Ginsenoside Rb3 attenuates skin flap ischemia-reperfusion damage by inhibiting STING-IRF3 signaling

Li, Yuanbin; Liu, Haifen; Zeng, Zhiwei; Lin, Hui; Chen, Xin; Yuan, Xianglian; Qiu, Jizhe; Fu, Fengchun; Chen, Zhuang; Kuang, Jianjun

doi:10.1007/s10735-022-10081-x

Cited by 6 publications

(4 citation statements)

References 25 publications

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“…used ginsenoside Rb3 to suppress adhesion molecule expression in endothelial cells (ECs) and improve microcirculation of murine transplanted skin flaps. They confirmed that the protective effect of IRI resulted from the inhibition of STING–IRF3 signaling ( 44 ). Besides, Yang et al.…”

Section: Cgas–sting Pathway and Transplantation Outcomesmentioning

confidence: 64%

cGAS–STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes

Chen,

Liu,

Lin

et al. 2023

Front. Immunol.

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Transplantation is an important life-saving therapeutic choice for patients with organ or tissue failure once all other treatment options are exhausted. However, most allografts become damaged over an extended period, and post-transplantation survival is limited. Ischemia reperfusion injury (IRI) tends to be associated with a poor prognosis; resultant severe primary graft dysfunction is the main cause of transplant failure. Targeting the cGAS–STING pathway has recently been shown to be an effective approach for improving transplantation outcomes, when activated or inhibited cGAS–STING pathway, IRI can be alleviated by regulating inflammatory response and programmed cell death. Thus, continuing efforts to develop selective agonists and antagonists may bring great hopes to post-transplant patient. In this mini-review, we reviewed the role of the cGAS–STING pathway in transplantation, and summarized the crosstalk between this pathway and inflammatory response and programmed cell death during IRI, aiming to provide novel insights into the development of therapies to improve patient outcome after transplantation.

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Section: Cgas–sting Pathway and Transplantation Outcomesmentioning

confidence: 64%

cGAS–STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes

Chen,

Liu,

Lin

et al. 2023

Front. Immunol.

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“…Thereafter, one cross-regional flap of 9 cm × 2 cm was cut, where the iliolumbar artery (area I) was used as the pedicle, while the valve area spanned from the posterior intercostal artery to the thoracic dorsal artery (both of which were ligated) (area II). Following complete skin flap lifting, hemostasis was achieved, and sutures were used to close the skin 0.5 cm from the skin edge at 1 cm intervals [ 35 ]. The vascular bundle of the rats in I/R group was clamped with a microvascular clamp for 3 h to induce skin flap ischemia, while the rats in the sham group were not clamped [ 36 ].…”

Section: Methodsmentioning

confidence: 99%

“…The flap necrotic area was measured with the use of the Image-Pro Plus V6.0 image analysis system, and the following formula was used to calculate the flap survival rate: flap survival rate = flap survival area (cm 2 )/total flap area (cm 2 ) × 100 %. The necrosis of skin flaps was determined based on black color, tissue retraction, hard texture, low elasticity, and nonbleeding when the flap was cut [ 35 ]. After taking photographs, the middle of the ﬂap tissue (1 × 1 cm 2 in size) from the proximal area of the vascular axis of the skin ﬂap was collected, and diced into small blocks for further study.…”

Section: Methodsmentioning

confidence: 99%

Protective effects of the bioactive peptide from maggots against skin flap ischemia‒reperfusion injury in rats

Chen,

Zhang,

Yan

et al. 2024

Heliyon

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“…18 After skin flap I/R injury, the STING-IRF3 signaling pathway induces vascular endothelial cell damage. 19 However, whether the STING-IRF3 pathway participates in the inhibition of ER stress-induced autophagy after I/R has not been studied. In this study, we explored the effect of ER stress on the STING-IRF3 signaling pathway and cardiac autophagy after reperfusion in vivo and in vitro and further discussed the potential mechanism of this process.…”

Section: Introductionmentioning

confidence: 99%

The STING-IRF3 Signaling Pathway, Mediated by Endoplasmic Reticulum Stress, Contributes to Impaired Myocardial Autophagic Flux After Ischemia/Reperfusion

Li,

Lin,

Tang

et al. 2023

Journal of Cardiovascular Pharmacology

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This study aimed to determine whether endoplasmic reticulum (ER) stress is involved in impaired autophagy after myocardial ischemia/reperfusion I/R (M-I/R) and elucidate the underlying mechanisms. The expression levels of STING and IRF3 phosphorylation increased in M-I/R heart tissues and hypoxia/reoxygenation (H/R)-treated H9c2 cells. The ER stress inhibitor 4-phenylbutyric acid (4-PBA)significantly suppressed the stimulation of STING-IRF3 transcription and alleviatedcardiac dysfunction caused by M-I/R injury. In addition, 4-PBA reversed I/R-induced autophagic flux dysfunction, as demonstrated by a decrease in p62 and LC3 levels. Similarly, the protective effect of STING deficiency on myocardial cell damage was achieved by the recovery of autophagic flux. Conversely, the protective effect of 4-PBA against H/R injury in cardiomyocytes was offset by STING overexpression, wherein the activated STING-IRF3 pathway promoted the expression of Rubicon (a negatively-regulated autophagic molecule) by binding to the Rubicon promoter. Rubicon ablation effectively counteracts the adverse effects of STING overexpression in cardiomyocytes. The data showed that STING-IRF3 signaling of ER stress receptors is particularly important in the progression of physiological M-I/R caused by the inhibition of autophagic flow in vivo and in vitro.

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Ginsenoside Rb3 attenuates skin flap ischemia-reperfusion damage by inhibiting STING-IRF3 signaling

Cited by 6 publications

References 25 publications

cGAS–STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes

cGAS–STING pathway in ischemia-reperfusion injury: a potential target to improve transplantation outcomes

Protective effects of the bioactive peptide from maggots against skin flap ischemia‒reperfusion injury in rats

The STING-IRF3 Signaling Pathway, Mediated by Endoplasmic Reticulum Stress, Contributes to Impaired Myocardial Autophagic Flux After Ischemia/Reperfusion

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