Corilagin attenuates intestinal ischemia/reperfusion injury in mice by inhibiting ferritinophagy-mediated ferroptosis through disrupting NCOA4-ferritin interaction

Wang, Yunxiang; Li, Bin; Liu, Guanting; Han, Qipeng; Diao, Yunpeng; Liu, Jing

doi:10.1016/j.lfs.2023.122176

Cited by 8 publications

(4 citation statements)

References 36 publications

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“…Currently, prominent traditional Chinese medicine treatments for II/R-induced systemic diseases include conventional Chinese medicine treatment and acupuncture treatment. The effectiveness of Artesunate ( 18 ), Corilagin ( 17 , 118 ), and Nervilifordin F ( 30 ), active ingredients of Artemisia annua , ellagic tannin, and Nervilia fordii , has been confirmed in preclinical studies of II/R-related diseases. The potential mechanism aligns with the aspects mentioned above.…”

Section: Treatment Approachmentioning

confidence: 94%

“…As a prominent member of the stem cell family, MSCs find wide application in various clinical diseases (116). Research has demonstrated the protective effect of bone marrow-derived mesenchymal stem cells (BMSCs) on II/R-ALI (117). The mechanism primarily involves two categories: (1) exogenous MSCs migrate to locally damaged intestinal tissues and differentiate into IEC, thereby ensuring the integrity of the intestinal barrier, reducing bacterial translocation, and mitigating distal lung injury; (2) exogenous MSCs exert anti-inflammatory, anti-oxidative, anti-apoptotic effects, promote cell proliferation, and angiogenesis…”

Section: Stem Cell Therapymentioning

confidence: 99%

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Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion

Lv,

Zhao,

et al. 2024

Front. Med.

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Intestinal ischemia/reperfusion is a prevalent pathological process that can result in intestinal dysfunction, bacterial translocation, energy metabolism disturbances, and subsequent harm to distal tissues and organs via the circulatory system. Acute lung injury frequently arises as a complication of intestinal ischemia/reperfusion, exhibiting early onset and a grim prognosis. Without appropriate preventative measures and efficacious interventions, this condition may progress to acute respiratory distress syndrome and elevate mortality rates. Nonetheless, the precise mechanisms and efficacious treatments remain elusive. This paper synthesizes recent research models and pertinent injury evaluation criteria within the realm of acute lung injury induced by intestinal ischemia/reperfusion. The objective is to investigate the roles of pathophysiological mechanisms like oxidative stress, inflammatory response, apoptosis, ferroptosis, and pyroptosis; and to assess the strengths and limitations of current therapeutic approaches for acute lung injury stemming from intestinal ischemia/reperfusion. The goal is to elucidate potential targets for enhancing recovery rates, identify suitable treatment modalities, and offer insights for translating fundamental research into clinical applications.

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Section: Treatment Approachmentioning

confidence: 94%

Section: Stem Cell Therapymentioning

confidence: 99%

Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion

Lv,

Zhao,

et al. 2024

Front. Med.

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“…Likewise, Oroxylin A, an active constituent of Scutellaria baicalensis, can regulate ferritinophagy and inhibit hepatic fibrosis via the cGAS-STING pathway [ 120 ]. In addition, some potent compounds, such as Corilagin, have anti-inflammatory and antioxidant effects [ 121 , 122 ], Wang et al found that Corilagin could inhibit NCOA4-mediated ferritinophagy, regulate iron homeostasis, inhibit ferroptosis, and attenuate intestinal ischemia/reperfusion injury (IIRI) in mice [ 123 ]. A coumarin derivative extracted from a variety of plants, Esculetin (6,7-dihydroxycoumarin), was shown to induce ferritinophagy in hepatocellular carcinoma cells through the NCOA4/LC3II/FTH1 pathway, promoting ferroptosis and exerting anticancer effects [ 124 ].…”

Section: Therapeutic Approaches To Target Ferritinophagymentioning

confidence: 99%

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

Liu,

Xie,

Wang

et al. 2024

Neurochem Res

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Cerebral ischemia–reperfusion injury (CIRI) is the second leading cause of death worldwide, posing a huge risk to human life and health. Therefore, investigating the pathogenesis underlying CIRI and developing effective treatments are essential. Ferroptosis is an iron-dependent mode of cell death, which is caused by disorders in iron metabolism and lipid peroxidation. Previous studies demonstrated that ferroptosis is also a form of autophagic cell death, and nuclear receptor coactivator 4(NCOA4) mediated ferritinophagy was found to regulate ferroptosis by interfering with iron metabolism. Ferritinophagy and ferroptosis are important pathogenic mechanisms in CIRI. This review mainly summarizes the link and regulation between ferritinophagy and ferroptosis and further discusses their mechanisms in CIRI. In addition, the potential treatment methods targeting ferritinophagy and ferroptosis for CIRI are presented, providing new ideas for the prevention and treatment of clinical CIRI in the future.

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“…Factors that induce ferroptosis can directly or indirectly affect the levels of glutathione (GSH) through various pathways, resulting in reduced antioxidant capacity, accumulation of reactive oxygen species (ROS), and ultimately leading to cell death [8]. Many studies have found that modulation of ferroptosis attenuates intestinal IRI [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Sodium butyrate inhibits ferroptosis and ameliorates intestinal ischemia-reperfusion injury by modulating the NRF2/SLC7A11/GPX4 pathway

Zhao,

Leng,

Chang

et al. 2024

Preprint

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Purpose Sodium butyrate, a short-chain fatty acid produced by the metabolism of intestinal flora, has been shown to have a protective effect against intestinal ischemia reperfusion injury (IRI), but its effect on intestinal IRI-associated ferroptosis has not yet been demonstrated. Methods In this experiment, we used a model of superior mesenteric artery occlusion in mice to examine the effects and principles of sodium butyrate on ferroptosis related to intestinal IRI. We assessed the role of sodium butyrate by constructing mice intestinal IRI models and determining the extent of intestinal tissue damage and changes in ferroptosis-related factors. Results Results show that Intestinal IRI mice showed increased tissue damage, massive infiltration of inflammatory cells, severe destruction of villus structure, and elevated MDA. In addition, intestinal IRI led to downregulation of GSH, GPX4, FTH1 and SLC7A11, regulators of ferroptosis, and a rise in Fe2+, as well as downregulation of NRF2 by intestinal IRI. Sodium butyrate had an attenuating effect on intestinal IRI, whereas mice exogenously supplemented with sodium butyrate showed less tissue damage, some restoration of villus structure and decreased MDA, up-regulation of GSH, GSH/GSSG, GPX4, FTH1, SLC7A11, and NRF2, and decreased Fe2+. Conclusion This experiment demonstrates that sodium butyrate regulates the SLC7A11/GPX4 pathway by up-regulating NRF2, thereby inhibiting ferroptosis and attenuating intestinal IRI.

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Corilagin attenuates intestinal ischemia/reperfusion injury in mice by inhibiting ferritinophagy-mediated ferroptosis through disrupting NCOA4-ferritin interaction

Cited by 8 publications

References 36 publications

Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion

Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

Sodium butyrate inhibits ferroptosis and ameliorates intestinal ischemia-reperfusion injury by modulating the NRF2/SLC7A11/GPX4 pathway

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