Liver injury in septic mice were suppressed by a camptothecin-bile acid conjugate via inhibiting NF-κB signaling pathway

Xiao, Linxia; Liang, Qi; Zhang, Xiangli; Zhou, Yuqin; Yue, Hanlin; Yu, Endian; Li, Qingyong

doi:10.1016/j.lfs.2020.118130

Cited by 5 publications

(7 citation statements)

References 47 publications

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“…66 CPT-bile acid conjugate alleviated sepsis-induced liver injury by suppressing the NF-κB signaling pathway. 67 CPT inhibits the expressions of proinflammatory cytokines and improves ulcerative colitis induced by dextran sodium sulfate in terms of colon length and the disease activity index in rats. 68 In our experiment, we found that SCI induced downregulation of protein and mRNA expressions of Top-1, which may be result from SCI that rapidly leads to a large number of nerve cell death and immune microenvironment in early stage that inhibits cell proliferation and DNA replication in mice.…”

Section: Discussionmentioning

confidence: 96%

“…Moreover, CPT regulates microglia polarization and provides neuroprotective effects through activating AKT/Nrf2/HO‐1 and inhibiting NF‐κB pathways in vivo and in vitro 66 . CPT–bile acid conjugate alleviated sepsis‐induced liver injury by suppressing the NF‐κB signaling pathway 67 . CPT inhibits the expressions of proinflammatory cytokines and improves ulcerative colitis induced by dextran sodium sulfate in terms of colon length and the disease activity index in rats 68 .…”

Section: Discussionmentioning

confidence: 99%

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Topoisomerase 1 inhibition modulates pyroptosis to improve recovery after spinal cord injury

Jiang

Ding

et al. 2022

The FASEB Journal

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Excessive neuroinflammation and neuronal loss contribute to mechanisms of spinal cord injury (SCI). Accumulating evidence has suggested that topoisomerase 1 (Top1) inhibition can suppress exacerbated immune responses and protect against lethal inflammation. Pyroptosis is a recently identified pro‐inflammatory programmed mode of cell death. However, the effects and underlying mechanisms of Top1 inhibition in SCI remains unclear. Locomotor functional recovery in mice was evaluated through Basso Mouse Scale (BMS). Neuronal loss was evaluated by immunochemistry staining of NeuN. Pyroptosis was determined by immunofluorescence staining, western blot, flow cytometry, cell viability, and cytotoxicity assays. In the present study, we estimated the effects of chemical inhibition of Top1 in an SCI model. Administration of Top1 inhibitor camptothecin (CPT) to mice significantly improved locomotor functional recovery after SCI. Moreover, CPT reduced Top1 level, inhibited nucleotide‐binding oligomerization domain‐like receptor 3 (NLRP3) inflammasome activation and pyroptosis, attenuated proinflammatory cytokines levels, diminished the number of neutrophil and neuronal loss in mice. Furthermore, CPT in oxygen‐glucose deprivation neurons down‐regulated Top1 level, attenuated NLRP3 inflammasome activation, and suppressed pyroptosis and inflammatory response. Together, our findings indicate that inhibition of Top1 with CPT can inhibit pyroptosis, control neuroinflammation, and improve functional recovery after SCI.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Topoisomerase 1 inhibition modulates pyroptosis to improve recovery after spinal cord injury

Jiang

Ding

et al. 2022

The FASEB Journal

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“…Emerging studies have demonstrated that NF-κB signaling pathway play a critical role in the progress of sepsis-induced multi-organ dysfunction [10]. Upregulation of NF-κB related signaling is linked with liver injury induced by sepsis [11].…”

Section: Introductionmentioning

confidence: 99%

“…NF-κB signaling can be activated in response to pathogens and proinflammatory cytokines [12]. NF-κB binds to its inhibitor IκB and forms a complex in cytosol in a resting state [10]. When the IκB kinase is activated in response to inflammatory stimuli, this stimulates the phosphorylation of IκB, and then it moves to the nucleus, thus allowing its regulatory role in various gene expressions [10].…”

Section: Introductionmentioning

confidence: 99%

“…NF-κB binds to its inhibitor IκB and forms a complex in cytosol in a resting state [10]. When the IκB kinase is activated in response to inflammatory stimuli, this stimulates the phosphorylation of IκB, and then it moves to the nucleus, thus allowing its regulatory role in various gene expressions [10]. The inflammatory cytokines including TNFα, IL-1β and IL-6 stimulates the activity of NF-κB, which also regulates the expression levels of inflammatory cytokines, and forming an amplified feedback loop [13].…”

Section: Introductionmentioning

confidence: 99%

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Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling pathway

Zhang¹,

Qun²

2022

Trop. J. Pharm Res

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Purpose: To investigate the protective role of aromadendrin in septic liver injury in mice, and its mechanism of action.Methods: Eight-week-old male C57BL/6 mice (n=6 for each group) were administrated with aromadendrin (SMB00175, Sigma-Aldrich) at 0 mg/kg, 30 mg/kg and 60 mg/kg via a hypodermic intraperitoneal injection. HE staining was used to examine liver histopathological structural changes in the liver while DAPI/Tunel staining was employed to evaluate liver cell apoptosis. The mRNA expression levels of TNF-α, IL-1β and IL-6 were determined by quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR). Moreover, enzyme-linked immunosorbent assay (ELISA)was applied to assess the levels of TNF-α, IL-1β and IL-6, as well as the activities of catalase (CAT), antioxidant glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA). Moreover, the protein levels of p65, p-p65, p-IκBα and IκBα were analyzed by Western blotting.Results: The liver tissues exhibited severe structural damages, with edema, necrosis, and neutrophil infiltration, but recovered as a result of aromadendrin treatment (p < 0.05). The increased serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in CLP mice were reduced by aromadendrin, which also attenuated liver injury and cell apoptosis. Aromadendrin inhibited the levels ofu TNF-α, IL-1β and IL-6 in the mice, while the activities of GSH and antioxidant enzymes (SOD and CAT) were also significantly lowered in the mice, but attenuated by aromadendrin (p < 0.05). Aromadendrin also prevented the increased level of MDA, and suppressed the phosphorylation of p65 and IκBα (p < 0.05).Conclusion: Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling in vivo, thus suggesting a potential strategy for the therapy of sepsis-induced liver injury.

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Maresin1 prevents sepsis-induced acute liver injury by suppressing NF-κB/Stat3/MAPK pathways, mitigating inflammation

Sun,

Wang,

Wang

et al. 2023

Heliyon

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Liver injury in septic mice were suppressed by a camptothecin-bile acid conjugate via inhibiting NF-κB signaling pathway

Cited by 5 publications

References 47 publications

Topoisomerase 1 inhibition modulates pyroptosis to improve recovery after spinal cord injury

Topoisomerase 1 inhibition modulates pyroptosis to improve recovery after spinal cord injury

Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling pathway

Maresin1 prevents sepsis-induced acute liver injury by suppressing NF-κB/Stat3/MAPK pathways, mitigating inflammation

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