Galangin Targets HSP90β to Alleviate Ulcerative Colitis by Controlling Fatty Acid Synthesis and Subsequent NLRP3 Inflammasome Activation

Yang, Ling; Ma, Xingyu; Mu, Kexin; Dai, Yue; Xia, Yufeng; Wei, Zhifeng

doi:10.1002/mnfr.202200755

Cited by 5 publications

(2 citation statements)

References 40 publications

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“…Our study revealed that ethanol stimulated a significantly increased expression of NLRP3, ASC, and caspase-1, as well as that of the proinflammatory cytokines IL-18 and IL-1β. Like other flavonoids, galangin exerts its anti-inflammatory effect by repressing NLRP3 inflammasome activation. , Thus, we wondered whether galangin could protect against ethanol-induced intestinal injury via an NLRP3-related pathway. As expected, galangin relieved the NLRP3 inflammasome activation and its downstream proinflammatory cytokine level enhanced induced by ethanol.…”

Section: Discussionmentioning

confidence: 99%

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Zhao,

Li,

Liu

et al. 2024

J. Agric. Food Chem.

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The potential of natural phytochemicals in addressing ethanol-related public safety concerns has been garnering attention. Galangin, a potent flavonoid renowned for its antioxidative and anti-inflammatory characteristics, is derived from the galanga plant, and propolis is derived from bees. Here, we documented the effects of galangin on ethanol-stimulated intestinal tight junction damage and investigated its potential protective mechanism in both in vivo and in vitro models, which has not been extensively investigated. Our results revealed that galangin efficaciously mitigated ethanol-induced intestine injury and dysfunction of the intestinal barrier. Concurrently, galangin significantly counteracted the ethanol-induced upregulation of NLRP3 inflammasomeassociated proteins and activated the mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways in both the mouse colon and Caco-2 cells. Interestingly, similar to galangin, inhibitors of MAPKs and the NF-κB p65 reduced ethanol-induced NLRP3 inflammasome activation and intestinal tight junction damage. To sum up, our results showed that galangin blocks the ethanol-induced perturbation of the intestinal barrier and activation of the NLRP3 inflammasome via the NF-κB/MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Zhao,

Li,

Liu

et al. 2024

J. Agric. Food Chem.

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“…Through extensive research and clinical application, natural botanical remedies have demonstrated distinct efficacy and reduced toxicity in the treatment of various ailments, gaining gradual acceptance among individuals [ 10 , 11 ]. As one of the most active ingredients in A. officinarum , galangin has shown important effects in the prevention and treatment of many diseases, including but not limited to anti-cancer, regulation of apoptosis and inflammation, cardiovascular diseases, and neurodegenerative diseases [ 12 – 20 ]. Given the limited research on the therapeutic effects and potential mechanisms of galangin in anti-inflammatory pain, this study aimed to evaluate its anti-inflammatory and analgesic effects and explore its mechanism pathways.…”

Section: Discussionmentioning

confidence: 99%

Analgesic and anti-inflammatory effects of galangin: a potential pathway to inhibit transient receptor potential vanilloid 1 receptor activation

Lin,

Fu,

Wang

et al. 2024

Korean J Pain

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Background Galangin, commonly employed in traditional Chinese medicine for its diverse medicinal properties, exhibits potential in treating inflammatory pain. Nevertheless, its mechanism of action remains unclear. Methods Mice were randomly divided into 4 groups for 7 days a normal control group, a galangin-treated (25 and 50 mg/kg), and a positive control celecoxib (20 mg/kg). Analgesic and anti-inflammatory effects were evaluated using a hot plate test, acetic acid-induced writhing test, acetic acid-induced vascular permeability test, formalin-induced paw licking test, and carrageenan-induced paw swelling test. The interplay between galangin, transient receptor potential vanilloid 1 (TRPV1), NF-κB, COX-2, and TNF-α proteins was evaluated via molecular docking. COX-2, PGE2, IL-1β, IL-6, and TNF-α levels in serum were measured using ELISA after capsaicin administration (200 nmol/L). TRPV1 expression in the dorsal root ganglion was analyzed by Western blot. The quantities of substance P (SP) and calcitonin gene-related peptide (CGRP) were assessed using qPCR. Results Galangin reduced hot plate-induced licking latency, acetic acid-induced contortions, carrageenan-triggered foot inflammation, and capillary permeability in mice. It exhibited favorable affinity towards TRPV1, NF-κB, COX-2, and TNF-α, resulting in decreased levels of COX-2, PGE2, IL-1β, IL-6, and TNF-α in serum following capsaicin stimulation. Galangin effectively suppressed the upregulation of TRPV1 protein and associated receptor neuropeptides CGRP and SP mRNA, while concurrently inhibiting the expression of NF-κB, TNF-α, COX-2, and PGE2 mRNA. Conclusions Galangin exerts its anti-inflammatory pain effects by inhibiting TRPV1 activation and regulating COX-2, NF-κB/TNF-α expression, providing evidence for the use of galangin in the management of inflammatory pain.

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Natural approaches for the management of ulcerative colitis: evidence of preclinical and clinical investigations

Subudhi,

Poonia,

Singh

et al. 2024

Nat. Prod. Bioprospect.

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Ulcerative colitis (UC) is a recurring autoimmune disorder characterized by persistent inflammation in the mucosal lining of the lower part of the large intestine. Conventional treatment options such as salicylates, corticosteroids, and immunosuppressants often come with severe side effects, limited bioavailability, and the development of drug resistance, which hampers their therapeutic effectiveness. Therefore, it is imperative to explore natural strategies as safe and alternative treatments for UC. Currently, around 40% of UC patients find relief through natural constituents, which can help reduce toxic side effects and maintain clinical remission. This review aims to provide a summary of both preclinical and clinical evidence supporting the efficacy of various natural substances in the prophylaxis of UC. These natural options include plant extracts, essential oils, nutraceuticals, and phytochemicals. Furthermore, we will delve into the potential mechanisms that underlie the protective and curative actions of these novel herbal agents. In summary, this review will explore the effectiveness of natural remedies for UC, shedding light on their preclinical and clinical findings and the mechanisms behind their therapeutic actions. These alternatives offer hope for improved treatment outcomes and reduced side effects for individuals suffering from this challenging autoimmune condition. Graphical Abstract

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Galangin Targets HSP90β to Alleviate Ulcerative Colitis by Controlling Fatty Acid Synthesis and Subsequent NLRP3 Inflammasome Activation

Cited by 5 publications

References 40 publications

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Galangin Prevents Against Ethanol-Induced Intestinal Barrier Dysfunction and NLRP3 Inflammasome Activation via NF-κB/MAPK Signaling Pathways in Mice and Caco-2 Cells

Analgesic and anti-inflammatory effects of galangin: a potential pathway to inhibit transient receptor potential vanilloid 1 receptor activation

Natural approaches for the management of ulcerative colitis: evidence of preclinical and clinical investigations

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