that sodium valproate could act as a potential preventive drug for cisplatin-induced AKI.
METHODS: In order to establish cisplatin‐induced AKI animal model, C57BL/6 mice were administered with either cisplatin (15 mg/kg, i.p.) or saline (control). The degree of renal damage was assessed by various renal function parameters and pathological evaluation. The effect of sodium valproate on cisplatin-induced cytotoxicity was evaluated using HK2 cells, MKN-1 cells and LLC cells.
RESULTS: Cisplatin treatment worsened various renal function parameters and tubular damage scores, which were significantly improved by co-treatment with sodium valproate. The decrease in cell viability of HK2 cells by cisplatin was significantly improved by co-treatment with sodium valproate. On the other hand, sodium valproate had no adverse effect on the reduction of cell viability of various cancer cells by cisplatin.
CONCLUSIONS: The results of this study indicated that sodium valproate could act as a potential preventive drug for cisplatin-induced AKI.
- リンク情報
- ID情報
-
- DOI : 10.1254/jpssuppl.95.0_1-ss-48
- ISSN : 0918-9823
- eISSN : 2435-4953
- 医中誌Web ID : W408600690
- J-Global ID : 202202219158169742
- CiNii Research ID : 1390291767676156800