Glycyrrhizin attenuates hepatic ischemia-reperfusion injury by suppressing HMGB1-dependent GSDMD-mediated kupffer cells pyroptosis

Hua, Shuyao; Ma, Mingyang; Fei, Xiaoyuan; Zhang, Yuanyue; Gong, Feili; Fang, Min

doi:10.1016/j.intimp.2019.01.002

Cited by 64 publications

(46 citation statements)

References 46 publications

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“…One study that used mouse model for investigation also mentioned that deletion of GSDMD in the kidney tissues of mice alleviated the liver injury in mice, suggesting the contribution of GSDMD to the development of liver injury [31]. Without stimulation, GSDMD with full length can be intact with the N-terminal (GSDMD-N) and Cterminal (GSDMD-C) regions that interact with each other [32]. The N-GSDMD fragments can be generated when caspase-1 is used for cleavage of inflammasomeactivated macrophages, and the subsequent pore formation of oligomerized N-GSDMD can lead to pyroptosis and the facilitation of IL-1β release [33].…”

Section: Discussionmentioning

confidence: 99%

Co-treatment with disulfiram and glycyrrhizic acid suppresses the inflammatory response of chondrocytes

Lan

2021

J Orthop Surg Res

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Background Osteoarthritis (OA) is a kind of systemic musculoskeletal disorder and a most important factor for causing disability and physical painfulness. Nevertheless, due to the fact that OA can be triggered by multiple etiological factors, this disease is hard to be cured. Therefore, it is of great necessity for us to find novel targets or drugs for OA treatment. Materials and methods The chondrocytes were treated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP) to induce pyroptosis in OA. The cell proliferation was detected by Cell Counting Kit-8 assay (CCK-8 assay). Enzyme-linked immunosorbent assay (ELISA) was used for the detection of pyroptosis-related inflammatory factors. Then, the antagonists for gasdermin D (GSDMD) (disulfiram) and high mobility group box 1 (HMGB1) (glycyrrhizic acid) were used to treat the cell model to observe the effects of disulfiram and glycyrrhizic acid on the proliferation of chondrocytes in OA. The protein levels of pyroptosis-related inflammatory factors were measured by western blot, and the levels of aldehyde dehydrogenase (ALDH) and reactive oxygen species (ROS) were measured by corresponding commercial kits. Results After chondrocytes were induced by LPS and ATP, the cell proliferation was decreased and the expressions of pyroptosis-related inflammatory factors were increased. Disulfiram and glycyrrhizic acid treatment led to enhanced cell proliferation and increased expressions of pyroptosis-related inflammatory factors, while disulfiram showed better alleviative effects on the inflammation in chondrocytes in OA. However, co-treatment with disulfiram at a high concentration and glycyrrhizic acid did not result in higher proliferation of chondrocytes and alleviated inflammation, but led to oxidative stress. Conclusion In conclusion, co-treatment with disulfiram and glycyrrhizic acid at a standard concentration suppresses the inflammatory response of chondrocytes, which may provide guidance for the use of the drugs in the treatment of OA.

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Section: Discussionmentioning

confidence: 99%

Co-treatment with disulfiram and glycyrrhizic acid suppresses the inflammatory response of chondrocytes

Lan

2021

J Orthop Surg Res

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“…This eventually results in the cell lysing to death, triggering a strong inflammation reaction (40). Liver I/R may promote the pyroptosis of KCs mediated by GSDMD and NRLP3 (41). M2-type KCs promote M1-type KC apoptosis through an IL-10-mediated arginase-dependent mechanism (42).…”

Section: Crosstalk Of Apoptosis and Polarization Of Kcs In I/rmentioning

confidence: 99%

Effect of Hepatic Macrophage Polarization and Apoptosis on Liver Ischemia and Reperfusion Injury During Liver Transplantation

Mao

et al. 2020

Front. Immunol.

111

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Ischemia-reperfusion (I/R) injury is injury caused by a limited blood supply and subsequent blood supply recovery during liver transplantation. Serious ischemia-reperfusion injury is the main cause of transplant failure. Hepatic I/R is characterized by tissue hypoxia due to a limited blood supply and reperfusion inducing oxidative stress and an immune response. Studies have confirmed that Kupffer cells (KCs), resident macrophages in the liver, play a key role in aseptic inflammation induced by I/R. In liver macrophage polarization, M1 macrophages activated by interferon-γ (IFN-γ) and lipopolysaccharide (LPS) exert a pro-inflammatory effect and release a variety of inflammatory cytokines. M2 macrophages activated by IL-4 have an anti-inflammatory response. M1-type KCs are the dominant players in I/R as they secrete various pro-inflammatory cytokines that exacerbate the injury and recruit other types of immune cells via the circulation. In contrast, M2-type KCs can ameliorate I/R through unregulated anti-inflammatory factors. A new notion has been proposed that KC apoptosis may influence I/R in yet another manner as well. Management of KCs is expected to help improve I/R. This review summarizes the effects of hepatic macrophage polarization and apoptosis on liver I/R.

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“…Firstly, large amounts of hypoxanthine accumulated converted to xanthine during anaerobic respiration after the interruption of blood supply, and the resulting ROS prompt cells to release acetylated HMGB1 (26,27). Secondly, Kupffer cells can be activated to release IL-1b, IL-6, and TNF-a, which can promote the acetylation of HMGB1 (28,29). Thirdly, during the late stage of ischemia/reperfusion (the phase of injury caused by blood reperfusion), activated neutrophils and macrophages begin to converge and accumulate towards the ischemic area and stimulate HMGB1 release through the release of inflammatory factors.…”

Section: Discussionmentioning

confidence: 99%

HMGB1, the Next Predictor of Transcatheter Arterial Chemoembolization for Liver Metastasis of Colorectal Cancer?

et al. 2020

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HMGB1 is an important mediator of inflammation during ischemia–reperfusion injury on organs. The serum expression of HMGB1 was increased significantly on the 1st day after TACE and decreased significantly which was lower on the 30th day after TACE. Tumor markers of post-DEB-TACE decreased significantly. The correlational analysis showed that patients with low HMGB1 expression had lower risks of fever and liver injury compared those with the higher expression, while the ORR is relatively worse. Patients with lower expression of HMGB1 had longer PFS, better efficacy, and higher quality of life. With the high post-expression, the low expression had lower incidence of fever and liver injury too. There was no statistical difference in the one-year survival among the different groups. The quality of life of all patients was improved significantly. The over-expression of HMGB1 in LMCRC is an adverse prognostic feature and a positive predictor of response to TACE.

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Glycyrrhizin attenuates hepatic ischemia-reperfusion injury by suppressing HMGB1-dependent GSDMD-mediated kupffer cells pyroptosis

Cited by 64 publications

References 46 publications

Co-treatment with disulfiram and glycyrrhizic acid suppresses the inflammatory response of chondrocytes

Co-treatment with disulfiram and glycyrrhizic acid suppresses the inflammatory response of chondrocytes

Effect of Hepatic Macrophage Polarization and Apoptosis on Liver Ischemia and Reperfusion Injury During Liver Transplantation

HMGB1, the Next Predictor of Transcatheter Arterial Chemoembolization for Liver Metastasis of Colorectal Cancer?

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