ReferenceID 4559
Emodin prevents renal ischemia-reperfusion injury via suppression of CAMKII/DRP1-mediated mitochondrial fission
Eur J Pharmacol
Acute kidney injury (AKI) is a serious threat to human health. Clinically, ischemia-reperfusion (I/R) injury is considered one of the most common contributors to AKI. Emodin has been reported to alleviate I/R injury in t
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Record Fields
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- Reference Id
- 4559
- Evidence Id
- 21149
- Core Evidence Id
- 21149
- Source Reference Id
- 2389
- Herb2 Reference Id
- HBREF003186
- Subject Paper Key
- HBIN016606_34793771
- Pubmed Id
- 34793771
- Doi
- 10.1016/j.ejphar.2021.174603
- Paper Title
- Emodin prevents renal ischemia-reperfusion injury via suppression of CAMKII/DRP1-mediated mitochondrial fission
- Paper Abstract
- Acute kidney injury (AKI) is a serious threat to human health. Clinically, ischemia-reperfusion (I/R) injury is considered one of the most common contributors to AKI. Emodin has been reported to alleviate I/R injury in the heart, brain, and small intestine in rats and mice through its anti-inflammatory effects. The present study investigated whether emodin improved AKI induced by I/R and elucidated the molecular mechanisms. We used a mouse model of renal I/R injury and human renal tubular epithelial cell model of hypoxia/reoxygenation (H/R) injury. Ischemia/reperfusion resulted in renal dysfunction. Pretreatment with emodin ameliorated renal injury in mice following I/R injury. Emodin reduced mitochondrial-mediated apoptosis, suppressed the overproduction of mitochondrial reactive oxygen species and accelerated the recovery of adenosine triphosphate both in vivo and in vitro. Emodin prevented mitochondrial fission and restored the balance of mitochondrial dynamics. The phosphorylation of dynamin-related protein 1 (DRP1) at Ser616, a master regulator of mitochondrial fission, was upregulated in both models of I/R and H/R injury, and this upregulation was blocked by emodin. Using computational cognate protein kinase prediction and specific kinase inhibitors, we found that emodin inhibited the phosphorylation of calcium/calmodulin-dependent protein kinase II (https://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=1554), thereby inhibiting its kinase activity and reducing the phosphorylation of DRP1 at Ser616. The results demonstrated that emodin pretreatment could protect renal function by improving mitochondrial dysfunction induced by I/R.
- Journal
- Eur J Pharmacol
- Publish Year
- 2021
- Experiment Subject
- mouse; rat; human; human renal tubular epithelial cell model
- Experiment Type
- Animal Experiment
- Phenotype Related
- I/r Injury; Acute Kidney Injury; Renal Dysfunction; Ischemia-reperfusion (i/r) Injury; Renal Injury; Mitochondrial Dysfunction; Renal I/r Injury
- Paper Title Cn
- Paper Title En
- Emodin prevents renal ischemia-reperfusion injury via suppression of CAMKII/DRP1-mediated mitochondrial fission
- Bilingual Status
- semi_complete