Polyphenol (−)-Epigallocatechin Gallate (EGCG) mitigated kidney injury by regulating metabolic homeostasis and mitochondrial dynamics involvement with Drp1-mediated mitochondrial fission in mice

The study aimed to examine effects of (−)-epigallocatechin-3-gallate (EGCG) on energy metabolism and mitochondrial dynamics in mouse model of renal injury caused by doxorubicin (DOX). Here, mice were divided into Control group, EGCG-only treated group, DOX group, and three doses of EGCG plus DOX gro...

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Veröffentlicht in:Food and chemical toxicology Jg. 191; S. 114906
Hauptverfasser: Chu, Yue-Lei, Pi, Jin-Chan, Yao, Yu-Fei, Chen, Xuan-Ying, Peng, Xiao-Ping, Li, Wen-Juan
Format: Journal Article
Sprache:Englisch
Veröffentlicht: England Elsevier Ltd 01.09.2024
Schlagworte:
(−)-Epigallocatechin gallate
Acute Kidney Injury - chemically induced
Acute Kidney Injury - drug therapy
Acute Kidney Injury - metabolism
Acute Kidney Injury - prevention & control
Animals
Antioxidants - pharmacology
apoptosis
Apoptosis - drug effects
blood serum
Catechin - analogs & derivatives
Catechin - pharmacology
creatinine
doxorubicin
Doxorubicin - toxicity
Dynamins - metabolism
Energy metabolism
Energy Metabolism - drug effects
epigallocatechin gallate
glycolysis
hexokinase
homeostasis
Homeostasis - drug effects
Kidney - drug effects
Kidney - metabolism
Kidney injury
kidneys
malate dehydrogenase
Male
malondialdehyde
membrane potential
Membrane Potential, Mitochondrial - drug effects
Mice
mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Mitochondrial dynamics
Mitochondrial Dynamics - drug effects
mitochondrial membrane
oxidative phosphorylation
Oxidative stress
Oxidative Stress - drug effects
polyphenols
protective effect
reactive oxygen species
Reactive Oxygen Species - metabolism
renoprotective effect
toxicology
urea nitrogen
Oxidative stress
Energy metabolism
GSH-PX
HK
SCr
Mitochondrial dynamics
EGCG
SOD
(−)-Epigallocatechin gallate
MDA
DOX
Drp1
MDH
DCFH-DA
ΔΨm
Rhodamine 123
CAT
ROS
BUN
Kidney injury
ISSN:0278-6915, 1873-6351, 1873-6351
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Zusammenfassung:The study aimed to examine effects of (−)-epigallocatechin-3-gallate (EGCG) on energy metabolism and mitochondrial dynamics in mouse model of renal injury caused by doxorubicin (DOX). Here, mice were divided into Control group, EGCG-only treated group, DOX group, and three doses of EGCG plus DOX groups. Our results showed that EGCG behaved beneficial effects against kidney injury via attenuation of pathological changes in kidney tissue, which was confirmed by reducing serum creatinine (SCr), blood urea nitrogen (BUN), and apoptosis. Subsequently, changes in reactive oxygen species generation, malondialdehyde content, and activities of antioxidant enzymes were considerably ameliorated in EGCG + DOX groups when compared to DOX group. Furthermore, EGCG-evoked renal protection was associated with increases of mitochondrial membrane potential and decreases of mitochondrial fission protein Dynamin-related protein 1 (Drp1). Moreover, changing glycolysis into mitochondrial oxidative phosphorylation was observed, evidenced by controlling activities of malate dehydrogenase (MDH) and hexokinase (HK) in EGCG + DOX groups when compared to DOX group, indicating that reprogramming energy metabolism was linked to EGCG-induced renal protection in mice. Therefore, EGCG was demonstrated to have a protective effect against kidney injury by reducing oxidative damage, metabolic disorders, and mitochondrial dysfunction, suggesting that EGCG has potential as a feasible strategy to prevent kidney injury. [Display omitted] •EGCG mitigated doxorubicin (DOX)-induced kidney injury by attenuating apoptosis.•Renal protection of EGCG via modification of redox system and mitochondrial disorder.•EGCG-mediated mitochondrial protection via mitigating abnormal energy metabolism.•Reducing Drp1-evoked mitochondrial fission was implicated in renal protection of EGCG.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0278-6915
1873-6351
1873-6351
DOI:10.1016/j.fct.2024.114906