Anti-inflammatory effect of a standardized triterpenoid-rich fraction isolated from Rubus coreanus on dextran sodium sulfate-induced acute colitis in mice and LPS-induced macrophages

Abstract Salvia miltiorrhiza (SM, or Danshen) extract has been approved by China FDA for the treatment of cardiovascular and cerebrovascular diseases owing to its potent anti-inflammatory effects. Whether SM may be used to treat inflammatory bowel disease (IBD) remains elusive. In the current study, Dextran-Sodium-Sulfate (DSS) induced colitis in mice was used as a model of IBD, and SM was given orally for 7 days. SM administration has significantly reduced the disease activity index (DAI) score and weight lost and colon shortening in the DSS-induced colitis mice. The macrophage infiltration was significantly reduced in the SM treatment group. To explore the mechanisms, macrophage processor cell line Raw 264.7 was used to verify the anti-inflammatory effect of SM. SM treatment inhibited lipopolysaccharide (LPS)-induced macrophage activation in RAW264.7 cells and significantly reduced the production of pro-inflammatory factors. The current study provided evidence that oral administration of SM ameliorates pathological deterioration of IBD in mice, and warrants future clinical application of SM for the management of IBD.

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miR-135a Protects Dextran Sodium Sulfate-Induced Inflammation in Human Colorectal Cell Lines by Activating STAT3 Signal

Cellular Physiology and Biochemistry ◽

10.1159/000495481 ◽

2018 ◽

Vol 51 (3) ◽

pp. 1001-1012 ◽

Cited By ~ 4

Author(s):

Jingru Zhang ◽

Bo Lian ◽

Yan Shang ◽

Chun Li ◽

Qingkai Meng

Keyword(s):

Proinflammatory Cytokines ◽

Sodium Sulfate ◽

Inflammatory Responses ◽

Dextran Sodium Sulfate ◽

Stat3 Phosphorylation ◽

Colorectal Cell ◽

Anti Inflammatory ◽

Colonic Cells ◽

Ht 29 ◽

Inflammatory Effect

Background/Aims: miR-135a is reduced in several cancers and has been suggested to mediate immune and inflammatory responses. However, the effect of miR-135a on inflammatory bowel diseases was obscure. This study firstly attempted to investigate the hypothesis that miR-135a alleviates dextran sodium sulfate (DSS)-induced inflammation in colonic cells and potential mechanisms are also studied. Methods: Caco-2 and HT-29 cells in this study were treated with DSS, miR-135a mimic, and S3I-201, and then CKK-8 assay was used to test cell viability. Expressions of miR-135a, cytokines, and signal transducers and activators of transcription factors (STATs) were determined by RT-PCR. Also, cytokine productions were further tested by using ELISA kits. Activation or inactivation of STAT3 signal was validated by western blotting analysis. Results: The results showed that DSS markedly downregulated miR-135a expression (P< 0.05) and induced inflammatory response in Caco-2 and HT-29 cells evidenced by the up regulations and productions of interleukin-1β (IL-1β) and tumor necrosis factor-ɑ (TNF-ɑ) (P< 0.05). Transfection with miR-135a mimic significantly alleviated DSS-induced upregulation and productions of IL-1β and TNF-ɑ in Caco-2 and HT-29 cells (P< 0.05). STATs were analyzed and miR-135a mimic treatment reversed STAT3 downregulation in DSS-challenged Caco-2 and HT-29 cells compared with the mimic control (P< 0.05). Also, STAT3 phosphorylation was inhibited in DSS-challenged Caco-2 cells and miR-135a mimic activated STAT3 signal (P< 0.05). S3I-201, an inhibitor of STAT3 signal, further used to inactivate STAT3 signal and the results showed that S3I-201 blocked the anti-inflammatory effect of miR-135a mimic on Caco-2 and HT-29 cells evidenced by the lowered expressions and productions of proinflammatory cytokines ((IL-1β and TNF-ɑ) (P< 0.05). Conclusion: Our results indicated that miR-135a alleviated DSS-induced inflammation and activated STAT3 signal in colonic cells. Inhibition of STAT3 reversed the anti-inflammatory function of miR-135a by regulating proinflammatory cytokines. Thus, STAT3 signal might serve, at least in part, as the potential mechanism of miR-135a-mediated anti-inflammatory effect in colonic cells.

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THE EFFECT OF MAHKOTA DEWA (PHALERIA MACROCARPA) (SCHEFF.) FRUIT PERICARP EXTRACT ON INOS IN MICE COLON INTERMITTENTLY-INDUCED BY DEXTRAN SODIUM SULFATE

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2017.v10i12.20560 ◽

2017 ◽

Vol 10 (12) ◽

pp. 309

Author(s):

Kusmardi Kusmardi ◽

Dilla Shavera ◽

Ari Estuningtyas ◽

Aryo Tedjo ◽

Bambang Priyosoeryanto

Keyword(s):

Sodium Sulfate ◽

Total Yield ◽

Ethanolic Extract ◽

Dextran Sodium Sulfate ◽

Inflammatory Activity ◽

Fruit Pericarp ◽

Phaleria Macrocarpa ◽

Anti Inflammatory ◽

Oxide Synthase ◽

Different Doses

Objective: The objective of this research was to investigate the anti-inflammatory effect of Mahkota Dewa fruit pericarp extract (Phaleria macrocarpa) on inducible nitric oxide synthase (iNOS) in mice colon induced by dextran sodium sulfate (DSS).Method: The simplisia of P. macrocarpa pericarp was weighed (1000 g) and extracted by maceration process. The total yield of the ethanolic extract was 26.43%. Phytochemical screening was carried out for the detection of the phytoconstituents by simple qualitative methods. The anti-inflammatory activity was performed by DSS-induced colitis model through assessment of hematoxylin-eosin staining and expression of iNOS by immunohistochemistry assay at four different doses, i.e., 650, 1250, 2500, and 5000 mg/kg. Swiss Webster male mice weighing 25-30 g were used for the study.Results: Inflammation score in dose 625, 1250, 2500, and 5000 mg/kg were 1.63, 1.43, 1.32, and 2.20, respectively. This result is significantly different (p=0.008) with DSS group that was 4.37. The results of iNOS optical density score in dose 625, 1250, 2500, and 5000 mg/kg were 1.21, 1.119, 1.22, and 1.37, respectively. This result was significantly different (p=0.000) with DSS group that was 2.24.Conclusion: Pericarp extract of P. macrocarpa fruit exhibited anti-inflammatory activity in the experimental model shown by suppressing the expression of inflammatory cell and iNOS.

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Osteopontin Protects Colonic Mucosa from Dextran Sodium Sulfate-Induced Acute Colitis in Mice by Regulating Junctional Distribution of Occludin

Digestive Diseases and Sciences ◽

10.1007/s10620-018-5246-6 ◽

2018 ◽

Vol 64 (2) ◽

pp. 421-431 ◽

Cited By ~ 4

Author(s):

Sang-Ho Woo ◽

Su-Hyung Lee ◽

Jun-Won Park ◽

Du-Min Go ◽

Dae-Yong Kim

Keyword(s):

Sodium Sulfate ◽

Colonic Mucosa ◽

Dextran Sodium Sulfate ◽

Acute Colitis

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Oral priming with oligodeoxynucleotide particles from Lactobacillus rhamnosus GG attenuates symptoms of dextran sodium sulfate‐induced acute colitis in mice

Animal Science Journal ◽

10.1111/asj.13468 ◽

2020 ◽

Vol 91 (1) ◽

Author(s):

Suguru Shigemori ◽

Fu Namai ◽

Tasuku Ogita ◽

Takashi Sato ◽

Takeshi Shimosato

Keyword(s):

Sodium Sulfate ◽

Lactobacillus Rhamnosus ◽

Dextran Sodium Sulfate ◽

Acute Colitis ◽

Lactobacillus Rhamnosus Gg

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Acetylsalicylic Acid Reduces the Severity of Dextran Sodium Sulfate-Induced Colitis and Increases the Formation of Anti-Inflammatory Lipid Mediators

BioMed Research International ◽

10.1155/2013/748160 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 14

Author(s):

Thomas Köhnke ◽

Beate Gomolka ◽

Süleyman Bilal ◽

Xiangzhi Zhou ◽

Yanping Sun ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Acetylsalicylic Acid ◽

Bowel Disease ◽

Sodium Sulfate ◽

Lipid Mediators ◽

Dextran Sodium Sulfate ◽

Cyclooxygenase Inhibitors ◽

Omega 3 ◽

Inflammatory Bowel ◽

Anti Inflammatory

The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used to assess disease severity, and lipid metabolites were measured using liquid chromatography-coupled tandem mass spectrometry. Decreased colitis activity was demonstrated by phenotype and MRI assessment in mice treated with ASA, and confirmed in postmortem analysis. Analysis of lipid mediators showed sustained formation of lipoxin A4 and an increase of DHA-derived 17-hydroxydocosahexaenoic acid (17-HDHA) after treatment with ASA. Furthermore,in vitroexperiments in RAW264.7 murine macrophages demonstrated significantly increased phagocytosis activity after incubation with 17-HDHA, supporting its proresolution effect. These results show a protective effect of ASA in a murine colitis model and could give a rationale for a careful reassessment of ASA therapy in patients with inflammatory bowel disease and particularly ulcerative colitis, possibly combined with DHA supplementation.

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Melatonin Attenuates Dextran Sodium Sulfate Induced Colitis in Obese Mice

Pharmaceuticals ◽

10.3390/ph14080822 ◽

2021 ◽

Vol 14 (8) ◽

pp. 822

Author(s):

Shijia Pan ◽

Fan Hong ◽

Letong Li ◽

Yuan Guo ◽

Xiaoxiao Qiao ◽

...

Keyword(s):

Sodium Sulfate ◽

Antioxidant Activities ◽

Intestinal Barrier ◽

Inflammatory Cells ◽

Inhibitory Effect ◽

Immune Defense ◽

Dextran Sodium Sulfate ◽

Obese Mice ◽

Promoting Effect ◽

Anti Inflammatory

Epidemiological studies have indicated that obesity is an independent risk factor for colitis and that a high-fat diet (HFD) increases the deterioration of colitis-related indicators in mice. Melatonin has multiple anti-inflammatory effects, including inhibiting tumor growth and regulating immune defense. However, the mechanism of its activity in ameliorating obesity-promoted colitis is still unclear. This study explored the possibility that melatonin has beneficial functions in HFD-induced dextran sodium sulfate (DSS)-induced colitis in mice. Here, we revealed that HFD-promoted obesity accelerated DSS-induced colitis, while melatonin intervention improved colitis. Melatonin significantly alleviated inflammation by increasing anti-inflammatory cytokine release and reducing the levels of proinflammatory cytokines in HFD- and DSS-treated mice. Furthermore, melatonin expressed antioxidant activities and reversed intestinal barrier integrity, resulting in improved colitis in DSS-treated obese mice. We also found that melatonin could reduce the ability of inflammatory cells to utilize fatty acids and decrease the growth-promoting effect of lipids by inhibiting autophagy. Taken together, our study indicates that the inhibitory effect of melatonin on autophagy weakens the lipid-mediated prosurvival advantage, which suggests that melatonin-targeted autophagy may provide an opportunity to prevent colitis in obese individuals.

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