Ononin alleviates DSS‐induced colitis through inhibiting NLRP3 inflammasome via triggering mitophagy

Yu, Ting; Lu, Xuejia; Liang, Yan; Yang, Le; Yin, Yuehan; Chen, Hong

doi:10.1002/iid3.776

Cited by 14 publications

(5 citation statements)

References 32 publications

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“…Not only does HJXJ reduce the loss of renal units by inhibiting pyroptosis, but it can also minimize additional tissue damage caused by the inflammatory environment. Interestingly, components of HJXJ, such as Astragalus mongolicus , Rhizoma coptis chinensis , and Centella asiatica , have shown anti-inflammatory effects and are involved in regulating the inflammasome pathway [ 51 , 73 , 74 ].…”

Section: Discussionmentioning

confidence: 99%

Huajuxiaoji Formula Alleviates Phenyl Sulfate‐Induced Diabetic Kidney Disease by Inhibiting NLRP3 Inflammasome Activation and Pyroptosis

Zhang,

Bi,

Zhou

et al. 2024

Journal of Diabetes Research

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Background: One of the most common microvascular complications of diabetes is diabetic kidney disease (DKD). The Huajuxiaoji formula (HJXJ) has shown clinical efficacy for DKD; however, its regulatory mechanisms against DKD remain elusive. We investigated NLRP3 inflammasome and the mechanisms of HJXJ by which HJXJ alleviates DKD.Methods: Phenyl sulfate (PS) was used to establish DKD models. HJXJ was administered to mice through intragastric or made into a pharmaceutical serum for the cell cultures. Biological indicator levels in mouse blood and urine were analyzed, and kidney tissues were used for HE, Masson, and PAS staining. ELISA and western blotting were used to detect inflammatory cytokines and protein levels, respectively. Reactive oxygen species (ROS) production and pyroptosis were evaluated using flow cytometry. Lentiviral vector‐mediated overexpression of NLRP3 was performed to determine whether NLRP3 participates in the antipyroptotic effect of HJXJ.Results: HJXJ significantly reduced the severity of the injury and, in a dose‐dependent manner, decreased the levels of biological markers including creatinine, blood urea nitrogen, urine protein, and endotoxin, as well as inflammatory cytokines such as interleukin (IL)‐1β, IL‐18, tumor necrosis factor‐α, and IL‐6 in DKD mice. Treatment with HJXJ reversed the downregulation of podocin, nephrin, ZO‐1, and occludin and upregulated ROS, NLRP3, Caspase‐1 P20, and GSDMD‐N induced by PS. Moreover, the upregulation of NLRP3 expression increased the number of cells positive for pyroptosis. HJXJ suppressed pyroptosis and inflammasome activation by inhibiting NLRP3 expression.Conclusions: Generally, HJXJ has the potential to reduce DKD injury and exerts anti‐DKD effects by inhibiting the NLRP3‐mediated NLRP3 inflammasome activation and pyroptosis in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

Huajuxiaoji Formula Alleviates Phenyl Sulfate‐Induced Diabetic Kidney Disease by Inhibiting NLRP3 Inflammasome Activation and Pyroptosis

Zhang,

Bi,

Zhou

et al. 2024

Journal of Diabetes Research

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“…Therefore, triggering mitochondrial autophagy is a potential strategy for treating inflammatory diseases. [ 40 ] Studies have also found that flavonoids exhibit a strong inhibitory effect on liver fibrosis by inhibiting NF-κB and various downstream inflammatory factors. [ 41 ] Astragaloside IV may regulate the differentiation of activated CD4 + subset T cells (including Th 1, Th 17, and Treg) through JAK/STAT and NF-κB signaling, induce the apoptosis of activated CD4 T cells, and ultimately significantly reduce the demyelination and inflammatory infiltration in the central nervous system of mice with autoimmune encephalomyelitis.…”

Section: Discussionmentioning

confidence: 99%

Predicting the anti-inflammatory mechanism of Radix Astragali using network pharmacology and molecular docking

Ren,

Ding,

et al. 2023

Medicine

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According to current research, the primary active ingredients of Radix Astragali (RA), such as saponins, flavonoids, and polysaccharides, play an important role in anti-inflammatory effects. However, the exact molecular mechanism underlying the action was not elucidated to date. Our research attempted to determine the active components in RA and to investigate the interaction between the active components and targets involved in the anti-inflammation activity by network pharmacology and molecular docking. The active components and targets of RA were screened out by TCMSP. Thereafter, through the “anti-inflammation effect” and “inflammation” as the keywords, disease targets were obtained from the GeneCards database. The PPI network was constructed with Cytoscape 3.8.0 software to screen core targets. The GO function and KEGG analysis were enriched and analyzed through the Metascape platform, obtaining the 3-dimensional view of the core targets from the PDB database, and then, performing molecular docking in AutoDock Vina, a heatmap was constructed using the binding free energies in GraphPad Prism 8. The Discovery Studio software was used for docking analysis, and eventually, the docking results were visualized. We also explored the targets and signaling pathways of Astragaloside IV acting on anti-inflammatory effects via constructing compound-disease-target-pathway network. 18 active components and 45 targets of RA were screened out. The main anti-inflammatory active components of RA were quercetin, Astragaloside IV, kaempferol, 7-O-methylisomucronulatol, and formononetin, and the strongly interacting core proteins were TNF, IL6, IL1B, TLR4, CXCL8, CCL2, IL10, VEGFA, and MMP9. The signal pathways mainly involved include Lipid and atherosclerosis, IL-17 signaling pathway, Chagas disease, leishmaniasis, and TNF signaling pathway. Moreover, molecular docking showed that the 2 most active compounds, Astragaloside IV and kaempferol, could efficiently bind with the targets TNF, TLR4, and IL10. Astragaloside IV may play a part in anti-inflammatory effects through pathways such as HIF-1 signaling pathway, Inflammatory bowel disease and Hepatitis B ect. RA exhibits the characteristic of multicomponent and multitarget synergistic effects in exerting anti-inflammatory effects and the effective component of RA is Astragaloside IV, targeting TNF, TLR4, and IL10.

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“…TEM showed that the number of autophagosomes increased in lutein-treated IEC-6 cells[ 8 ]. In addition, several Chinese herbs such as ononin, celastrol, licorice, and Jianpi-Qingchang decoction have been shown to protect IECs and treat experimental colitis by activating mitophagy[ 85 - 88 ]. Subsequently, Truzzi and colleagues demonstrated that stimulation of autophagy by a combination of spermidine and eugenol supplements reduced intestinal inflammatory parameters[ 89 ].…”

Section: Autophagy and Gi Diseasesmentioning

confidence: 99%

Morphological and biochemical characteristics associated with autophagy in gastrointestinal diseases

Chang,

Li,

Liu

et al. 2024

World J Gastroenterol

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Autophagy is a cellular catabolic process characterized by the formation of double-membrane autophagosomes. Transmission electron microscopy is the most rigorous method to clearly visualize autophagic engulfment and degradation. A large number of studies have shown that autophagy is closely related to the digestion, secretion, and regeneration of gastrointestinal (GI) cells. However, the role of autophagy in GI diseases remains controversial. This article focuses on the morphological and biochemical characteristics of autophagy in GI diseases, in order to provide new ideas for their diagnosis and treatment.

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Ononin alleviates DSS‐induced colitis through inhibiting NLRP3 inflammasome via triggering mitophagy

Cited by 14 publications

References 32 publications

Huajuxiaoji Formula Alleviates Phenyl Sulfate‐Induced Diabetic Kidney Disease by Inhibiting NLRP3 Inflammasome Activation and Pyroptosis

Huajuxiaoji Formula Alleviates Phenyl Sulfate‐Induced Diabetic Kidney Disease by Inhibiting NLRP3 Inflammasome Activation and Pyroptosis

Predicting the anti-inflammatory mechanism of Radix Astragali using network pharmacology and molecular docking

Morphological and biochemical characteristics associated with autophagy in gastrointestinal diseases

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