文献类型：期刊文献

英文题名：Highland barley polyphenols mitigate cisplatin-induced nephrotoxicity via mitochondrial protection and metabolic reprogramming

作者：Shao, Yong[1,2];Liu, Yunfan[3];Chen, Gang[1];Yu, Hailong[7];Wang, Miao[2];Zhang, Tangwei[4];Gao, Liping[3];Abd El-Aty, A. M.[5,6];She, Yongxin[2]

第一作者：Shao, Yong

通讯作者：She, YX[1]

机构：[1]Beijing Technol & Business Univ, Key Lab Geriatr Nutr & Hlth, Minist Educ, Beijing 100048, Peoples R China;[2]Chinese Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, Beijing 100081, Peoples R China;[3]Beijing Union Univ, Coll Biochem Engn, Beijing 100023, Peoples R China;[4]Tibetan Acad Agr land Anim Husb Sci, Inst Qual Stand & Testing Technol Agroprod, Lhasa 850000, Peoples R China;[5]Cairo Univ, Fac Vet Med, Dept Pharmacol, Giza 12211, Egypt;[6]Ataturk Univ, Med Fac, Dept Med Pharmacol, TR-25240 Erzurum, Turkiye;[7]Beijing Polytech, Coll Bioengn, Beijing 100176, Peoples R China

第一机构：Beijing Technol & Business Univ, Key Lab Geriatr Nutr & Hlth, Minist Educ, Beijing 100048, Peoples R China

通讯机构：[1]corresponding author), Chinese Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, Beijing 100081, Peoples R China.

年份：2026

卷号：1277

外文期刊名：JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES

收录：;EI(收录号：20261520468655);WOS:【SCI-EXPANDED(收录号:WOS:001742570800001)】；

基金：This research was funded by the National Natural Science Founda-tion of China (31772071) and the Agriculture Research System of China (CARS-05-05A-03) .

语种：英文

外文关键词：Polyphenols extracted from highland barley; Cisplatin; HEK293 cells; Kidney; Metabolomics

摘要：Cisplatin (DDP)-induced acute kidney injury (AKI) presents a major challenge in chemotherapy, limiting its clinical utility due to nephrotoxicity. In this study, we explored the therapeutic potential of polyphenol-rich extracts from highland barley (HBPE) in counteracting DDP-induced renal damage. We hypothesized that HBPE could exert protective effects through the modulation of oxidative stress, mitochondrial dysfunction, and metabolic dysregulation. Using UHPLC-QTOF/MS-based untargeted metabolomics, we identified key metabolic disruptions in human embryonic kidney (HEK293) cells treated with DDP, which were substantially reversed by HBPE. The extract significantly attenuated mitochondrial injury and oxidative stress, as shown by decreased malondialdehyde (MDA) levels; increased levels of glutathione (GSH), superoxide dismutase (SOD), and ATP; and reduced reactive oxygen species (ROS) (P < 0.05). Furthermore, HBPE inhibited apoptosis by stabilizing mitochondrial integrity. In vivo, HBPE pretreatment ameliorated renal dysfunction in rats, as evidenced by reduced serum creatinine and blood urea nitrogen (BUN) levels and improved renal histopathology. Metabolomic profiling identified 39 potential biomarkers and revealed that HBPE restored key metabolic pathways, including folate biosynthesis, nicotinate metabolism, and phenylalanine metabolism. These results support the potential of HBPE as a natural nephroprotective intervention during chemotherapy. Derived from a sustainable agricultural source, HBPE offers a promising, low-toxicity strategy for enhancing patient safety and promoting integrative therapeutic development.