Protective role of apigenin in cisplatin-induced renal injury.

  title={Protective role of apigenin in cisplatin-induced renal injury.},
  author={Xuexiu He and Chunmei Li and Zhengkai Wei and Jingjing Wang and Jinhua Kou and Weijian Liu and Mingyu Shi and Zhengtao Yang and Yunhe Fu},
  journal={European journal of pharmacology},

Ameliorative Effect of Daidzein on Cisplatin-Induced Nephrotoxicity in Mice via Modulation of Inflammation, Oxidative Stress, and Cell Death

It is suggested that daidzein attenuated cisplatin-induced kidney injury through the downregulation of oxidative/nitrative stress, immune cells, inflammatory cytokines, and apoptotic cell death, thus improving kidney regeneration.

Effect of apigenin on apoptosis induced by renal ischemia/reperfusion injury in vivo and in vitro

ApI pretreatment can protect renal function against I/R injury and prevent renal tubular cells from apoptosis in vivo and in vitro which might through PI3K/Akt mediated mitochondria-dependent apoptosis signaling pathway.

Protective effect of urolithin a on cisplatin-induced nephrotoxicity in mice via modulation of inflammation and oxidative stress.

  • Taile JingJiezhi Liao Hao Pan
  • Biology, Chemistry
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2019

Apigenin alleviates methotrexate-induced liver and kidney injury in mice

It is suggested that API has a protective effect against oxidative stress and liver-kidney toxicity induced by MTX, and alleviates liver and kidney toxicity by attenuating oxidative Stress and tissue injury markers, histopathological alterations, and apoptosis and inflammation.

Apigenin Protects Against Renal Tubular Epithelial Cell Injury and Oxidative Stress by High Glucose via Regulation of NF-E2-Related Factor 2 (Nrf2) Pathway

Apigenin protects renal tubular epithelial cells against high glucose-induced injury through suppression of oxidative stress and inflammation via activation of the Nrf2 pathway.

DHA-PC protects kidneys against cisplatin-induced toxicity and its underlying mechanisms in mice.

Investigation of whether DHA-PC treatment could alleviate cisplatin-induced nephrotoxicity using a Balb/c mice model showed that Dha-PC could significantly prolong the survival time, while the traditional DHA had no remarkable changes, suggesting that D HA-PC might be a new dietary strategy for the treatment of neph rotoxicity.

The potential protective role of apigenin against oxidative damage induced by nickel oxide nanoparticles in liver and kidney of male Wistar rat, Rattus norvegicus

Apigenin (APG) can ameliorate the NiONP-induced hepatotoxicity and nephrotoxicity in male Wistar rats and substantially alleviated all the studied parameters.

Apigenin ameliorates hyperuricemic nephropathy by inhibiting URAT1 and GLUT9 and relieving renal fibrosis via the Wnt/β-catenin pathway.



Renoprotective mechanisms of morin in cisplatin-induced kidney injury.

An Extract of Rhodobacter sphaeroides Reduces Cisplatin-Induced Nephrotoxicity in Mice

Lycogen™ exerts anti-inflammatory activities that represent a promising strategy for the treatment of cisplatin-induced renal injury and attenuated body weight loss and significantly prolonged the survival of mice with renal injury.

Enhancement by pyrazole of lipopolysaccharide‐induced liver injury in mice: Role of cytochrome P450 2E1 and 2A5

Induction of CYP2E1 plays an important role in the enhancement of LPS liver injury by pyrazole, but some contribution by CYP1E1 cannot be excluded and CMZ protected against the pyrazoles enhanced L PS liver injury and oxidative stress.

The Flavonoid Apigenin Ameliorates Cisplatin-Induced Nephrotoxicity through Reduction of p53 Activation and Promotion of PI3K/Akt Pathway in Human Renal Proximal Tubular Epithelial Cells

It is suggested that apigenin ameliorates cisplatin-induced apoptosis through reduction of p53 activation and promotion of PI3K/Akt pathway in HK-2 cells.

Manganese superoxide dismutase attenuates Cisplatin-induced renal injury: importance of superoxide.

The results demonstrate the importance of reactive oxygen species in the mechanism that underlies cisplatin-induced renal injury and specifically implicate the superoxide radical, and not hydrogen peroxide, as the mediator.

Lipopolysaccharide-induced liver injury in rats treated with the CYP2E1 inducer pyrazole.

Results show that pyrazole treatment enhanced LPS-induced necrosis, not apoptosis, and the enhanced liver necrosis appears to involve an increase in oxidative and nitrosative stress generated by the combination of LPS plus elevated CYP2E1 levels.

Cisplatin nephrotoxicity: mechanisms and renoprotective strategies.

Examination of tumor-bearing animals and identification of novel renoprotective strategies that do not diminish the anticancer efficacy of cisplatin are essential to the development of clinically applicable interventions.

An integrative view of the pathophysiological events leading to cisplatin nephrotoxicity

This review presents an integrative view of the pathophysiological effects of cisplatin on tubular, vascular, glomerular, and interstitial function and the interplay among these actions.

Lithium Chloride Suppresses Colorectal Cancer Cell Survival and Proliferation through ROS/GSK-3β/NF-κB Signaling Pathway

Results showed administration of LiCl increased apoptosis and the level of ROS in colorectal cancer cells, and demonstrated that therapeutic targeting of ROS/GSK-3β/NF-κB pathways may be an effective way for colorective cancer intervention, although further preclinical and clinical testing are desirable.