Puerarin reduces ischemia/reperfusion-induced myocardial injury in diabetic rats via upregulation of vascular endothelial growth factor A/angiotensin-1 and suppression of apoptosis

Guo, Bao-Qiang; Xu, Jiahua; Xiao, Ming; Ding, Min; Duan, Lijun

doi:10.3892/mmr.2018.8754

Cited by 25 publications

(33 citation statements)

References 29 publications

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“…Previous reports have pointed out that VEGFA can participate in suppression of cell apoptosis [45, 46]. Thus, we further carried out apoptosis analysis to find out whether VEGFA overexpression induced by PNS could inhibit cell apoptosis in HUVECs.…”

Section: Resultsmentioning

confidence: 93%

Network Pharmacology-Based Prediction and Verification of the Targets and Mechanism for Panax Notoginseng Saponins against Coronary Heart Disease

Dong

Duan

Chen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Coronary heart disease (CHD) is the worldwide leading cause for cardiovascular death. Panax notoginseng saponin (PNS), which is the main bioactive compound of panax notoginseng, has been generally accepted to exert a remarkable effect on CHD for a long time. However, to reveal the underlying treatment target and corresponding mechanism of PNS against CHD is still a substantial challenge. In this work, the targets and mechanism of PNS against CHD were successfully achieved by pharmacology-based prediction and experimental verification. 36 common targets were screened out through integrating the gene expression profile of CHD and the chemical-protein data of PNS. Then, two key nodes were further selected for verification by experiment after analyzing GO function, KEGG pathway, coexpression, and topology analysis. Results showed that PNS has protected the human umbilical vein endothelial cells from H2O2-induced oxidative stress by inhibiting early cell apoptosis via upregulating VEGFA mRNA expression. Therefore, our research has successfully pointed out one treatment target and apoptotic inhibition caused by PNS with method of integrating bioinformatics prediction and experimental verification, which has partially explained the pharmacological mechanism of PNS against CHD.

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Section: Resultsmentioning

confidence: 93%

Network Pharmacology-Based Prediction and Verification of the Targets and Mechanism for Panax Notoginseng Saponins against Coronary Heart Disease

Dong

Duan

Chen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…OA is a common joint disease with persistent, low-degree inflammation in the synovium (3). Puerarin has been reported to exhibit anti-inflammatory effects in various mouse models of inflammatory disease, including ischemia/reperfusion, atopic dermatitis, mastitis and collagen antibody-induced arthritis (11,16,28,29). Puerarin treatment inhibits chronic inflammation induced by lipopolysaccharide or pro-inflammatory mediators, such as IL-1β, in various types of cells (9,19,30).…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, the protective roles of puerarin have been reported in a number of cell lineages, including endothelial progenitor cells, cardiac muscle cells and neuronal cells (9,10). Puerarin has been hypothesized to act in an arginase 2-dependent manner, a mitochondrial enzyme, via modulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-associated oxidative stress (6,(11)(12)(13). In addition, puerarin alters the production of innate immune cells by regulating the differentiation of progenitor cells via estrogen receptors (14).…”

Section: Introductionmentioning

confidence: 99%

Puerarin alters the function of monocytes/macrophages and exhibits chondroprotection in mice

et al. 2019

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Recent studies have suggested that puerarin may impede osteoclastogenesis and facilitate bone regeneration, in addition to attenuating tissue inflammation. The present study investigated the therapeutic effects of puerarin on inflammatory responses and monocyte recruitment in in vitro and in vivo osteoarthritis (OA) models. Puerarin treatment increased the proliferation of OA chondrocytes, as determined by Cell Counting Kit-8 assay. In addition, the present results suggested that puerarin suppressed the interleukin-1β-induced production of inflammatory cytokines in OA chondrocytes and monocytes/macrophages, as assessed by ELISA. In a mouse model of mono-iodoacetate-induced OA, the present histological analyses suggested that administration with puerarin attenuated the inflammatory profile of OA joints and reduced cartilage destruction. Using flow cytometry, a decreased number of myeloid-derived CC chemokine receptor 2 + /lymphocyte Ag 6C + monocytes was identified in the blood of OA mice treated with puerarin compared with control OA mice. Furthermore, quantitative real-time polymerase chain reaction analysis suggested that puerarin treatment decreased CC chemokine ligand 2 expression in arthritic tissues. Collectively, the results suggested that puerarin treatment limited the recruitment of inflammatory monocytes. In summary, the present study provided pre-clinical evidence that puerarin may serve as a potential target in the treatment of OA.

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“…However, the effects of PUR on apoptosis are different among various kinds of cells. For example, PUR could suppress apoptosis and reduce myocardial injury induced by ischemia [24], while promoting apoptosis in cancer cells [25,26]. Thus, the specific effects of PUR on the fate of NPMSCs in the development of IDD need to be further clarified.…”

Section: Introductionmentioning

confidence: 99%

Puerarin Relieved Compression-Induced Apoptosis and Mitochondrial Dysfunction in Human Nucleus Pulposus Mesenchymal Stem Cells via the PI3K/Akt Pathway

Huang

Peng

et al. 2020

Stem Cells International

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Puerarin (PUR), an 8-C-glucoside of daidzein extracted from Pueraria plants, is closely related to autophagy, reduced reactive oxygen species (ROS) production, and anti-inflammatory effects, but its effects on human nucleus pulposus mesenchymal stem cells (NPMSCs) have not yet been identified. In this study, NPMSCs were cultured in a compression apparatus to simulate the microenvironment of the intervertebral disc under controlled pressure (1.0 MPa), and we found that cell viability was decreased and apoptosis level was gradually increased as compression duration was prolonged. After PUR administration, apoptosis level evaluated by flow cytometry and caspase-3 activity was remitted, and protein levels of Bas as well as cleaved caspase-3 were decreased, while elevated Bcl-2 level was identified. Moreover, ATP production detection, ROS, and JC-1 fluorography as well as quantitative analysis suggested that PUR could attenuate intercellular ROS accumulation and mitochondrial dysfunction. Besides, the rat tail compression model was utilized, which indicated that PUR could restore impaired nucleus pulposus degeneration induced by compression. The PI3K/Akt pathway was identified to be deactivated after compression stimulation by western blot, and PUR could rescue the phosphorylation of Akt, thus reactivating the pathway. The effects of PUR, such as antiapoptosis, cell viability restoration, antioxidation, and mitochondrial maintenance, were all counteracted by application of the PI3K/Akt pathway inhibitor (LY294002). Summarily, PUR could alleviate compression-induced apoptosis and cell death of human NPMSCs in vitro as well as on the rat compression model and maintain intracellular homeostasis by stabilizing mitochondrial membrane potential and attenuating ROS accumulation through activating the PI3K/Akt pathway.

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Puerarin reduces ischemia/reperfusion-induced myocardial injury in diabetic rats via upregulation of vascular endothelial growth factor A/angiotensin-1 and suppression of apoptosis

Cited by 25 publications

References 29 publications

Network Pharmacology-Based Prediction and Verification of the Targets and Mechanism for Panax Notoginseng Saponins against Coronary Heart Disease

Network Pharmacology-Based Prediction and Verification of the Targets and Mechanism for Panax Notoginseng Saponins against Coronary Heart Disease

Puerarin alters the function of monocytes/macrophages and exhibits chondroprotection in mice

Puerarin Relieved Compression-Induced Apoptosis and Mitochondrial Dysfunction in Human Nucleus Pulposus Mesenchymal Stem Cells via the PI3K/Akt Pathway

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