scholarly journals Gardenia jasminoides Ellis Fruit Extracts Attenuated Colitis in 2,4,6-Trinitrobenzenesulfonic Acid-Induced Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jing Liu ◽  
Chao Yang ◽  
Zhigui Wu ◽  
Jianguo Pei ◽  
Yao Chen ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Chemical Components ◽  
Protective Agent ◽  
Protective Effects ◽  
Trinitrobenzenesulfonic Acid ◽  
Fruit Extracts ◽  
Gardenia Jasminoides ◽  
Tnf Α ◽  
Ameliorative Effect ◽  
Gardenia Jasminoides Ellis

Ulcerative colitis (UC) is a relapsing inflammatory disease with an unknown precise etiology. The purpose of this study is to investigate the protective effects of Gardenia jasminoides Ellis fruit extracts (GFE) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. GFE (50 mg/kg, 100 mg/kg) were administered orally for 7 days after induction. Meanwhile, the chemical components of GFE were performed by UPLC-QTOF-MS/MS. GFE significantly decreased DAI scores and ameliorated macroscopic and histologic damage. It also reduced the levels of MPO, NO, MDA, IL-1β, TNF-α, and IL-6, while increasing the level of SOD. Moreover, 56 components were identified in GFE using a UPLC-QTOF-MS/MS method, which can be categorized into six structural groups. Our results indicated that GFE has an ameliorative effect on TNBS-induced colitis in rats, which may further verify its anti-inflammatory and antioxidative properties. Therefore, GFE can be a promising protective agent of colitis that deserves further investigation.

scholarly journals Protective effects of pterostilbene on ulcerative colitis in rats via suppressing NF-κB pathway and activating PPAR-γ

2019 ◽  
Vol 17 ◽  
pp. 205873921984015
Author(s):  
Liu Shi ◽  
Qing Liu ◽  
Jian-hua Tang ◽  
Jian-jun Wen ◽  
Chen Li
Keyword(s):  
Ulcerative Colitis ◽  
Activity Index ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Model Group ◽  
Trinitrobenzenesulfonic Acid ◽  
Ppar Γ ◽  
Tnf Α

Our study aimed to investigate the protective effects and potential mechanisms of pterostilbene on rats with ulcerative colitis (UC). We established 2,4,6-trinitrobenzenesulfonic acid (TNBS) induced colitis rat model. Rats were randomly divided into three groups, including control group, model group, and pterostilbene group (30 mg/kg). Disease activity index (DAI) including body weight, stool consistency, and gross bleeding was measured. The concentration of superoxide dismutases (SODs), glutathione superoxide (GSH-px), malondialdehyde (MDA), and methylpropanediol (MPO) in serum were detected by enzyme-linked immunosorbent assay (ELISA). The levels of interleukin-1 beta (IL-1β), IL-17, IL-6, and tumor necrosis factor–alpha (TNF-α) in serum were also analyzed by ELISA kits. Histological evaluations of colons were conducted. The levels of peroxisome-proliferator-activated receptor–γ (PPAR-γ), nuclear factor-κB (NF-κB), ZO-1, and Occludin were analyzed by immunohistochemistry. Compared with model group, pterostilbene notably suppressed the production of TNF-α, IL-17, IL-1β, IL-6, MDA and MPO in serum, and markedly increased the SOD and GSH-Px activity in serum. Pterostilbene significantly attenuated macroscopic damage and histological injury, when compared with model rats. Furthermore, pterostilbene also markedly activated the expression of PPAR-γ, ZO-1, and Occludin, and suppressed the expression of NF-κB. The protective effects of pterostilbene might be associated with suppression of NF-κB and activation of PPAR-γ. Pterostilbene might be a promising therapeutic agent for colitis treatment.

scholarly journals F. prausnitzii and its supernatant increase SCFAs-producing bacteria to restore gut dysbiosis in TNBS-induced colitis

AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Youlian Zhou ◽  
Haoming Xu ◽  
Jing Xu ◽  
Xue Guo ◽  
Hailan Zhao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Throughput Sequencing ◽  
Therapeutic Potential ◽  
Protective Effects ◽  
Trinitrobenzenesulfonic Acid ◽  
Gut Dysbiosis ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Gut Microbiota Dysbiosis

AbstractAn increasing number of studies have shown that Faecalibacterium prausnitzii (F. prausnitzii) is a promising anti-inflammatory bacterium that colonizes in the gut and that gut microbiota dysbiosis plays an important role in the pathogenesis of inflammatory bowel disease (IBD). In this study, we report the gut microbiota profile of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis mice treated with F. prausnitzii and its supernatant on the basis of high-throughput sequencing. We interestingly found that both F. prausnitzii and its metabolites exerted protective effects against colitis in mice, which ameliorated gut dysbiosis, with an increase in bacterial diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria and a decrease in serum TNF-α and the abundance of Proteinbacteria, Acidobacteria, and Bacteroidetes. These findings will provide further evidence of the anti-inflammatory effect of F. prausnitzii, which presents therapeutic potential for IBD treatment.

Attenuation of genotoxicity, oxidative stress, apoptosis and inflammation by rutin in benzo(a)pyrene exposed lungs of mice: plausible role of NF-κB, TNF-α and Bcl-2

2016 ◽  
Vol 13 (1) ◽  
Author(s):  
Ayaz Shahid ◽  
Rashid Ali ◽  
Nemat Ali ◽  
Syed Kazim Hasan ◽  
Summya Rashid ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biological Activities ◽  
Protective Effects ◽  
Oral Gavage ◽  
Carcinogenic Agent ◽  
Tnf Α ◽  
Lung Injuries ◽  
Ameliorative Effect ◽  
Apoptosis And Inflammation

Abstract: Benzo(a)pyrene [B(a)P] is an environmental contaminant and potential carcinogenic agent that causes lung injuries which leads to lung cancer. Rutin, a well-known flavonoid present in various natural sources, possesses biological activities such as anti-oxidative and anti-inflammatory properties. The aim of this study was to evaluate the protective effects of rutin against B(a)P-induced genotoxicity, oxidative stress, apoptosis and inflammation in Swiss albino mice.: Pretreatment of rutin was given by oral gavage at doses of 40 and 80 mg/kg body weight (b.wt.) for 7 days before the administration of a single oral dose of B(a)P (125 mg/kg b.wt.). The ameliorative effect of rutin on oxidative stress, apoptotic and inflammatory markers in lung tissues and genotoxicity was studied using an alkaline unwinding assay and DNA fragmentation.: B(a)P enhanced lipid peroxidation, xanthine oxidase, H: The findings of the present study supported the protective effect of rutin against B(a)P-induced lung toxicity and genotoxicity.

scholarly journals Protective Effect of Spirulina platensis Extract against Dextran-Sulfate-Sodium-Induced Ulcerative Colitis in Rats

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2309 ◽  
Author(s):  
Mohamed A. Morsy ◽  
Sumeet Gupta ◽  
Anroop B. Nair ◽  
Katharigatta N. Venugopala ◽  
Khaled Greish ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Drinking Water ◽  
Spirulina Platensis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Control Group ◽  
Protective Effects ◽  
Hydroalcoholic Extract ◽  
Tnf Α

Inflammatory bowel disease is a multifactorial inflammatory condition. This study aimed to test the protective effects of Spirulina platensis against ulcerative colitis (UC). UC was induced in thirty-six male Wistar rats by adding dextran sulfate sodium (DSS) to their drinking water, while a control group received only drinking water. UC rats were equally-divided into six groups that received a single oral daily dose of vehicle (DSS), sulfasalazine (SSZ, 50 mg/kg/day), chloroform or the hydroalcoholic extracts of Spirulina platensis (100 or 200 mg/kg/day) for 15 days, and then blood and colon samples were harvested for determination of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), erythrocyte sedimentation rate (ESR), myeloperoxidase (MPO), and histopathology. At the end of the study, compared to time-matched controls, UC rats showed increased TNF-α (1.64-fold), IL-6 (5.73-fold), ESR (3.18-fold), and MPO (1.61-fold), along with loss of body weight (24.73%) and disease activity index (1.767 ± 0.216 vs. 0 ± 0), p < 0.001. These effects were prevented by SSZ treatment (p < 0.001 vs. DSS). The hydroalcoholic extract of Spirulina platensis dose-dependently modulated all DSS-induced inflammatory changes. However, the chloroform extract significantly lowered only IL-6 and ESR, but not TNF-α or MPO levels. The protective effects of the hydroalcoholic extract of Spirulina platensis against experimental UC involved mitigation of DSS-induced inflammation.

scholarly journals Ghrelin Inhibits Intestinal Epithelial Cell Apoptosis Through the Unfolded Protein Response Pathway in Ulcerative Colitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Lin Zhang ◽  
Jian Cheng ◽  
Jie Shen ◽  
Sheng Wang ◽  
Chuanyong Guo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Unfolded Protein Response ◽  
Cell Apoptosis ◽  
Intestinal Epithelial ◽  
Trinitrobenzenesulfonic Acid ◽  
Unfolded Protein ◽  
Tnf Α ◽  
The Unfolded Protein Response ◽  
Protein Response ◽  
Upr Pathway

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that occurs in the lining of the rectum and colon. Apoptosis of the intestinal epithelial cells (IECs) is common in active UC patients. Ghrelin is reported to be downregulated in apoptosis of IECs induced by tumor necrosis factor-α (TNF-α). Therefore, we hypothesized that ghrelin might play an antiapoptotic role in UC progression, which was investigated using in vitro and in vivo studies. The TNF-α-treated Caco-2 cell model and mouse colitis model induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS) were established and employed. We found that ghrelin could inhibit the apoptosis of Caco-2 cells induced by TNF-α, which could be disturbed by [D-lys3]-GHRP-6, the antagonist of ghrelin receptor GHS-R1a. Similarly, in the DSS- and TNBS-induced mouse colitis models, ghrelin could also protect intestinal tissues from apoptosis in DSS- and TNBS-induced colitis depending on GHS-R1a. Furthermore, ghrelin modulated the unfolded protein response (UPR) pathway and regulated the expressions of caspase-3, BAX, and Bcl-2, which contributed to the inhibition of cell apoptosis. In conclusion, ghrelin protects IECs from apoptosis during the pathogenesis of colitis by regulating the UPR pathway.

Antioxidant activity of Gardenia jasminoides Ellis fruit extracts

2011 ◽  
Vol 128 (3) ◽  
pp. 697-703 ◽  
Author(s):  
Trishna Debnath ◽  
Pyo-Jam Park ◽  
Narayan Chandra Deb Nath ◽  
Nadira Binte Samad ◽  
Hee Won Park ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Fruit Extracts ◽  
Gardenia Jasminoides ◽  
Gardenia Jasminoides Ellis

scholarly journals Geniposide, a component of Gardenia jasminoides Ellis, inhibits NF-ĸB to attenuate LPS-induced injury in intestinal epithelial cells

2020 ◽  
Author(s):  
Yizhe Cui ◽  
Xinyue Qiao ◽  
Qiuju Wang ◽  
Rui Wu
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Intestinal Epithelial ◽  
Migration Ability ◽  
Gardenia Jasminoides ◽  
Tnf Α ◽  
Gardenia Jasminoides Ellis

Abstract Background: The nuclear factor-ĸB (NF-ĸB) transcriptional system is a major effector pathway involved in inflammatory responses. Previous studies found that a Gardenia decoction (GD) inhibited the expression of NF-κB in a lipopolysaccharide (LPS)-stimulated mouse intestinal injury model. Herein, we hypothesized that geniposide (GE), a component of Gardenia jasminoides Ellis, also exerts anti-inflammatory effects and inhibits NF-ĸB activity in LPS-induced intestinal epithelial cells (IEC-6). IEC-6 cells were stimulated with LPS, following which the effects of GE on NF-ĸB signaling in the IEC-6 cells were examined by western blotting to detect IĸB phosphorylation/degradation. The expression of NF-κB was determined by immunofluorescence assay (IFA). Enzyme-linked immunosorbent assay (ELISA) was used to detect the inhibitory effect of GE on the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) activated by LPS in IEC-6 cells. In addition, the migration ability of IEC-6 cells was observed by the scratch method. Results: These results showed that GE dose-dependently downregulated levels of the proinflammatory cytokines TNF-α, IL-6 and IL-1β that had been upregulated by LPS and suppressed the phosphorylation of IĸB and NF-ĸB induced by LPS. Our findings indicated that GE could reduce LPS-induced NF-ĸB signaling and proinflammatory expression in IEC-6 cells and significantly enhance the migration of IEC-6 cells. Moreover, GE inhibited the expression of NF-κB, nuclear transfer, and transcriptional activity in IEC-6 cells. Conclusion: GE could block the synthesis of inflammatory factors of IEC-6 cells by inhibiting activation of the IĸB/NF-κB signaling pathway induced by LPS.

Anti-TNF-α therapy in ulcerative colitis

2008 ◽  
Vol 149 (20) ◽  
pp. 921-927
Author(s):  
Péter László Lakatos ◽  
László Lakatos
Keyword(s):  
Ulcerative Colitis ◽  
Colitis Ulcerosa ◽  
Tnf Α

A colitis ulcerosa kezelését meghatározó legfontosabb tényezők a betegség kiterjedése és súlyossága. Az enyhe és középsúlyos betegek nagy többsége ma is a hagyományos gyógyszereket kapja (orális-topicalis 5-ASA, sulfasalazin). A hagyományos terápiára (szteroid, azathioprin, 5-ASA) rezisztens és a súlyos, akut colitis ulcerosa kezelése ugyanakkor nincs megoldva. Az újabb adatok alapján az infliximab indukciós vagy fenntartó kezelés formájában mindkét betegcsoportban hatékony kezelési alternatívát jelenthet, így az esetek egy részében elkerülhetővé válik a colectomia. Az összefoglalóban a szerzők colitis ulcerosában az anti-TNF-α-kezeléssel kapcsolatos eredményeket foglalták össze.

scholarly journals Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haidy A. Saleh ◽  
Eman Ramdan ◽  
Mohey M. Elmazar ◽  
Hassan M. E. Azzazy ◽  
Anwar Abdelnaser
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Raw 264.7 Cells ◽  
Inos Mrna ◽  
No Production ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Protective Effects ◽  
Tnf Α ◽  
Ifn Γ

AbstractDoxorubicin (DOX) chemotherapy is associated with the release of inflammatory cytokines from macrophages. This has been suggested to be, in part, due to DOX-mediated leakage of endotoxins from gut microflora, which activate Toll-like receptor 4 (TLR4) signaling in macrophages, causing severe inflammation. However, the direct function of DOX on macrophages is still unknown. In the present study, we tested the hypothesis that DOX alone is incapable of stimulating inflammatory response in macrophages. Then, we compared the anti-inflammatory effects of curcumin (CUR), resveratrol (RES) and sulforaphane (SFN) against lipopolysaccharide/interferon-gamma (LPS/IFN-γ)-mediated inflammation in the absence or presence of DOX. For this purpose, RAW 264.7 cells were stimulated with LPS/IFN-γ (10 ng/mL/10 U/mL) in the absence or presence of DOX (0.1 µM). Our results showed that DOX alone is incapable of stimulating an inflammatory response in RAW 264.7 macrophages. Furthermore, after 24 h of incubation with LPS/IFN-γ, a significant increase in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) mRNA levels was observed. Similarly, nitric oxide (NO) production and TNF-α and IL-6 protein levels were significantly upregulated. Moreover, in LPS/IFN-γ-treated macrophages, the microRNAs (miRNAs) miR-146a, miR-155, and miR-21 were significantly overexpressed. Interestingly, upon testing CUR, RES, and SFN against LPS/IFN-γ-mediated inflammation, only SFN was able to significantly reverse the LPS/IFN-γ-mediated induction of iNOS, TNF-α and IL-6 and attenuate miR-146a and miR-155 levels. In conclusion, SFN, at the transcriptional and posttranscriptional levels, exhibits potent immunomodulatory action against LPS/IFN-γ-stimulated macrophages, which may indicate SFN as a potential treatment for DOX-associated inflammation.

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