ReferenceID 5131

Dioscin ameliorates cisplatin-induced intestinal toxicity by mitigating oxidative stress and inflammation

Int Immunopharmacol

Cisplatin is the most widely prescribed drug in chemotherapy, but its gastrointestinal toxicity reduces therapeutic efficacy. Oxidative stress and inflammation are considered to be the main pathogenesis of cisplatin-indu

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Reference Id
5131
Evidence Id
21721
Core Evidence Id
21721
Source Reference Id
3542
Herb2 Reference Id
HBREF004339
Subject Paper Key
HBIN024134_35933746
Pubmed Id
35933746
Doi
10.1016/j.intimp.2022.109111
Paper Title
Dioscin ameliorates cisplatin-induced intestinal toxicity by mitigating oxidative stress and inflammation
Paper Abstract
Cisplatin is the most widely prescribed drug in chemotherapy, but its gastrointestinal toxicity reduces therapeutic efficacy. Oxidative stress and inflammation are considered to be the main pathogenesis of cisplatin-induced intestinal toxicity. Dioscin is a steroidal saponin with potential anti-cancer, antioxidant, and anti-inflammatory activities. In this study, we established a rat model of intestinal injury by tail vein injection of cisplatin, and intragastrically administered dioscin to evaluate its effect on intestinal injury. Biochemical markers, western blotting, qRT-PCR and histopathological staining were used to analyze intestinal injury according to various molecular mechanisms. The results revealed that dioscin significantly inhibited cisplatin-induced intestinal mucosal damage and decreased DAO levels in rats. Furthermore, dioscin activated the Nrf2/HO-1 pathway to increase the level of antioxidant enzymes and reduce the levels of MDA and H 2 O 2 . In addition, dioscin pretreatment significantly reduced ileum epithelial NLRP3 inflammasome formation and decreased the levels of inflammatory factors compared with the cisplatin group. In parallel, Nrf2 inhibitor ML385 blocked the therapeutic effect of dioscin in rat with cisplatin-induced intestinal toxicity. In terms of mechanisms, dioscin reversed cisplatin-induced up-regulation of MAPKs and up-regulated p-PI3K and p-AKT levels. Meanwhile, dioscin potently promoted Wnt3A/β-catenin signaling to relieve cisplatin-induced proliferation inhibition. In conclusion, our study suggests that dioscin could ameliorate the cisplatin-induced intestinal toxicity by reducing oxidative stress and inflammation.
Journal
Int Immunopharmacol
Publish Year
2022
Experiment Subject
rat
Experiment Type
Animal Experiment
Phenotype Related
Intestinal Injury; Cisplatin-induced Intestinal Toxicity; Inflammation
Paper Title Cn
Paper Title En
Dioscin ameliorates cisplatin-induced intestinal toxicity by mitigating oxidative stress and inflammation
Bilingual Status
semi_complete