Ginsenoside Rb1 attenuates microglia activation to improve spinal cord injury via microRNA‐130b‐5p/TLR4/NF‐κB axis

Wang, Dan; Zhao, Shixin; Pan, Junwei; Wang, Zhen; Liu, Yu; Xu, Xiaoxiao; Yang, Jingquan; Zhang, Xi; Wang, Yisheng; Liu, Ming

doi:10.1002/jcp.30001

Cited by 25 publications

(15 citation statements)

References 46 publications

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“…Recent studies have shown that miR‐130b‐5p has different functions in diverse types of tumours 23,24 . In addition, miR‐130b‐5p was reported to ameliorate activated microglia‐induced neuronal injury via the TLR4/NF‐κB signalling pathway 25 . A report has demonstrated that microRNA‐130b‐5p as a regulator for inhibition and treatment of NAFLD 15 .…”

Section: Discussionmentioning

confidence: 99%

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miRNA‐130b‐5p promotes hepatic stellate cell activation and the development of liver fibrosis by suppressing SIRT4 expression

Wang

et al. 2021

J Cellular Molecular Medi

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Liver fibrosis is a progressive disease accompanied by the deposition of extracellular matrix (ECM). Numerous reports have demonstrated that alterations in the expression of microRNAs (miRNAs) are related to liver disease. However, the effect of individual miRNAs on liver fibrosis has not been studied. Hepatic stellate cells (HSCs), being responsible for producing ECM, exert an important influence on liver fibrosis. Then, microarray analysis of non‐activated and activated HSCs induced by transforming growth factor β1 (TGF‐β1) showed that miR‐130b‐5p expression was strongly up‐regulated during HSC activation. Moreover, the progression of liver fibrosis had a close connection with the expression of miR‐130b‐5p in different liver fibrosis mouse models. Then, we identified that there were specific binding sites between miR‐130b‐5p and the 3′ UTR of Sirtuin 4 (SIRT4) via a luciferase reporter assay. Knockdown of miR‐130b‐5p increased SIRT4 expression and ameliorated liver fibrosis in mice transfected with antagomiR‐130b‐5p oligos. In general, our results suggested that miR‐130b‐5p promoted HSC activation by targeting SIRT4, which participates in the AMPK/TGF‐β/Smad2/3 signalling pathway. Hence, regulating miR‐130b‐5p maybe serve as a crucial therapeutic treatment for hepatic fibrosis.

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Section: Discussionmentioning

confidence: 99%

“…23,24 In addition, miR-130b-5p was reported to ameliorate activated microglia-induced neuronal injury via the TLR4/NF-κB signalling pathway. 25 A report has demonstrated that microRNA-130b-5p as a regulator for inhibition and treatment of NAFLD. 15 However, the underlying mechanism of miR-130b-5p in HSC activation is poorly understood.…”

Section: Discussionmentioning

confidence: 99%

miRNA‐130b‐5p promotes hepatic stellate cell activation and the development of liver fibrosis by suppressing SIRT4 expression

Wang

et al. 2021

J Cellular Molecular Medi

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“…GRb1 exerts significant antidepressant effects in chronic mild stress (CMS)-exposed rodents [ 21 ]. Already known that GRb1 regulates activation of microglia, protecting neurons from inflammatory, oxidative injury and promoting neurogenesis [ 22 , 23 ]. Few studies have focused on the relationship between antidepressant effects of GRb1 and microglia-mediated neuroinflammatory processes.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 induces a pro-neurogenic microglial phenotype via PPARγ activation in male mice exposed to chronic mild stress

Zhang

Tang

Xie

et al. 2021

J Neuroinflammation

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Background Anti-inflammatory approaches are emerging as a new strategy for the treatment of depressive disorders. Ginsenoside Rb1 (GRb1), a major component of Panax ginseng, can inhibit inflammatory cascade and alleviate depressive-like behaviors. Microglia can promote or inhibit adult hippocampal neurogenesis according to their functional phenotypes. Here, we examine whether GRb1 may exert antidepressant effects by promoting a pro-neurogenic phenotype of microglia and thereby increasing neurogenesis. Methods The antidepressant effects of GRb1 or the licensed antidepressant imipramine (IMI) were assessed in chronic mild stress (CMS)-exposed male mice. The depressive-like behaviors of mice were evaluated by sucrose preference test, forced swimming test (FST), and tail suspension test (TST). The microglial phenotypes were identified by pro- and anti-inflammatory cytokine expression and morphological properties, analyzed by RT-qPCR, western blotting, and immunofluorescence staining. The effect of GRb1-treated microglia on adult hippocampal neurogenesis in vivo and in vitro was detected using immunofluorescence staining. Results Behavioral assessment indicated that GRb1 or IMI treatment alleviated depressive-like behaviors in CMS-exposed mice. Immunofluorescence examination demonstrated that GRb1 induced a pro-neurogenic phenotype of microglia via activating PPARγ in vivo and in vitro, which were effectively reversed by the PPARγ inhibitor GW9662. In addition, GRb1-treated microglia increased the proliferation and differentiation of neural precursor cells. Conclusions These findings demonstrated that GRb1 alleviated depressive-like behaviors of CMS-exposed male mice mainly through PPARγ-mediated microglial activation and improvement of adult hippocampus neurogenesis.

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“…Moreover, NF-κB pathway activation plays a positive role in the SCI development [ 2 , 10 ]. For example, GRB1 relieved SCI via altering miR-130b-5p/TLR4/NF-κB pathway [ 23 ]. circ_0000962 inhibited the inflammation in the SCI cell model via activating PI3K/Akt and inactivating NF-κB by sponging miR-302b-3p [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p

Zhong

Bao

et al. 2021

Open Medicine

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Long noncoding RNAs have been demonstrated to play crucial roles in the pathogenesis of spinal cord injury (SCI). In this study, we aimed to explore the roles and underlying mechanisms of lncRNA X-inactive specific transcript (XIST) in SCI progression. SCI mice model was constructed and evaluated by the Basso–Beattie–Bresnahan method. The SCI cell model was constructed by treating BV2 cells with lipopolysaccharide (LPS). The levels of XIST and miR-219-5p were determined by the reverse transcription quantitative polymerase chain reaction. The concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Protein levels were measured via western blot assay. Cell viability and apoptosis were evaluated by cell counting kit-8 assay and flow cytometry analysis, respectively. The relationship between XIST and miR-219-5p was analyzed by online tool starBase, dual-luciferase reporter assay, and RNA immunoprecipitation assay. As a result, the XIST level was enhanced and the miR-219-5p level was declined in the SCI mice model. XIST was also upregulated in LPS-induced BV2 cells. LPS treatment restrained BV2 cell viability and accelerated apoptosis and inflammatory response. XIST knockdown effectively weakened LPS-induced BV2 cell injury. miR-219-5p was identified as a target of XIST. Moreover, inhibition of miR-219-5p restored the impacts of XIST knockdown on cell viability, apoptosis, and inflammation in LPS-treated BV2 cells. In addition, LPS-induced XIST promoted the activation of the nuclear factor-κB (NF-κB) pathway by sponging miR-219-5p. In conclusion, XIST silencing promoted microglial cell viability and repressed apoptosis and inflammation by sponging miR-219-5p, thus promoting the recovery of SCI.

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Ginsenoside Rb1 attenuates microglia activation to improve spinal cord injury via microRNA‐130b‐5p/TLR4/NF‐κB axis

Cited by 25 publications

References 46 publications

miRNA‐130b‐5p promotes hepatic stellate cell activation and the development of liver fibrosis by suppressing SIRT4 expression

miRNA‐130b‐5p promotes hepatic stellate cell activation and the development of liver fibrosis by suppressing SIRT4 expression

Ginsenoside Rb1 induces a pro-neurogenic microglial phenotype via PPARγ activation in male mice exposed to chronic mild stress

Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p

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