Ginsenoside Rg1 promoted the wound healing in diabetic foot ulcers via miR-489–3p/Sirt1 axis

Huang, Liang; Cai, Hongbin; Zhang, Mingsheng; Liao, Ruo-Yi; Huang, Xing; Hu, Feng-Dan

doi:10.1016/j.jphs.2021.07.008

Cited by 26 publications

(12 citation statements)

References 46 publications

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“…Interestingly, we also found that GS-Rg1 significantly decreased expression of miR-126 (Figure 3). Previous studies also demonstrated that GS-Rg1 had an influence on miRNAs [33,34].…”

Section: Discussionmentioning

confidence: 77%

Ginsenoside Rg1 Suppresses Non-Small-Cell Lung Cancer via MicroRNA-126-PI3K-AKT-mTOR Pathway

Chen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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As one of the most common cause of cancer death in the world, lung cancer causes approximately 1.6 million deaths annually. Among them, NSCLC accounts for approximately 85% of patients in whole lung cancer patients. Ginsenoside Rg1 has been confirmed to play an important role in various diseases including cancer. As one of miRNAs, miR-126 closely involves in pathogenesis of the several types of cancers including colorectal, prostate, bladder and gastric cancer, and so on. Thus, the present study aims to investigate effects of the Ginsenoside Rg1 on NSCLC and underlying mechanism. In the study, two lung cancer cell lines including A549 and H1650 were used. It was found that expression of miR-126 was decreased in PBMC of NSCLC patients compared to healthy control. Expression of miR-126 was decreased in cancer tissue compared to paracancerous tissues in NSCLC patients. Importantly, it was found Ginsenoside Rg1 could inhibit growth of lung cancer cells. miR-126 KD remarkably increased the expression of apoptosis genes including caspase 3 and caspase 9 and decreased cell viability in lung cancer cells including A549 and H1650 cells. Interesting, in silico analysis indicated that miR-126 could target PI3K signaling pathway, which was confirmed by WB assay. KD of PI3KR2 compromised promotion of miR-126 on cell apoptosis. Similarly, it was found that KD of mTOR compromised promotion of miR-126 on cell apoptosis. Inhibition of Ginsenoside Rg1 on growth of lung cancer cells was through miR-126 and mTOR. Thus, the present study confirmed that Ginsenoside Rg1 remarkably inhibit lung cancer, which is through microRNA-126-PI3K-AKT-mTOR pathway.

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“…Interestingly, we also found that GS-Rg1 significantly decreased expression of miR-126 (Figure 3). Previous studies also demonstrated that GS-Rg1 had an influence on miRNAs [33,34].…”

Section: Discussionmentioning

confidence: 77%

Ginsenoside Rg1 Suppresses Non-Small-Cell Lung Cancer via MicroRNA-126-PI3K-AKT-mTOR Pathway

Chen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…All of these have been shown as involved in regulation of immune responses, angiogenesis, or wound healing. The three downregulated miRNAs were; miR-137 (angiogenesis and muscle regeneration [ 63 , 64 ]), miR-218 (regulation of cytokines, chemokines and interferon production, hypoxia-responding [ 65 , 66 , 67 ]) and mir-489 (apoptosis and wound healing [ 68 , 69 , 70 ]). Similarly, the three upregulated miRNAs have been reported as involved in regulation of disease relevant responses; miR-730 is an Actinopterygii-specific miRNA responding to bacterial infection in Zebrafish [ 52 , 71 , 72 ]), miR-144 regulates apoptosis/cell cycle control [ 73 ] while the teleost specific miR-2188 responds to viral infection and is likely involved in macrophage differentiation [ 25 , 74 ].…”

Section: Discussionmentioning

confidence: 99%

Expression Analysis of Moritella viscosa-Challenged Atlantic Salmon Identifies Disease-Responding Genes, MicroRNAs and Their Predicted Target Genes and Pathways

Ramberg

Krasnov

Colquhoun

et al. 2022

IJMS

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Moritella viscosa is a bacterial pathogen causing winter-ulcer disease in Atlantic salmon. The lesions on affected fish lead to increased mortality, decreased fish welfare, and inferior meat quality in farmed salmon. MicroRNAs (miRNAs) are small non-coding RNAs involved in post-transcriptional regulation by guiding the miRNA-induced silencing complex to specific mRNA transcripts (target genes). The goal of this study was to identify miRNAs responding to Moritella viscosa in salmon by investigating miRNA expression in the head-kidney and the muscle/skin from lesion sites caused by the pathogen. Protein coding gene expression was investigated by microarray analysis in the same materials. Seventeen differentially expressed guide-miRNAs (gDE-miRNAs) were identified in the head-kidney, and thirty-nine in lesion sites, while the microarray analysis reproduced the differential expression signature of several thousand genes known as infection-responsive. In silico target prediction and enrichment analysis suggested that the gDE-miRNAs were predicted to target genes involved in immune responses, hemostasis, angiogenesis, stress responses, metabolism, cell growth, and apoptosis. The majority of the conserved gDE-miRNAs (e.g., miR-125, miR-132, miR-146, miR-152, miR-155, miR-223 and miR-2188) are known as infection-responsive in other vertebrates. Collectively, the findings indicate that gDE-miRNAs are important post-transcriptional gene regulators of the host response to bacterial infection.

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Section: Dysregulated Micrornas In Diabetic Angiogenesismentioning

confidence: 98%

“…While there is limited previous literature describing the relationship between miR-489-3p and angiogenesis, its downregulation was associated with improved angiogenesis and wound healing in a rat model of DFU ( 174 ). Huang et al ( 174 ) studied Rg1 as a treatment for DFU, and similarly to its effects on miR-23 as described above, treatment with Rg1 was associated with miR-489-3p downregulation and upregulation of its direct target Sirt1. Therefore, the proposed mechanism by which miR-489-3p is therefore proposed to affect angiogenesis is through inhibition of Sirt1 and subsequent downregulation of PI3K/AKT/eNOS signaling, which is reversed by treatment with Rg1 ( 174 ).…”

Section: Dysregulated Micrornas In Diabetic Angiogenesismentioning

confidence: 98%

Effects of microRNAs on angiogenesis in diabetic wounds

et al. 2023

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Diabetes mellitus is a morbid condition affecting a growing number of the world population, and approximately one third of diabetic patients are afflicted with diabetic foot ulcers (DFU), which are chronic non-healing wounds that frequently progress to require amputation. The treatments currently used for DFU focus on reducing pressure on the wound, staving off infection, and maintaining a moist environment, but the impaired wound healing that occurs in diabetes is a constant obstacle that must be faced. Aberrant angiogenesis is a major contributor to poor wound healing in diabetes and surgical intervention is often necessary to establish peripheral blood flow necessary for healing wounds. Over recent years, microRNAs (miRNAs) have been implicated in the dysregulation of angiogenesis in multiple pathologies including diabetes. This review explores the pathways of angiogenesis that become dysregulated in diabetes, focusing on miRNAs that have been identified and the mechanisms by which they affect angiogenesis.

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Ginsenoside Rg1 promoted the wound healing in diabetic foot ulcers via miR-489–3p/Sirt1 axis

Cited by 26 publications

References 46 publications

Ginsenoside Rg1 Suppresses Non-Small-Cell Lung Cancer via MicroRNA-126-PI3K-AKT-mTOR Pathway

Ginsenoside Rg1 Suppresses Non-Small-Cell Lung Cancer via MicroRNA-126-PI3K-AKT-mTOR Pathway

Expression Analysis of Moritella viscosa-Challenged Atlantic Salmon Identifies Disease-Responding Genes, MicroRNAs and Their Predicted Target Genes and Pathways

Effects of microRNAs on angiogenesis in diabetic wounds

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