Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier

Ye, Bin; Lai, Liqun

doi:10.1155/2021/8870901

Cited by 3 publications

(2 citation statements)

References 41 publications

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“…As a bowel disease characterized by inflammation, ulcerative colitis (UC) has been reported to correlate with the tumorigenesis of colon cancer [ 7 ]. The partial reversal of pyroptosis can be done by YST (Yu Shi An Chang Fang), which protects the intestinal mucosal barrier and prevents tumorigenesis [ 103 ]. GSDME-mediated pyroptosis releases HMGB1 and leads to colitis-associated colorectal cancer through the ERK1/2 pathway.…”

Section: Pyroptosis and Colon Cancermentioning

confidence: 99%

Non-Canonical Programmed Cell Death in Colon Cancer

Pan

Zheng

Xing

et al. 2022

Cancers

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Programmed cell death (PCD) is an evolutionarily conserved process of cell suicide that is regulated by various genes and the interaction of multiple signal pathways. Non-canonical programmed cell death (PCD) represents different signaling excluding apoptosis. Colon cancer is the third most incident and the fourth most mortal worldwide. Multiple factors such as alcohol, obesity, and genetic and epigenetic alternations contribute to the carcinogenesis of colon cancer. In recent years, emerging evidence has suggested that diverse types of non-canonical programmed cell death are involved in the initiation and development of colon cancer, including mitotic catastrophe, ferroptosis, pyroptosis, necroptosis, parthanatos, oxeiptosis, NETosis, PANoptosis, and entosis. In this review, we summarized the association of different types of non-canonical PCD with tumorigenesis, progression, prevention, treatments, and prognosis of colon cancer. In addition, the prospect of drug-resistant colon cancer therapy related to non-canonical PCD, and the interaction between different types of non-canonical PCD, was systemically reviewed.

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Section: Pyroptosis and Colon Cancermentioning

confidence: 99%

Non-Canonical Programmed Cell Death in Colon Cancer

Pan

Zheng

Xing

et al. 2022

Cancers

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“…Shenling Baizhu San inhibits the production of pro-inflammatory factors IL-1β, IL-18, and TNF-a and reduces the mRNA expression levels of NLRP3, ASC, and GSDMD-N [156]. Yushi Anchang Fang can down-regulate the expressions of NLRP3, ASC, and caspase-1 to close to normal levels, thereby inhibiting pyroptosis [157]. Due to the flexible composition of TCM prescriptions, we just listed the above as some representative prescriptions studied in recent years.…”

Section: Herb Medicine As Inhibitor Of Pyroptosismentioning

confidence: 99%

Molecular Characteristics of Cell Pyroptosis and Its Inhibitors: A Review of Activation, Regulation, and Inhibitors

Wei

Feng

Zhang

2022

IJMS

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Pyroptosis is an active and ordered form of programmed cell death. The signaling pathways of pyroptosis are mainly divided into canonical pathways mediated by caspase-1 and noncanonical pathways mediated by caspase-11. Cell pyroptosis is characterized by the activation of inflammatory caspases (mainly caspase-1, 4, 5, 11) and cleavage of various members of the Gasdermin family to form membrane perforation components, leading to cell membrane rupture, inflammatory mediators release, and cell death. Moderate pyroptosis is an innate immune response that fights against infection and plays an important role in the occurrence and development of the normal function of the immune system. However, excessive pyroptosis occurs and leads to immune disorders in many pathological conditions. Based on canonical pathways, research on pyroptosis regulation has demonstrated several pyroptotic inhibitors, including small-molecule drugs, natural products, and formulations of traditional Chinese medicines. In this paper, we review the characteristics and molecular mechanisms of pyroptosis, summarize inhibitors of pyroptosis, and propound that herbal medicines should be a focus on the research and development for pyroptosis blockers.

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Effects of the N-Butanol Extract of Pulsatilla Decoction on Neutrophils in a Mouse Model of Ulcerative Colitis

Wang,

Wu,

Sun

et al. 2024

Pharmaceuticals

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Ulcerative colitis (UC) is a chronic inflammatory disease, the incidence of which is increasing worldwide. However, the etiology and pathogenesis of UC remains unclear. The n-butanol extract of Pulsatilla decoction (BEPD), a traditional Chinese medicine, has been shown to be effective in treating UC. This study aimed to explore the molecular mechanism underlying the effects of BEPD on UC, in particular its effects on neutrophil extracellular trap (NET) formation by neutrophils. High-performance liquid chromatography was used to determine the principal compounds of BEPD. UC was induced in mice using dextran sodium sulfate, and mice were treated with 20, 40, or 80 mg/kg BEPD daily for seven days. Colonic inflammation was determined by assessing the disease activity index, histopathology, colonic mucosal damage index, colonic mucosal permeability, and pro- and anti-inflammatory cytokine levels. The infiltration and activation status of neutrophils in the colon were determined by analyzing the levels of chemokine (C-X-C motif) ligand (CXCL) 1 and CXCL2, reactive oxygen species, Ly6G, and numerous NET proteins. The findings suggest that BEPD improved the disease activity index, histopathology, and colonic mucosal damage index scores of mice with UC, and restored colonic mucosal permeability compared with untreated mice. The expression levels of the pro-inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α in colon tissues were significantly decreased, while the expression levels of anti-inflammatory cytokines in colon tissues were significantly increased, exceeding those of control mice. In addition, BEPD reduced the expression of the neutrophil chemokines CXCL1 and CXCL2 in the colon tissue of mice with UC, reduced neutrophil infiltration, reduced reactive oxygen species levels, and significantly reduced the expression of NET proteins. BEPD also significantly reduced NET formation. The results of this study suggest that BEPD exerts therapeutic effects in a murine model of UC by inhibiting neutrophil infiltration and activation in the colon, as well as by inhibiting the expression of key proteins involved in NET formation and reducing NET formation, thereby alleviating local tissue damage and disease manifestations.

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Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier

Cited by 3 publications

References 41 publications

Non-Canonical Programmed Cell Death in Colon Cancer

Non-Canonical Programmed Cell Death in Colon Cancer

Molecular Characteristics of Cell Pyroptosis and Its Inhibitors: A Review of Activation, Regulation, and Inhibitors

Effects of the N-Butanol Extract of Pulsatilla Decoction on Neutrophils in a Mouse Model of Ulcerative Colitis

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