Intestinal Anti-Inflammatory Activity of the Aqueous Extract from Ipomoea asarifolia in DNBS-Induced Colitis in Rats

Silva, Valéria da; Araujo, A De; Araújo, Daline Fernandes de Souza; Lima, Maíra C.J.S.; Vasconcelos, Roseane Carvalho; Júnior, Raimundo de Araújo; Langasnner, Silvana; Pedrosa, Matheus De Freitas Fernandes; Medeiros, Caroline de; Guerra, Gerlane Coelho Bernardo

doi:10.3390/ijms19124016

Cited by 31 publications

(18 citation statements)

References 56 publications

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“…Therefore, there is an ongoing search for new therapies that may be beneficial in treating these chronic diseases. 34 In this sense, the interest in the use of plant products for treating IBD has increased, 35,36 as many of them are known to act on different targets of the inflammatory process and protect the tissue microenvironment of oxidative stress. Therefore, this study has evaluated the potential effects of plumericin, an iridoid spironolactone isolated from H. sucuuba, on intestinal inflammation.…”

Section: Discussionmentioning

confidence: 99%

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

et al. 2019

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Inflammatory bowel diseases (IBDs) are characterized by an inflammatory and oxidative stress condition in the intestinal tissue. In this study, we evaluated the effect of plumericin, one of the main bioactive components of Himatanthus sucuuba (Woodson) bark, on intestinal inflammation and oxidative stress, both in vitro and in vivo. The effect of plumericin (0.5‐2 µM) in vitro was evaluated in rat intestinal epithelial cells (IEC‐6) treated with lipopolysaccharides from E. coli (10 μg/mL) plus interferon‐γ (10 U/mL). Moreover, a 2,4,6‐dinitrobenzene sulfonic acid (DNBS)‐induced colitis model was used to evaluate the anti‐inflammatory and antioxidant activity of plumericin (3 mg/kg) in vivo. The results showed that plumericin significantly reduces intestinal inflammatory factors such as tumor necrosis factor‐α, cyclooxygenase‐2 and inducible nitric oxide synthase expression, and nitrotyrosine formation. Plumericin also inhibited nuclear factor‐κB translocation, reactive oxygen species (ROS) release, and inflammasome activation. Moreover, plumericin activated the nuclear factor erythroid‐derived 2 pathway in IEC‐6. Using the DNBS‐induced colitis model, a significant reduction in the weight loss and in the development of the macroscopic and histologic signs of colon injury, together with a reduced inflammatory and oxidative stress state, were observed in plumericin‐treated mice. These results indicate that plumericin exerts a strong anti‐inflammatory and antioxidant activity. Thus, it might be a candidate for the development of a new pharmacologic approach for IBDs treatment.

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Section: Discussionmentioning

confidence: 99%

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

et al. 2019

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“…In gastrointestinal disorders, the therapeutic effects of flavonoids are largely attributed to their antioxidant and anti-inflammatory properties. In terms of anti-inflammatory activity, flavonoids can inhibit cyclic adenosine monophosphate and COX activity, as well as protein phosphorylation [ 66 , 67 , 68 , 69 , 70 ]. In the case of RUT, its anti-inflammatory effects have been attributed to its capacity to suppress the production of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), as well as its ability to activate nuclear factor B (NF-kB) and extracellular kinases [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Rutin in 5-Fluorouracil-Induced Intestinal Mucositis: Prevention of Histological Damage and Reduction of Inflammation and Oxidative Stress

et al. 2020

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Intestinal mucositis, characterized by inflammatory and/or ulcerative processes in the gastrointestinal tract, occurs due to cellular and tissue damage following treatment with 5-fluorouracil (5-FU). Rutin (RUT), a natural flavonoid extracted from Dimorphandra gardneriana, exhibits antioxidant, anti-inflammatory, cytoprotective, and gastroprotective properties. However, the effect of RUT on inflammatory processes in the intestine, especially on mucositis promoted by antineoplastic agents, has not yet been reported. In this study, we investigated the role of RUT on 5-FU-induced experimental intestinal mucositis. Swiss mice were randomly divided into seven groups: Saline, 5-FU, RUT-50, RUT-100, RUT-200, Celecoxib (CLX), and CLX + RUT-200 groups. The mice were weighed daily. After treatment, the animals were euthanized and segments of the small intestine were collected to evaluate histopathological alterations (morphometric analysis); malondialdehyde (MDA), myeloperoxidase (MPO), and glutathione (GSH) concentrations; mast and goblet cell counts; and cyclooxygenase-2 (COX-2) activity, as well as to perform immunohistochemical analyses. RUT treatment (200 mg/kg) prevented 5-FU-induced histopathological changes and reduced oxidative stress by decreasing MDA concentrations and increasing GSH concentrations. RUT attenuated the inflammatory response by decreasing MPO activity, intestinal mastocytosis, and COX-2 expression. These results suggest that the COX-2 pathway is one of the underlying protective mechanisms of RUT against 5-FU-induced intestinal mucositis.

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“…EHEC-induced intestinal inflammation was assessed by determining the DAI, as described previously ( 23 , 28 ). The DAI was determined as the sum of scores assigned for the body weight, stool consistency, and occult blood in the stool.…”

Section: Methodsmentioning

confidence: 99%

A Novel Cecropin-LL37 Hybrid Peptide Protects Mice Against EHEC Infection-Mediated Changes in Gut Microbiota, Intestinal Inflammation, and Impairment of Mucosal Barrier Functions

Xin

Zhang

et al. 2020

Front. Immunol.

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Intestinal inflammation can cause impaired epithelial barrier function and disrupt immune homeostasis, which increases the risks of developing many highly fatal diseases. Enterohemorrhagic Escherichia coli (EHEC) O157:H7 causes intestinal infections worldwide and is a major pathogen that induces intestinal inflammation. Various antibacterial peptides have been described as having the potential to suppress and treat pathogen-induced intestinal inflammation. Cecropin A (1-8)-LL37 (17-30) (C-L), a novel hybrid peptide designed in our laboratory that combines the active center of C with the core functional region of L, shows superior antibacterial properties and minimized cytotoxicity compared to its parental peptides. Herein, to examine whether C-L could inhibit pathogen-induced intestinal inflammation, we investigated the anti-inflammatory effects of C-L in EHEC O157:H7-infected mice. C-L treatment improved the microbiota composition and microbial community balance in mouse intestines. The hybrid peptide exhibited improved anti-inflammatory effects than did the antibiotic, enrofloxacin. Hybrid peptide treated infected mice demonstrated reduced clinical signs of inflammation, reduced weight loss, reduced expression of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interferon-gamma (IFN-γ)], reduced apoptosis, and reduced markers of jejunal epithelial barrier function. The peptide also affected the MyD88-nuclear factor κB signaling pathway, thereby modulating inflammatory responses upon EHEC stimulation. Collectively, these findings suggest that the novel hybrid peptide C-L could be developed into a new anti-inflammatory agent for use in animals or humans.

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Intestinal Anti-Inflammatory Activity of the Aqueous Extract from Ipomoea asarifolia in DNBS-Induced Colitis in Rats

Cited by 31 publications

References 56 publications

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

Plumericin prevents intestinal inflammation and oxidative stress in vitro and in vivo

Role of Rutin in 5-Fluorouracil-Induced Intestinal Mucositis: Prevention of Histological Damage and Reduction of Inflammation and Oxidative Stress

A Novel Cecropin-LL37 Hybrid Peptide Protects Mice Against EHEC Infection-Mediated Changes in Gut Microbiota, Intestinal Inflammation, and Impairment of Mucosal Barrier Functions

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