PXD011414

PXD011414 is an original dataset announced via ProteomeXchange.

Title	Ginsenoside Rb1 blocked mitochondrial reverse electron transfer-derived ROS production and protected cardiomyocytes from ischemia/reperfusion injury through reversibly inhibiting mitochondrial complex I
Description	The management of cardiac ischemic injury has been challenged by ischemia and reperfusion (I/R) injury. Reactive oxygen species (ROS) generated from mitochondrial reverse electron transport (RET) during the early phase of reperfusion is considered to be the initiating cause for ischemia and reperfusion injury. Ginsenosides and their prescriptions are widely used in the clinic for treatment of myocardial ischemia, however, the action to combat ROS remains to be elucidated. In this work, we used TMT-based proteomic approach to detect differential proteins from mitochondrial fractions of mice hearts with ischemia-reperfusion. Results indicated that the mass error of identified peptides was within 10 ppm, and most of the identified peptides were composed of 7-23 amino acids. Using these qualified data, 17,262 peptides, with a confidence level ≥ 95%, were mapped to 3,054 protein groups. PCA analysis showed that the model group was clearly separated from the blank group, while the protein pattern was partly reversed with Rb1 treatment. With a criteria of p-value < 0.05, 591 significantly changed proteins including 186 increased and 405 decreased ones in the model group were identified compared with the blank group. These proteins were divided into 4 clusters. Proteins in Cluster I highly increased in the model group, but clearly decreased in the Rb1 group. Proteins in Cluster IV clearly decreased in the model group, but markedly increased in the Rb1 group. Proteins in Cluster III and in Cluster IV were not significantly or slightly regulated by the Rb1 treatment. GO analysis of Cluster I and II indicated that the molecular function of these proteins were closely related to oxidoreductase activity and NADH dehydrogenase activity. Our result showed that Rb1 administration before ischemia markedly decreased infarct size (48 h post-I/R), and preserved cardiac function (2 weeks post-I/R), and subsequently limited tissue fibrosis (28 days post-I/R). These results indicated that targeted inhibition of mitochondrial complex I in the early stage of reperfusion by Rb1 is a potential therapeutic strategy for alleviating IR injury. This work not only indicates a potent molecular target for the precision therapy of myocardial ischemia by Rb1, but also provides novel knowledge for the management of cardiac ischemic injury by traditional Chinese medicine.
HostingRepository	PRIDE
AnnounceDate	2021-09-08
AnnouncementXML	Submission_2021-09-08_07:34:56.778.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Yin Xiaojian
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	No PTMs are included in the dataset
Instrument	Q Exactive Plus

Revision	Datetime	Status	ChangeLog Entry
0	2018-10-19 00:53:12	ID requested
⏵ 1	2021-09-08 07:34:57	announced

Jiang L, Yin X, Chen YH, Chen Y, Jiang W, Zheng H, Huang FQ, Liu B, Zhou W, Qi LW, Li J, Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I. Theranostics, 11(4):1703-1720(2021) [pubmed]

curator keyword: Biological

submitter keyword: Rb1,ROS,LC-MS/MS,proteome,cardiomyocytes

Lian-Wen Qi
contact affiliation	State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu, China
contact email	Qilw@cpu.edu.cn
lab head
Yin Xiaojian
contact affiliation	China Pharmaceutical University
contact email	ajian.517@163.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD011414
     1. Label: PRIDE project
     2. Name: Ginsenoside Rb1 blocked mitochondrial reverse electron transfer-derived ROS production and protected cardiomyocytes from ischemia/reperfusion injury through reversibly inhibiting mitochondrial complex I