期刊
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
卷 17, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12906-017-2055-y
关键词
Acute kidney injury; Herbal medicine; High-mobility group box protein 1; Neutrophil gelatinase-associated lipocalin; Kidney injury molecule-1
资金
- Traditional Korean Medicine R&D program - Ministry of Health & Welfare through the Korea Health Industry Development Institute (KHIDI) [HI16C0948]
Background: Acute kidney injury (AKI) is an initial factor in many kidney disorders. Pre- and intra-renal AKI biomarkers have recently been reported. Recovery from AKI by herbal medicine has rarely been reported. Thus, this study aimed to investigate the dose- and time-dependent effects of herbal medicines to protect against AKI in cisplatin-induced human kidney 2 (HK-2) cells by assessing the activities of high-mobility group box protein 1 (HMGB1), neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). Methods: Proximal tubular HK-2 cell lines were treated with either 400 mu M of cisplatin for 6 h or 10 mu M of cisplatin for 24 h and then exposed to ten types of single herbal medicines, including Nelumbo nymphaea (NY) at a dose of 100 mu g/mL. The AKI biomarkers HMGB1, NGAL and KIM-1 were repeatedly measured by an ELISA assay at 2, 4, and 6 h in the group treated with 400 mu M of cisplatin to confirm necrotic cell death and at 6, 24, and 48 h in the group treated with 10 mu M of cisplatin to examine apoptotic cell death. Recovery confirm was conducted through in vivo study using ICR mice for 3 day NY or Paeonia suffruticosa intake. Results: Cisplatin treatment at a concentration of 10 mu M decreased cell viability. Treatment with 400 mu M of cisplatin reduced HMBG1 activity and resulted in lactate dehydrogenase release. In longer exposure durations (up to 48 h), NGAL and KIM-1 exhibited activity from 24 h onward. Additionally, NY treatment resulted in an approximately 50% change in all three biomarkers. The time-dependent profiles of HMGB1, NGAL and KIM-1 activities up to 48 h were notably different; HMGB1 exhibited a 7-fold change at 6 h, and NGAL and KIM-1 exhibited 1.7-fold changes at 24 h, respectively. Consistently, serum and urine NGAL and KIM-1 activities were all reduced in ICR mice. Conclusions: Several single herbal medicines, including NY, have a potential as effectors of AKI due to their ability to inhibit the activation of HMGB1, NGAL and KIM-1 in an in vitro AKI-mimicked condition and simple in vivo confirm. Furthermore, an in vivo proof-of-concept study is needed.
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