Protective Effect of Panduratin A on Cisplatin-Induced Apoptosis of Human Renal Proximal Tubular Cells and Acute Kidney Injury in Mice

被引:18
|
作者
Thongnuanjan, Penjai [1 ,2 ]
Soodvilai, Sirima [3 ]
Fongsupa, Somsak [4 ]
Chabang, Napason [5 ]
Vivithanaporn, Pornpun [6 ]
Tuchinda, Patoomratana [7 ]
Soodvilai, Sunhapas [1 ,2 ,7 ]
机构
[1] Mahidol Univ, Fac Sci, Multidisciplinary Unit, Toxicol Grad Program, Bangkok 10400, Thailand
[2] Mahidol Univ, Res Ctr Transport Prot Med Innovat, Dept Physiol, Bangkok 10400, Thailand
[3] Rangsit Univ, Coll Pharm, Dept Pharmaceut Technol, Pathum Thani 12000, Thailand
[4] Thammasat Univ Rangsit Campus, Fac Allied Hlth Sci, Dept Med Technol, Pathum Thani 12121, Thailand
[5] Mahidol Univ, Fac Sci, Sch Bioinnovat & Biobased Prod Intelligence, Bangkok 10400, Thailand
[6] Mahidol Univ, Ramathibodi Hosp, Fac Med, Chakri Naruebodindra Med Inst, Prakan 10540, Thailand
[7] Mahidol Univ, Excellent Ctr Drug Discovery, Bangkok 10400, Thailand
关键词
chemotherapy; acute kidney injury; panduratin A; human renal proximal tubule; anti-apoptosis; ACTIVATED PROTEIN-KINASE; CANCER-THERAPY; NEPHROTOXICITY; MECHANISMS; INFLAMMATION; INHIBITION; MAPK;
D O I
10.1248/bpb.b21-00036
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: Cisplatin is an effective chemotherapy but its main side effect, acute kidney injury, limits its use. Panduratin A, a bioactive compound extracted from Boesenbergia rotunda, shows several biological activities such as anti-oxidative effects. The present study investigated the nephroprotective effect of panduratin A on cisplatin-induced renal injury. Methods: We investigated the effect of panduratin A on the toxicity of cisplatin in both mice and human renal cell cultures using RPTEC/TERT1 cells. Results: The results demonstrated that panduratin A ameliorates cisplatin-induced renal toxicity in both mice and RPTEC/TERT1 cells by reducing apoptosis. Mice treated with a single intraperitoneal (i.p.) injection of cisplatin (20 mg/kg body weight (BW)) exhibited renal tubule injury and impaired kidney function as shown by histological examination and increased serum creatinine. Co-administration of panduratin A (50 mg/kg BW) orally improved kidney function and ameliorated renal tubule injury of cisplatin by inhibiting activation of extracellular signal-regulated kinase (ERK)1/2 and caspase 3. In human renal proximal tubular cells, cisplatin induced cell apoptosis by activating pro-apoptotic proteins (ERK1/2 and caspase 3), and reducing the anti-apoptotic protein (Bcl-2). These effects were significantly ameliorated by co-treatment with panduratin A. Interestingly, panduratin A did not alter intracellular accumulation of cisplatin. It did not alter the anti-cancer efficacy of cisplatin in either human colon or non-small cell lung cancer cell lines. Conclusions: The present study highlights panduratin A has a potential protective effect on cisplatin's nephrotoxicity.
引用
收藏
页码:830 / 837
页数:8
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