Gambogic acid inhibits spinal cord injury and inflammation through suppressing the p38 and Akt signaling pathways

Fu, Qiao; Li, Chaojian; Yu, Lehua

doi:10.3892/mmr.2017.8026

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…SCI is a serious disease that eventually results in loss of movement and sensation below the lesion (15,22). After SCI occurs, the inflammatory response has an important role in the pathogenesis of the injured spinal cord (23,24). The present study demonstrated that BMSC transplantation suppressed the expression of TLR4 and NF-κB in the injured spinal cord after trauma.…”

Section: Discussionsupporting

confidence: 53%

Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway

Bai

Zhou

2018

Exp Ther Med

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Spinal cord injury (SCI) results in inflammation, and TLR4, which is an inflammatory factor, has an important role in the pathological injury that occurs following SCI. Recently, bone marrow stromal cells (BMSCs) have been demonstrated to be a novel treatment in SCI. However, the underlying mechanism of neuroprotection in SCI by BMSCs remains unclear. The present study was designed to investigate the therapeutic mechanism of BMSCs in SCI by analysis of Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) expression. The present results demonstrated that BMSC transplantation promoted functional recovery and tissue repair in SCI rats. Interestingly, it also reduced the expression of TLR4 and NF-κB after SCI. Furthermore, it was demonstrated that BMSCs downregulated the expression of apoptosis factor caspase-12 in the SCI rat model. The present results demonstrated that BMSCs may have incorporated into the spinal cord to improve locomotor function after SCI, partly via the TLR4/NF-κB signaling pathway. To the best of our knowledge, this is the first study to determine that BMSCs prevented secondary injury and enhanced functional recovery in SCI via inhibition of TLR4/NF-κB-mediated inflammation.

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Section: Discussionsupporting

confidence: 53%

Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway

Bai

Zhou

2018

Exp Ther Med

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“…Although MSCs were reported to potentially lower angiogenesis [ 105 ], the surprisingly high expression of the VEGFA in LMSC−P3 ( Figure 7 ) is questionable due to the fact that elevated vasculature over the surface of cornea can potentially affect the visual acuity [ 106 , 107 ]. However, the elevated levels of VEGFA (growth factor-induced or transfected or topically applied) in the wound bed were reported to enhance the wound repair of dermis/skin [ 108 , 109 , 110 , 111 ], but not many studies on corneal surface were reported. These elevated levels of VEGFA also contradict decreased expression of MMP9, the factors reported to feedback regulation mechanism [ 112 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Profiling of Human Limbus-Derived Stromal/Mesenchymal Stem Cells—Novel Mechanistic Insights into the Pathways Involved in Corneal Wound Healing

Tavakkoli

Damala

Koduri

et al. 2022

IJMS

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Limbus-derived stromal/mesenchymal stem cells (LMSCs) are vital for corneal homeostasis and wound healing. However, despite multiple pre-clinical and clinical studies reporting the potency of LMSCs in avoiding inflammation and scarring during corneal wound healing, the molecular basis for the ability of LMSCs remains unknown. This study aimed to uncover the factors and pathways involved in LMSC-mediated corneal wound healing by employing RNA-Sequencing (RNA-Seq) in human LMSCs for the first time. We characterized the cultured LMSCs at the stages of initiation (LMSC−P0) and pure population (LMSC−P3) and subjected them to RNA-Seq to identify the differentially expressed genes (DEGs) in comparison to native limbus and cornea, and scleral tissues. Of the 28,000 genes detected, 7800 DEGs were subjected to pathway-specific enrichment Gene Ontology (GO) analysis. These DEGs were involved in Wnt, TGF-β signaling pathways, and 16 other biological processes, including apoptosis, cell motility, tissue remodeling, and stem cell maintenance, etc. Two hundred fifty-four genes were related to wound healing pathways. COL5A1 (11.81 ± 0.48) and TIMP1 (20.44 ± 0.94) genes were exclusively up-regulated in LMSC−P3. Our findings provide new insights involved in LMSC-mediated corneal wound healing.

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“…Oleanolic acid can inhibit in ammation by blocking the p38 and JNK MAPK signaling pathways to promote the recovery of the injured spinal cord (Wang et al 2020). Other studies have shown that in ammation and astrocytes proliferation/activation after SCI are related to the p38 MAPK and Akt signaling pathways (Qiao Fu et al 2018;Wang et al 2017). The most important nding of this study is that X-ray irradiation acts as an inhibitor of the p38 MAPK and Akt signaling pathways, which can inhibit in ammation and the formation of the glial scar.…”

Section: Discussionmentioning

confidence: 99%

X-ray Irradiation Inhibits Inflammation and Glial Scar Formation through p38 MAPK and Akt Signaling Pathways and Promotes the Recovery of Nerve Function after Spinal Cord Injury in Rats

Wang¹,

Niu²,

Lin³

et al. 2021

Preprint

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Spinal cord injury (SCI) is a common clinical disease that can cause permanent disruption of nerve function. Inflammation and glial scar formation influence the recovery of injured spinal cord. X-ray irradiation can reduce inflammation, inhibit cell proliferation and increase cell apoptosis. However, the regulatory effects of X-ray irradiation on inflammation and glial scars and the underlying molecular mechanisms are still unclear. This study aimed to explore the effect of X-ray irradiation on the progression of SCI. Behavioural experiments show that X-ray irradiation can effectively improve the motor function of SCI rats. X-ray irradiation inhibits the inflammatory response by reducing the expression of inflammatory factors (including TNF-α and IL-1β) at the lesion site, thereby enhancing the survival of neuronal cells .X-ray irradiation effectively inhibited the formation of the glial scar (the expression of the related proteins GFAP and vimentin) in the lesion. In addition, the p38 MAPK and Akt signaling pathways were activated after SCI in rats, but these signaling pathways were significantly blocked after X-ray irradiation. Furthermore, the 10 Gy dose had the most significant effects among the 2 Gy, 10 Gy and 20 Gy doses. In summary, X-ray irradiation can inhibit inflammation and glial scar formation by blocking the p38 MAPK and Akt signaling pathways, thereby improving the recovery of nerve function in rats with SCI. Therefore, X-ray irradiation provides a new strategy for the treatment of SCI.

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Gambogic acid inhibits spinal cord injury and inflammation through suppressing the p38 and Akt signaling pathways

Cited by 6 publications

References 28 publications

Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway

Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway

Transcriptomic Profiling of Human Limbus-Derived Stromal/Mesenchymal Stem Cells—Novel Mechanistic Insights into the Pathways Involved in Corneal Wound Healing

X-ray Irradiation Inhibits Inflammation and Glial Scar Formation through p38 MAPK and Akt Signaling Pathways and Promotes the Recovery of Nerve Function after Spinal Cord Injury in Rats

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