Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I

Jiang, Lujing; X, Yin; Chen, Yahui; Chen, Yan; Jiang, Wei; Zheng, Hao; Huang, Feng-Qing; Liu, Baolin; Zhou, Wei; Qi, Lian‐Wen; Li, Jia

doi:10.7150/thno.43895

Cited by 126 publications

(82 citation statements)

References 52 publications

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“…After blocking for 1 h at room temperature with a blocking buffer containing 5% BSA, the membranes were incubated with the primary antibody overnight at 4°C. After washing, the membranes were incubated with the HRP-conjugated secondary antibody for 2 h. The protein bands were visualized using a chemiluminescent imaging system (ChemiDoc XRS+, Bio-Rad) and quantified by ImageJ software ( Jiang et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis

et al. 2021

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Pulmonary fibrosis (PF) is one of the pathologic changes in COVID-19 patients in convalescence, and it is also a potential long-term sequela in severe COVID-19 patients. Qimai Feiluoping decoction (QM) is a traditional Chinese medicine formula recommended in the Chinese national medical program for COVID-19 convalescent patients, and PF is one of its indications. Through clinical observation, QM was found to improve the clinical symptoms and pulmonary function and reduce the degree of PF of COVID-19 convalescent patients. To further explore the pharmacological mechanisms and possible active components of QM in anti-PF effect, UHPLC/Q-TOF-MS was used to analyze the composition of the QM extract and the active components that can be absorbed into the blood, leading to the identification of 56 chemical compounds and 10 active components. Then, network pharmacology was used to predict the potential mechanisms and targets of QM; it predicted that QM exerts its anti-PF effects via the regulation of the epithelial–mesenchymal transition (EMT), extracellular matrix (ECM) degradation, and TGF-β signaling pathway. Finally, TGF-β1–induced A549 cells were used to verify and explore the pharmacological effects of QM and found that QM could inhibit the proliferation of TGF-β1–induced A549 cells, attenuate EMT, and promote ECM degradation by inhibiting the TGF-β/Smad3 pathway.

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Section: Methodsmentioning

confidence: 99%

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis

et al. 2021

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“…For the H/R model, cardiomyocyte culture medium was converted into H/R buffer (4 mM HEPES, 12 mM KCl, 117 mM NaCl, 0.49 mM MgCl 2 , 0.9 mM CaCl 2 , 20 mM sodium lactate, and 5.6 mM 2-deoxyglucose, pH 6.2) and placed in a hypoxic chamber (95% N 2 /5% CO 2 , Billups-Rothenberg) at 37°C for 30 min [ 15 ]. The chamber was closed, and a normal oxygen supply was added for an additional 4 hours, followed by reperfusion with DMEM supplemented with 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

miRNA‐146a Mimic Inhibits NOX4/P38 Signalling to Ameliorate Mouse Myocardial Ischaemia Reperfusion (I/R) Injury

Xiao

Ren

et al. 2021

Oxidative Medicine and Cellular Longevity

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Evidence suggests that miR-146a is implicated in the pathogenesis of cardiovascular diseases; however, the role of miR-146a in myocardial ischaemia reperfusion (I/R) injury is unclear. The aim of this study was to explore the functional role of miR-146a in myocardial ischaemia reperfusion injury and the underlying mechanism. C57BL/6J mice were subjected to 45 min of ischaemia and 1 week of reperfusion to establish a myocardial I/R injury model. A miR-146a mimic (0.5 mg/kg) was administered intravenously at the beginning of the ischaemia process. Neonatal rat cardiomyocytes were also subjected to hypoxia/reperfusion (H/R). Cells were treated with the miR-146a mimic or antagonist. As a result, the miR-146a mimic attenuated H/R-induced cardiomyocyte injury, as evidenced by increased cell viability and reduced lactate dehydrogenase (LDH) levels. In addition, the miR-146a mimic inhibited oxidative stress in cells suffering from H/R injury. Moreover, the miR-146a antagonist exerted adverse effects in vitro. In mice with myocardial I/R injury, the miR-146a mimic preserved cardiac function and reduced the infarction area and fibrosis. Moreover, the miR-146a mimic decreased the inflammatory response and reactive oxygen species (ROS) accumulation in mouse hearts. Mechanistically, we found that miR-146a directly regulated the transcription of NOX4, which subsequently affected P38 signalling in cardiomyocytes. When we knocked down NOX4, the effects of the miR-146a antagonist in worsening the cell condition were counteracted in in vitro experiments. Taken together, the results suggest that miR-146a protects against myocardial ischaemia reperfusion injury by inhibiting NOX4 signalling. The miR-146a mimic may become a potential therapeutic approach for patients with myocardial ischaemia reperfusion.

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“…Over the past decade, many studies have been conducted on the individual ginsenoside, focusing on the molecular-signaling pathways in MIRI [8][9][10]. There are more than dozens of ginsenosides, but the main type of ginsenosides (G) is Rb, including Rb1, Rb2, and Rg1 that account for more than 80% of total ginsenosides [11].…”

Section: Introductionmentioning

confidence: 99%

“…There are more than dozens of ginsenosides, but the main type of ginsenosides (G) is Rb, including Rb1, Rb2, and Rg1 that account for more than 80% of total ginsenosides [11]. Cumulative evidence indicates the beneficial cardioprotective effects of G-Rb when administered prior to experimental induction of MIRI [8][9][10][12][13][14][15][16][17][18][19][20][21][22][23][24]. The term preconditioning refers to endogenous mechanism stimulated by G-Rb given before MIRI via activations of kinases and other mediators that confer more resistant heart condition toward MIRI.…”

Section: Introductionmentioning

confidence: 99%

Molecular-Signaling Pathways of Ginsenosides Rb in Myocardial Ischemia-Reperfusion Injury: A Mini Review

Ramli¹,

Ali²,

Ibrahim³

2022

Int. J. Med. Sci.

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Reperfusion injury following myocardial ischemia remained a challenge for optimal treatment of myocardial infarction. Ginsenosides Rb (G-Rb), the primary components of ginsenoside, have been reported to exert cardioprotective effects via numerous mechanisms. G-Rb1 mediate cardioprotective effects via various signaling pathways, including mitochondrial apoptotic pathway, PI3K/Akt/mTOR, HIF-1α and GRF91, RhoA, p38α MAPK, and eNOS. G-Rb2 activates the SIRT-1 pathway, while G-Rb3 promotes both JNK-mediated NF-κB and PERK/Nrf2/HMOX1. Generally, ginsenosides Rb1, 2, and 3 modulates oxidative stress, inflammation, and apoptosis, contributing to the improvement of structural, functional and biochemical parameters. In conclusion, G-Rb, particularly G-Rb1, have vast potential as a supplement in attenuating reperfusion injury. Translation into a clinical trial is warranted to confirm the beneficial effects of G-Rb.

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Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I

Cited by 126 publications

References 52 publications

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis

miRNA‐146a Mimic Inhibits NOX4/P38 Signalling to Ameliorate Mouse Myocardial Ischaemia Reperfusion (I/R) Injury

Molecular-Signaling Pathways of Ginsenosides Rb in Myocardial Ischemia-Reperfusion Injury: A Mini Review

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