Evidence map›Paper›PMID 39662059›Full record

ArticleKidney & blood pressure research2025

Shikonin Inhibits Endoplasmic Reticulum Stress-Induced Apoptosis to Attenuate Renal Ischemia/Reperfusion Injury by Activating the Sirt1/Nrf2/HO-1 Pathway.

Qian Huang, Zilu Shi, Dandan Zheng, Huiqin Chen, Qiuhong Huang

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Article in Kidney & blood pressure research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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3 · Its place in the literature

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3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Qian HuangDepartment of Teaching and Research Section of Physiology, Basic Medicine Department, Quanzhou Medical College, Quanzhou, China.
Zilu ShiDepartment of Nephrology, First Hospital of Quanzhou Affiliated to Fujian Medical College, Quanzhou, China.
Dandan ZhengDepartment of Teaching and Research Section of Physiology, Basic Medicine Department, Quanzhou Medical College, Quanzhou, China.
Huiqin ChenDepartment of Teaching and Research Section of Physiology, Basic Medicine Department, Quanzhou Medical College, Quanzhou, China.
Qiuhong HuangDepartment of Teaching and Research Section of Physiology, Basic Medicine Department, Quanzhou Medical College, Quanzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionShikonin is the major bioactive compound abundant in Lithospermum erythrorhizon and possesses diverse pharmacological properties. This study aimed to examine shikonin roles in experimental renal ischemia/reperfusion (I/R) injury.

methodsRenal tissues and blood were collected from experimental renal I/R injury models. Kidney functions, structural injuries, and cellular death were assessed. Markers of endoplasmic reticulum (ER) stress were evaluated by RT-qPCR and Western blotting. The effect of shikonin on Sirt1/Nrf2/HO-1 signaling was detected by Western blotting and immunofluorescence staining. HK-2 cells that underwent hypoxia/reoxygenation (H/R) process were used to perform CCK-8 and flow cytometry.

resultsFor in vivo analysis, renal dysfunctions and tissue structural damage induced by I/R were relieved by shikonin. Additionally, shikonin alleviated ER stress-induced apoptosis in I/R mice. For in vitro analysis, shikonin inhibited ER stress-stimulated apoptosis of H/R cells. Mechanistically, shikonin activated Sirt1/Nrf2/HO-1 signaling post-I/R, and inhibition of Sirt1 limited shikonin-mediated protection against ER stress-stimulated apoptosis in both animal and cellular models.

conclusionBy activating Sirt1/Nrf2/HO-1 signaling, shikonin inhibits apoptosis caused by ER stress and relieves renal I/R injury.

Indexed as

ApoptosisEndoplasmic Reticulum StressNaphthoquinonesReperfusion InjuryAnimalsHeme Oxygenase-1HumansKidneyMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2Signal TransductionSirtuin 1Heme Oxygenase-1NaphthoquinonesNF-E2-Related Factor 2shikoninSirt1 protein, mouseSirtuin 1ApoptosisEndoplasmic reticulum stressNrf2/HO-1Renal ischemia/reperfusion injuryShikoninSirt1

Identifiers

PMID39662059
PMCPMC11844683

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.