Morroniside alleviates lipopolysaccharide-induced inflammatory and oxidative stress in inflammatory bowel disease by inhibiting NLRP3 and NF-κB signaling pathways

Zhang, Shi-fen; Lai, Qiaohua; Li, Liming; Yang, Yue; Wang, Juan

doi:10.15586/aei.v50i6.674

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…Phosphorylation of AKT/NF-kB is involved in NLRP3 activation of inflammatory responses. [18][19][20] Further to investigate the mechanism of the effect of PP2 on Mtb-infected cells, we used western blot to measure the phosphorylation levels of AKT and NF-kB. Results indicated that PP2 might exert anti-inflammatory effects through down-regulation of the AKT/ NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Polyphyllin II inhibits NLPR3 inflammasome activation and inflammatory response of Mycobacterium tuberculosis–infected human bronchial epithelial cells

Cheng,

Ye,

et al. 2024

Allergol Immunopathol

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Background: The bronchial infection by Mycobacterium tuberculosis (Mtb) is increasing in prevalence and severity worldwide. Despite appropriate tuberculosis treatment, most patients still develop bronchial stenosis, which often leads to disability. Polyphyllin II (PP2) is a steroidal saponin extracted from Rhizoma Paridis. In this study, we aimed to explore the effect of PP2 on the advancement of Mtb-induced bronchial infection. Method: The effects of PP2 on cell viability were measured by using MTT and lactate dehydrogenase (LDH) kit. The mRNA and protein levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-8 were elucidated by RT-qPCR and ELISA, respectively. The expression of NLR family pyrin domain containing 3 (NLRP3) related inflammasome (NLRP3, IL-1β, and cleaved-caspase-1) and the activated degree of protein kinase B (AKT)/nuclear factor-kappa B (NF-kB; p-AKT and p-NF-κB) were detected by Western blotting. Results: PP2 at 0, 1, 5, and 10 μM had little cytotoxicity on 16HBE cells. PP2 inhibited Mtb-induced cell proliferation and decreased LDH levels. We further found that PP2 could suppress Mtb-induced inflammatory responses and activation of NLPR3 inflammasome. Additionally, the role of PP2 in Mtb is associated with the AKT/NF-kB signaling pathway. Conclusion: PP2 inhibited Mtb infection in bronchial epithelial cells, by inhibiting Mtb-induced inflammatory reactions and activation of NLPR3 inflammasome. These effects may be exerted by suppressing the AKT/NF-kB pathway, which will provide a prospective treatment.

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Section: Discussionmentioning

confidence: 99%

Polyphyllin II inhibits NLPR3 inflammasome activation and inflammatory response of Mycobacterium tuberculosis–infected human bronchial epithelial cells

Cheng,

Ye,

et al. 2024

Allergol Immunopathol

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“…26 Targeting the NLRP3 inflammasome pathway could effectively alleviate inflammatory response. 27 Researchers have found that both protopine 28 and morroniside 29 could alleviate LPS-induced inflammation and oxidative stress in inflammatory bowel disease by inhibiting NLRP3 and NF-κB signaling pathways. Licochalcone B plays a protective role in peritonitis and hepatitis by specifically inhibiting NLRP3.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of PHLDA1 alleviates sepsis-induced acute lung injury by downregulating NLRP3 inflammasome activation

Meng,

Gu,

Wang

et al. 2023

Allergol Immunopathol

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Objective: To investigate the regulatory mechanism of pleckstrin homology-like domain, family A, member 1 (PHLDA1) in sepsis-induced acute lung injury (ALI). Method: Mice model of sepsis were established by cecal ligation and puncture (CLP). The expression of PHLDA1 was reduced by injecting short hairpin RNA (shRNA)–PHLDA1 into the tail vein. The levels of PHLDA1, pro-inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), IL-1β, IL-18, super-oxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH), molecular mechanism related to pyroptosis, such as caspase 1, adaptor apoptosis-associated speck-like protein containing a CARD (ASC), and gasdermin D (GSDMD)-N, and nucleotide oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) were tested by Western blot analysis, quantitative real-time polymerase chain reaction, and enzyme-linked-immunosorbent serologic assay. Pathological changes in lung tissues were examined by hematoxylin and eosin staining. Wet–dry weight ratio of lung tissues was observed. Results: The expression of PHLDA1 was up-regulated in lung tissues from CLP-induced septic mice. Knockdown of PHLDA1 could reduce lung injury and wet–dry weight ratio in mice with sepsis-induced ALI. Moreover, silencing of PHLDA1 decreased the expressions of IL-1β, TNF-α, IL-18, IL-6, and MDA but increased SOD and GSH expressions in CLP-induced septic mice. The expressions of NLRP3, GSDMD-N, ASC, and caspase 1 were decreased by PHLDA1 silencing. Conclusion: Knockdown of PHLDA1 inhibited lung inflammation and pyroptosis in mice with sepsis-induced ALI by down-regulating NLRP3.

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“…4.5.2. Morroniside S. Zhang et al [29] studied LPS-stimulated NCM460 cells in vitro to evaluate the effects of morroniside, an iridoid glycoside derived from Cornus offinalis, against NLRP3 activation during this model of IBD. The results showed that with the treatment, the cells presented regulation of the NLRP3 activation through decreased BCL-2-associated X-protein (BAX), TNF-α, IL-1β and IL-6, MDA, and MPO expressions, NLRP3 signaling and p-p65-p65 and p-IκBα-IκBα expressions, as well as increased B-cell lymphoma protein 2 (BCL-2), SOD, and total antioxidant capacity (T-AOC) expressions.…”

Section: Agrimonia Pilosamentioning

confidence: 99%

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

et al. 2023

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Ongoing research explores the underlying causes of ulcerative colitis and Crohn’s disease. Many experts suggest that dysbiosis in the gut microbiota and genetic, immunological, and environmental factors play significant roles. The term “microbiota” pertains to the collective community of microorganisms, including bacteria, viruses, and fungi, that reside within the gastrointestinal tract, with a particular emphasis on the colon. When there is an imbalance or disruption in the composition of the gut microbiota, it is referred to as dysbiosis. Dysbiosis can trigger inflammation in the intestinal cells and disrupt the innate immune system, leading to oxidative stress, redox signaling, electrophilic stress, and inflammation. The Nod-like Receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome, a key regulator found in immunological and epithelial cells, is crucial in inducing inflammatory diseases, promoting immune responses to the gut microbiota, and regulating the integrity of the intestinal epithelium. Its downstream effectors include caspase-1 and interleukin (IL)-1β. The present study investigated the therapeutic potential of 13 medicinal plants, such as Litsea cubeba, Artemisia anomala, Piper nigrum, Morus macroura, and Agrimonia pilosa, and 29 phytocompounds such as artemisitene, morroniside, protopine, ferulic acid, quercetin, picroside II, and hydroxytyrosol on in vitro and in vivo models of inflammatory bowel diseases (IBD), with a focus on their effects on the NLRP3 inflammasome. The observed effects of these treatments included reductions in IL-1β, tumor necrosis factor-alpha, IL-6, interferon-gamma, and caspase levels, and increased expression of antioxidant enzymes, IL-4, and IL-10, as well as regulation of gut microbiota. These effects could potentially provide substantial advantages in treating IBD with few or no adverse effects as caused by synthetic anti-inflammatory and immunomodulated drugs. However, additional research is necessary to validate these findings clinically and to develop effective treatments that can benefit individuals who suffer from these diseases.

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Morroniside alleviates lipopolysaccharide-induced inflammatory and oxidative stress in inflammatory bowel disease by inhibiting NLRP3 and NF-κB signaling pathways

Cited by 7 publications

References 15 publications

Polyphyllin II inhibits NLPR3 inflammasome activation and inflammatory response of Mycobacterium tuberculosis–infected human bronchial epithelial cells

Polyphyllin II inhibits NLPR3 inflammasome activation and inflammatory response of Mycobacterium tuberculosis–infected human bronchial epithelial cells

Knockdown of PHLDA1 alleviates sepsis-induced acute lung injury by downregulating NLRP3 inflammasome activation

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

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