Progress on Regulation of NLRP3 Inflammasome by Chinese Medicine in Treatment of Ulcerative Colitis

Sun, Hua; Zhu, Ying

doi:10.1007/s11655-023-3551-1

Cited by 5 publications

(2 citation statements)

References 66 publications

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“…The first barrier of the body against endogenous influences and external infections is intrinsic immunity, and NLRP3 is critical for the intrinsic immune system . The aberrant immune and inflammatory responses are involved in the occurrence and progression of UC .…”

Section: Discussionmentioning

confidence: 99%

3,5-Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol Attenuates Ulcerative Colitis via Targeting NLRP3 in Mice

Zhou,

Ma,

Zhang

et al. 2024

J. Agric. Food Chem.

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Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol (DMD) is a polyketide compound obtained from the endophytic fungus Penicillium sp. HJT-A-10 of Rhodiola tibetica. R. tibetica is a nourishing food and also used in traditional Chinese medicine and Xizang medicine. In dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mice, DMD significantly alleviated the pathological symptom of UC. Network pharmacology studies have shown that nucleotide-binding domain-like receptor family pyrin domain containing (NLRP) 3 is the primary target protein of DMD associated with anti-UC. In molecular biology studies, DMD suppressed the activation of NLRP3 and decreased the expression of downstream inflammatory proteins and proinflammatory cytokines in UC. The finding was further verified in knockout mice. DMD lost the effect of attenuating DSS-induced UC in NLRP3 −/− mice. In conclusion, this study demonstrates that DMD reduces inflammatory response and balances the barrier integrity to attenuate UC via targeting NLRP3, and DMD is a potential natural agent or dietary supplement for attenuating UC.

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Section: Discussionmentioning

confidence: 99%

3,5-Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol Attenuates Ulcerative Colitis via Targeting NLRP3 in Mice

Zhou,

Ma,

Zhang

et al. 2024

J. Agric. Food Chem.

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“…Lipid peroxidation reaction and the resulting end products such as MDA can lead to DNA damage, protein denaturation and crosslinking, loss of enzyme activity, and loss of enzyme activity. The Lipid peroxidation reaction and its end products, such as MDA, can lead to DNA damage, denaturation and cross-linking, loss of enzyme activity, damage of membrane structure and release of inflammatory mediators [6]. In this study, experimental colitis in mice was induced by TNBS, and the results showed that the body mass of mice was reduced, the content of MDA, the end product of lipid peroxidation was increased, the content of endogenous antioxidant GSH was decreased, and ulcers and inflammatory cell infiltration were observed by naked eye and microscope, and the inflammatory damage was obvious, which was consistent with literature reports.…”

Section: Discussionmentioning

confidence: 99%

Effect of Baicalin on TNBS-Induced Colonic Inflammatory Injury in Rats

Feng,

Guo

2023

Health

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Objective: The aim is to observe the protective effect of baicalin on trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis in mice and explore its mechanism. Methods: The mice were divided into 4 groups: ethanol control group, TNBS model group, baicalin low-dose group and baicalin high-dose group. The model of experimental colitis in mice was induced by TNBS enema. After 2 hours of TNBS enema, baicalin was given by gavage, QD × 7D. The animals were sacrificed on the 8th day to observe the extent of colonic mucosal damage, and the Peroxidase activity, Malondialdehyde (MDA) and glutathione (GSH) contents were measured. Results: Compared with the TNBS model group, the body weight, gross injury score and histological changes were significantly improved; MPO enzyme activity and MDA content were significantly decreased in the low and high-dose baicalin groups; and the content of glutathione increased. Conclusion: Baicalin can alleviate TNBS-induced colitis in mice, and the mechanism is related to the antioxidation of baicalin.

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Protective effects of sinomenine against dextran sulfate sodium-induced ulcerative colitis in rats via alteration of HO-1/Nrf2 and inflammatory pathway

Niu,

Li,

Yang

et al. 2024

Inflammopharmacol

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Progress on Regulation of NLRP3 Inflammasome by Chinese Medicine in Treatment of Ulcerative Colitis

Cited by 5 publications

References 66 publications

3,5-Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol Attenuates Ulcerative Colitis via Targeting NLRP3 in Mice

3,5-Dimethyl-8-methoxy-3,4-dihydro-1H-isochromen-6-ol Attenuates Ulcerative Colitis via Targeting NLRP3 in Mice

Effect of Baicalin on TNBS-Induced Colonic Inflammatory Injury in Rats

Protective effects of sinomenine against dextran sulfate sodium-induced ulcerative colitis in rats via alteration of HO-1/Nrf2 and inflammatory pathway

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