Notoginsenoside R1 promotes MC3T3-E1 differentiation by up-regulating
            <i>miR-23a</i>
            via MAPK and JAK1/STAT3 pathways

Wang, Chunsheng; Sun, Huanwei; Zhong, Yiming

doi:10.1080/21691401.2019.1573189

Cited by 13 publications

(11 citation statements)

References 34 publications

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“…A small fraction of studies believed that NGR1 exerted its function via regulating miRNA expression pattern [32]. For the selected examples, miR-26a [33], miR-23a [34], and miR-132 [35] are found as the targets of NGR1. Herein, we observed that miR-503 was another target of NGR1, as its expression was negative regulated by NGR1.…”

Section: Discussionmentioning

confidence: 99%

Notoginsenoside R1 alleviates high glucose-evoked damage in RSC96 cells through down-regulation of miR-503

Wang

Hao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Notoginsenoside R1 (NGR1) is a major bioactive ingredient of Radix notoginseng that has promise in treating several diabetes-related diseases, like diabetic nephropathy and diabetic cardiomyopathy. This work is designed to explore if NGR1 has potential in treating diabetic peripheral neuropathy (DPN). A cell model of DPN was made by stimulating RSC96 cells with high glucose. The effects of NGR1 preconditioning were examined by conducting CCK-8 assay, flow cytometry, ROS assay and Western blot. The downstream effector and signalling of NGR1 were then explored by qRT-PCR and Western blot. High glucose incubation led to cell viability loss, apoptosis facilitation, caspase-3 and PARP cleavage, and ROS generation of RSC96 cells. Meanwhile, expression of NGF and BDNF was declined by high glucose. Preconditioning NGR1 significantly protected RSC96 cells against high glucose-evoked damage. And NGR1 prevented high glucose-induced expression of miR-503. The beneficial functions of NGR1 towards high glucose-injured RSC96 cells were impeded by miR-503 overexpression. Further, NGR1 activated PI3K/AKT and b-catenin signalling through a miR-503-dependent way. This paper illustrated the neuroprotective and neurotrophic function of NGR1 in RSC96 cells. The beneficial function may due to its regulation on miR-503 expression and the downstream signalling such as PI3K/AKT and b-catenin.

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Section: Discussionmentioning

confidence: 99%

Notoginsenoside R1 alleviates high glucose-evoked damage in RSC96 cells through down-regulation of miR-503

Wang

Hao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…We found that OVX‐induced reduction of BMD and bone trabecula, and bone erosion and loss were further aggravated by Exos. In MC3T3‐E1 cells, Exos reduced osteogenesis and mineralization, and the expression of osteogenesis‐related factors OSX and RUNX2 (Wang et al, 2019a). These results indicate that M2Mφs and Exos may aggravate OP progression.…”

Section: Discussionmentioning

confidence: 99%

M1 macrophage‐derived exosomes aggravate bone loss in postmenopausal osteoporosis via a microRNA‐98/DUSP1/JNK axis

Cui

et al. 2021

Cell Biology International

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Macrophages (Mφs) are master regulators of the immune response and may serve as therapeutic targets in aging societies. This study aimed to determine the function of M1Mφ‐exosomes (Exos) in the development of osteoporosis (OP) and the involvement of microRNA (miR)‐98 and dual specificity phosphatase 1 (DUSP1). A murine model of OP was established using ovariectomies (OVX). Bone loss was observed in OVX‐treated mice, as manifested by reduced bone mineral density and decreased number of bone trabecula. The bone loss was further aggravated by treatment with M1Mφ‐Exos. Exos also suppressed osteogenic differentiation of MC3T3‐E1 cells. miRNA microarray analysis revealed that the miR‐98 level was notably upregulated in cells after Exo treatment, and DUSP1 was confirmed as a target of miR‐98. Meanwhile, downregulation of miR‐98 or upregulation of DUSP1 restored the osteogenic differentiation ability of MC3T3‐E1 cells. In addition, upregulation of DUSP1 reduced bone loss in murine bone tissues and suppressed JNK phosphorylation. In summary, M1Mφ‐derived exosomal miR‐98 exacerbates bone loss and OP by downregulating DUSP1 and activating the JNK signaling pathway. miR‐98 may therefore serve as a therapeutic target in OP management.

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“…Moreover, NGR1 was reported to protect cells against lipopolysaccharide‐induced injury via TLR4 signaling pathway (Qian et al, 2019). In addition, NGR1 was reported to promote cell differentiation by MAPK, JAK1, and STAT3 pathway (Wang, Sun et al, 2019). Another novel discovery of this study was that PI3K, Akt, and p65 NF‐κB proteins are the target of NGR1.…”

Section: Discussionmentioning

confidence: 99%

Effects of notoginsenoside R1 on attenuating depressive behavior induced by chronic stress in rats through induction of PI3K/AKT/NF‐κB pathway

Zhan

2021

Drug Development Research

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Chronic unpredictable mild stress (CUMS) can cause a series of depressive symptoms in depression patients. Recently, notoginsenoside R1 (NGR1) has been reported to play crucial roles in the anti‐inflammatory, antioxidant, and anti‐apoptotic. However, the role and mechanisms of NGR1 in improving symptoms of depressive behavior remain unknown. Evaluating and identifying its value and exploring the mechanisms of NGR1 on CUMS‐induced depressive behavior were the aims of this study. Here, rats were separated into five different groups and treated with or without different concentrations of the NGR1. Then, the body weight, sucrose preference rate, immobility time, crossing number, rearing number, and grooming number were determined to evaluate the effect of NGR1 on improving the depressive behavior of CUMS rats. Subsequently, the morphology of hippocampal neurons and protein expression of brain‐derived neurotrophic factor in each group were examined by hematoxylin and eosin staining and western blot to show the neuroprotective effects of NGR1. Furthermore, the mRNA and protein expression of TNF‐α, IL‐6, and IL‐1β were also detected by quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assay to verify the anti‐inflammatory effects of NGR1 on CUMS rats. In addition, the cell apoptosis‐related proteins were examined to reveal that NGR1 can inhibit cell apoptosis in CUMS rats. Moreover, it was confirmed that NGR1 attenuated the symptoms of depressive behavior by mediated PI3K/Akt/NF‐κB pathway. Together, this study shows that NGR1 improves depressive behavior induced by chronic stress in rats through activation of PI3K/AKT/NF‐κB pathway.

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Notoginsenoside R1 promotes MC3T3-E1 differentiation by up-regulating miR-23a via MAPK and JAK1/STAT3 pathways

Cited by 13 publications

References 34 publications

Notoginsenoside R1 alleviates high glucose-evoked damage in RSC96 cells through down-regulation of miR-503

Notoginsenoside R1 alleviates high glucose-evoked damage in RSC96 cells through down-regulation of miR-503

M1 macrophage‐derived exosomes aggravate bone loss in postmenopausal osteoporosis via a microRNA‐98/DUSP1/JNK axis

Effects of notoginsenoside R1 on attenuating depressive behavior induced by chronic stress in rats through induction of PI3K/AKT/NF‐κB pathway

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