Maggot protein ameliorates dextran sulphate sodium-induced ulcerative colitis in mice

Wang, Rong; Wang, Lei; Luo, Yongzheng; Wang, Daojuan; Du, Ronghui; Du, Jiaojiao; Wang, Yong

doi:10.1042/bsr20181799

Cited by 13 publications

(15 citation statements)

References 41 publications

(46 reference statements)

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“…Our data clearly demonstrated that the maggot extracts alleviated inflammation and oxidative stress in experimental colitis via modulation of the Nrf2/HO-1 pathway. While contributions of the maggot extracts to anti-inflammation have been recognized in our previous study [46], the molecular basis accounting for the function of the maggot extracts has not been elucidated. In this study, two important points have been clarified.…”

Section: Discussionmentioning

confidence: 97%

Maggot Extracts Alleviate Inflammation and Oxidative Stress in Acute Experimental Colitis via the Activation of Nrf2

Wang

Luo

et al. 2019

Oxidative Medicine and Cellular Longevity

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Ulcerative colitis (UC) is a common chronic remitting disease driven through altered immune responses with production of inflammatory cytokines. Oxidant/antioxidant balance is also suggested to be an important factor for the recurrence and progression of UC. Maggots are known as a traditional Chinese medicine also known as “wu gu chong.” NF-E2-related factor-2 (Nrf2) transcription factor regulates the oxidative stress response and also represses inflammation. The aim of this study was to investigate the effects of maggot extracts on the amelioration of inflammation and oxidative stress in a mouse model of dextran sulfate sodium- (DSS-) induced colitis and evaluate if the maggot extracts could repress inflammation and oxidative stress using RAW 264.7 macrophages stimulated by lipopolysaccharide (LPS). In the present study, we found that the maggot extracts significantly prevented the loss of body weight and shortening of colon length in UC induced by DSS. Furthermore, DSS-induced expression of proinflammatory cytokines at both mRNA and protein levels in the colon was also attenuated by the maggot extracts. In addition, the maggot extracts could significantly suppress the expression of interleukin- (IL-) 1β, IL-6, TNF-α, NFκB p65, p-IκB, p22-phox, and gp91-phox in LPS-stimulated RAW 264.7 cells and colonic tissues. The maggot extracts increased the level of Nrf2 and prevented the degradation of Nrf2 through downregulating the expression of Keap1, which resulted in augmented levels of HO-1, SOD, and GSH-Px and reduced levels of MPO and MDA. However, after administering an Nrf2 inhibitor (ML385) to block the Nrf2/HO-1 pathway, we failed to observe the protective effects of the maggot extracts in mice with colitis and RAW 264.7 cells. Taken together, our data for the first time confirmed that the maggot extracts ameliorated inflammation and oxidative stress in experimental colitis via modulation of the Nrf2/HO-1 pathway. This study sheds light on the possible development of an effective therapeutic strategy for inflammatory bowel diseases.

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Section: Discussionmentioning

confidence: 97%

Maggot Extracts Alleviate Inflammation and Oxidative Stress in Acute Experimental Colitis via the Activation of Nrf2

Wang

Luo

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…During the entire experimental period, the activity, physiological status and body weight were monitored daily. The status of the UC mice was scored using the disease activity index (DAI) according to the degree of weight loss, fecal viscosity and bleeding ( 36 ).…”

Section: Methodsmentioning

confidence: 99%

Protective effect of Gloeostereum�incarnatum on ulcerative colitis via modulation of Nrf2/NF‑κB signaling in C57BL/6 mice

Liu

Zhang

et al. 2020

Mol Med Rep

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Chronic non-specific inflammatory cell infiltration of the colon is generally considered to be the cause of ulcerative colitis (UC). Gloeostereum incarnatum (GI), a fungus rich in amino acids and fatty acids, exhibits a variety of biological functions. In the present study, GI was identified to contain 15 fatty acids, 17 amino acids and 11 metallic elements. The protective effect of GI against UC was investigated in C57BL/6 mice with UC induced by free drinking 3.5% dextran sulfate sodium (DSS). After a 21-day oral administration, GI prevented weight loss, enhancement of the disease activity index and colonic pathological alterations in mice with UC. GI reduced the levels of pro-inflammatory factors including interleukin (IL)-1β, IL-2, IL-6 and IL-12, tumor necrosis factor α and -β, interferon α and -γ, and pro-oxidative factors including reactive oxygen species and nitric oxide. In addition, it enhanced the levels of immunological factors including immunoglobulin (Ig)A, IgM and IgG, and antioxidative factors including superoxide dismutase and catalase in the serum and/or colon tissues. GI enhanced the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins and suppressed the phosphorylation of NF-κB signaling in colon tissues. Together, GI was shown to alleviate the physiological and pathological state of DSS-induced UC in mice via its antioxidant and anti-inflammatory functions, which may be associated with its modulation of the activation of Nrf2/NF-κB signaling.

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“…The volumes of distilled water or DSS solution consumed by all of the animals were measured daily, and there were no significant differences in water consumption among the groups. HQD and ME were administered daily by oral gavage (Chen et al, 2016;Wang et al, 2018).…”

Section: Experimental Animals and Groupingmentioning

confidence: 99%

Anti-Inflammatory Effects of Huangqin Decoction on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through Regulation of the Gut Microbiota and Suppression of the Ras-PI3K-Akt-HIF-1α and NF-κB Pathways

Luo

et al. 2020

Front. Pharmacol.

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Objective: Huangqin decoction (HQD), a classical traditional Chinese medicinal formula, has been commonly used to treat gastrointestinal diseases for thousands of years. We investigated the anti-inflammatory effects and underlying mechanisms of HQD on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC).Methods: Experimental mice were given 3% DSS, and HQD (2.275, 4.55, and 9.1 g/kg), or mesalazine (ME, 200 mg/kg) orally for 7 days. Body weight loss, disease activity index (DAI), colon length, histology, and levels of inflammatory cytokines were measured to evaluate the effects of HQD on colitis. The effects of HQD on the Ras-phosphoinositide-3kinase (PI3K)-Akt-hypoxia inducible factor 1 alpha (HIF-1a) and nuclear factor-kappa B (NF-kB) pathways were evaluated by Western blot analysis. In addition, the gut microbiota was characterized using high-throughput Illumina MiSeq sequencing. Results:The results showed that HQD significantly reduced the body weight loss, ameliorated DAI, restored colon length, and improved the intestinal epithelial cell barrier in mice with DSS-induced colitis. The messenger RNA (mRNA) expression levels of inflammatory mediators were decreased following HQD treatment. Furthermore, the Ras-PI3K-Akt-HIF-1a and NF-kB pathways were significantly inhibited by HQD. Finally, treatment with HQD resulted in recovery of gut microbiota diversity.Conclusions: HQD ameliorates DSS-induced colitis through regulation of the gut microbiota, and suppression of Ras-PI3K-Akt-HIF-1a and NF-kB pathways. Our results suggested that HQD may be a potential candidate for treatment of UC.GRAPHICAL ABSTRACT | This study demonstrated that supplementation of Huangqin decoction (HQD) attenuated dextran sulfate sodium (DSS)-induced ulcerative colitis by regulating the gut microbiota and suppressing Ras-PI3K-Akt-HIF-1a and NF-kB pathways in mice.

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Maggot protein ameliorates dextran sulphate sodium-induced ulcerative colitis in mice

Cited by 13 publications

References 41 publications

Maggot Extracts Alleviate Inflammation and Oxidative Stress in Acute Experimental Colitis via the Activation of Nrf2

Maggot Extracts Alleviate Inflammation and Oxidative Stress in Acute Experimental Colitis via the Activation of Nrf2

Protective effect of Gloeostereum�incarnatum on ulcerative colitis via modulation of Nrf2/NF‑κB signaling in C57BL/6 mice

Anti-Inflammatory Effects of Huangqin Decoction on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through Regulation of the Gut Microbiota and Suppression of the Ras-PI3K-Akt-HIF-1α and NF-κB Pathways

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