Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway

Qian, Jingli; Li, Guoping; Jin, Xia; Ma, Chunfang; Cai, Wanru; Jiang, Na; Zheng, Jisheng

doi:10.1042/bsr20201605

Cited by 12 publications

(13 citation statements)

References 33 publications

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“…Endogenous toxins released from intestinal bacteria can shift to the circulatory system after intestinal ischemia–reperfusion injury, resulting in systemic inflammation, including lung injury [ 25 ]. In addition to endogenous toxins, inflammatory factors, including IL-1 and IL-6, produced during ischemia enter the circulatory system [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of IFN gene stimulators (STING) improve intestinal ischemia–reperfusion-induced acute lung injury by activating AMPK signaling

Yang

Zhi

et al. 2022

Eur J Med Res

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Background Acute lung injury (ALI) caused by intestinal ischemia–reperfusion is a life-threatening disease. Interferon gene stimulator (STING) is a cytoplasmic DNA sensor that participates in the initiation of the inflammatory response. This study aims to establish whether C-176 (STING inhibitor) improves ALI under intestinal ischemia–reperfusion conditions. Methods To induce ALI, 72 male C57BL/6 mice were subjected to intestinal ischemia for 60 min and reperfusion for 3 h. Through intraperitoneal injection, C-176, a selective STING inhibitor, was injected 30 min before surgical treatment; meanwhile, compound C, an antagonist of adenosine monophosphate-activated protein kinase (AMPK), was administered 30 min after surgery. Based on immunofluorescence and Western blot assays, post-ALI assessments included lung water content (TLW), bronchoalveolar lavage fluid (BALF) protein, H&E staining, Masson staining, pulmonary pyroptosis [Gasdermin-D (GSDMD), cleaved caspase-1], and apoptosis (TUNEL, cleaved caspase-3). Results C-176 administration significantly attenuated intestinal ischemia–reperfusion-mediated ALI; this effect was reflected by exacerbated TLW and BALF protein, aggravated lung injury score, elevated degree of pulmonary fibrosis, increased TUNEL- and GSDMD-positive cells, and upregulated phospho-AMPK, cleaved caspase-1, cleaved caspase-3 and IFNβ mRNA expression. Moreover, C-176 increased phospho-AMPK under ALI conditions. Nonetheless, compound C partially reversed these beneficial effects. Conclusion C-176, a selective STING inhibitor, improves intestinal ischemia–reperfusion-mediated ALI, and its underlying mechanism may be associated with AMPK signal activation.

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Section: Discussionmentioning

confidence: 99%

Inhibitors of IFN gene stimulators (STING) improve intestinal ischemia–reperfusion-induced acute lung injury by activating AMPK signaling

Yang

Zhi

et al. 2022

Eur J Med Res

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“…SP-A regulates inflammatory cell response by binding to cell surface pattern recognition receptors. Reduced secretion or functional deficiency of pulmonary surfactant-related proteins is an important factor in lung injury ( 58 ).…”

Section: Discussionmentioning

confidence: 99%

The Immune Change of the Lung and Bowel in an Ulcerative Colitis Rat Model and the Protective Effect of Sodium Houttuyfonate Combined With Matrine

Shan

Zhu

et al. 2022

Front. Immunol.

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ObjectiveTo explore the immune change of lung injury of Ulcerative colitis (UC) by observing the changes of inherent immunity and adaptive immunity of the lung and bowel in UC rat models after the treatment of Sodium Houttuyfonate combined with Matrine. MethodUC rat models were established with the mucous membrane of colon allergize combined with TNBS-alcohol enteroclysis for 1 week and 5 weeks. 1-week experimental rats were divided into normal group and model group, 5/each group. 5-weeks experimental rats were divided into normal group, model group, Sodium Houttuyfonate (2.9mg/ml) combined with Matrine (1.47mg/ml), and positive control sulfasalazine (10mg/ml), 5/each group. All rats were administered by gavage for 5 weeks. The histopathological and fibrotic changes in the lung and bowel were observed, and the expressions of Tumor Necrosis Factor (TNF)- α, interleukin (IL)-8 in the lung, bowel, and serum were detected by radio-immunity and immunohistochemistry, and the mRNA expressions of Toll-like receptor (TLR)-4, nuclear factor kappa (NF-κB), Macrophage migration inhibitory factor (MIF), Mucosal addressing cell adhesion molecule-1 (MadCAM1) and Pulmonary surfactant protein-A (SP-A) in the lung and bowel were detected by Real time-PCR.ResultCompared with the normal group, the model rats had significant histopathological and fibrotic changes both in the lung and bowel, and all treatment groups were improved. After treatment, TLR4, IL-8, MIF, and TNF-α in the lung decreased (P<0.05); NF-KB, IL-8, and MIF in the bowel increased (P<0.05); MadCAM1 both in lung and bowel decreased (P<0.05); SP-A decreased in bowel and increased in the lung (P<0.05).ConclusionThe cause of lung injury in this model was found to be related to inherent immunity and adaptive immunity, while the cause of bowel injury in this model was found to be mainly related to adaptive immunity. Sodium Houttuyfonate combined with Matrine could improve bowel and lung injury.

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“…Endogenous toxins released from intestinal bacteria can shift to the circulatory system after intestinal ischemia-reperfusion injury, resulting in systemic in ammation, including lung injury [24]. Besides endogenous toxins, in ammatory factors including IL-1 and IL-6 produced during ischemia enter the circulatory system [25].…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of IFN Gene Stimulators (STING) Improve Intestinal Ischemia-Reperfusion Induced Acute Lung Injury by Activating AMPK Signal

Yang

Zhi

et al. 2022

Preprint

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Background: Acute lung injury (ALI) caused by intestinal ischemia-reperfusion is a life-threatening disease. Interferon gene stimulator (STING) is a cytoplasmic DNA sensor, participating in the initiation of inflammatory response. This study aims to establish whether C-176 (STING inhibitor) improves the ALI under intestinal ischemia-reperfusion conditions.Methods: To induce ALI, 72 C57BL/6 mice male were subjected to intestinal ischemia-reperfusion for 90 min. Through intraperitoneal injection, C-176, a selective STING inhibitor was injected 30 minutes before surgical treatment; meanwhile, compound C, an antagonist of adenosine monophosphate-activated protein kinase (AMPK) was administered 30 min after surgery. Based on immunofluorescence and Western blot assays, post-ALI assessments included lung water content (TLW), bronchoalveolar lavage fluid (BALF) protein, H&E staining, Masson staining, pulmonary apoptosis (TUNEL, cleaved caspase-3), and pyroptosis (Gasdermin-D [GSDMD], cleaved caspase-1).Results: C-176 administration significantly attenuated intestinal ischemia-reperfusion-mediated ALI; this was reflected by exasperated TLW and BALF protein, aggravated lung injury score, elevated degree of pulmonary fibrosis, increased TUNEL- and GSDMD-positive cells, as well as upregulated phosphor-AMPK, cleaved caspase-3, and cleaved caspase-1 expression. Moreover, C-176 increased phosphor-AMPK under ALI conditions. Nonetheless, compound C partially reversed these beneficial effects.Conclusion: C-176, a selective STING inhibitor improves intestinal ischemia-reperfusion-mediated ALI, and its underlying mechanism may be associated with AMPK signal activation.

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Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway

Cited by 12 publications

References 33 publications

Inhibitors of IFN gene stimulators (STING) improve intestinal ischemia–reperfusion-induced acute lung injury by activating AMPK signaling

Inhibitors of IFN gene stimulators (STING) improve intestinal ischemia–reperfusion-induced acute lung injury by activating AMPK signaling

The Immune Change of the Lung and Bowel in an Ulcerative Colitis Rat Model and the Protective Effect of Sodium Houttuyfonate Combined With Matrine

Inhibitors of IFN Gene Stimulators (STING) Improve Intestinal Ischemia-Reperfusion Induced Acute Lung Injury by Activating AMPK Signal

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