scholarly journals The Antioxidant and Anti-Inflammatory Effects of Quercus brantii Extract on TNBS-Induced Ulcerative Colitis in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Mahvash Alizade Naini ◽  
Shayan Mehrvarzi ◽  
Asal Zargari-Samadnejadi ◽  
Nader Tanideh ◽  
Mohammad Ghorbani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Body Weight Loss ◽  
Trinitrobenzene Sulfonic Acid ◽  
High Morbidity ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Sod Activity ◽  
Anti Inflammatory ◽  
Quercus Brantii

Objectives. Ulcerative colitis is a common subtype of persistent inflammatory bowel disease with high morbidity consequences. Despite unknown definite pathogenesis, multiple anti-inflammatory medications are used for its treatment. Traditionally, Quercus brantii (QB), mostly available in the Middle East, has been used for gastrointestinal disorders. Other beneficial effects associated with QB include reduction of oxidative stress, inflammations, homeostatic instability, and improvement in clinical conditions. Materials and Methods. This experimental study was designed to assess the possible therapeutic effects of QB on UC and compare its effects with those of sulfasalazine. Of the 70 Wistar rats clustered in seven groups, ten received only alcohols and sixty were confirmed to be suffering from trinitrobenzene sulfonic acid- (TNBS-) induced colitis. Four groups received different dosages of QB extract via oral and rectal routes, one received sulfasalazine, and the other remaining two groups received nothing. The effects of QB were evaluated by assessing macroscopic and histologic scoring, measuring inflammatory mediators, and determining oxidative stress markers. Results. Comparing to the untreated TNBS-induced control groups, QB-treated groups showed a dose- and route-dependent improvement comparable with sulfasalazine. Treating rats with QB reduced the microscopic and macroscopic damage, decreased TNF-α, IL-6, NO, MPO activity, and MDA content, increased superoxide dismutase (SOD) activity, and reduced body weight loss. Conclusions. Our data recommended the anti-inflammatory and antioxidant effects of QB extract in a dose-dependent manner.

scholarly journals Beneficial Effects of Celastrol on Immune Balance by Modulating Gut Microbiota in Dextran Sodium Sulfate-Induced Ulcerative Colitis

2021 ◽  
Author(s):  
Desheng Hu ◽  
Mingyue Li ◽  
Weina Guo ◽  
Yalan Dong ◽  
Wenzhu Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Protective Effect ◽  
Intestinal Permeability ◽  
Chronic Inflammatory Bowel Disease ◽  
Protective Mechanism ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Colonic Inflammation ◽  
Anti Inflammatory

Ulcerative colitis (UC) is a chronic inflammatory bowel disease caused by multi-factors including colonic inflammation and microbiota dysbiosis. Previous studies have indicated that Celastrol (CSR) has strong anti-inflammatory and immune-inhibitory effects. Here, we investigated the effects of CSR on colonic inflammation and the mucosal immunity in an experimental colitis model, and addressed the mechanism by which CSR preforms the protective effect. We characterized the therapeutic effects and the potential mechanism of CSR in treating UC using histological staining, intestinal permeability assay, cytokine assay, flow cytometry, fecal microbiota transplantation (FMT), 16S rRNA sequencing, untargeted metabolomics, and cell differentiation approaches. CSR administration significantly ameliorated DSS-induced colitis, as evidenced by the recovery of body weight and colon length, decreased disease activity index (DAI) score, as well as decreased intestinal permeability. CSR down-regulated the secretion of proinflammatory cytokines, upregulated the anti-inflammatory mediators, and improved the balances of Treg/Th1 and Treg/Th17 to maintain colonic immune homeostasis. However, the protective effects of CSR disappeared when the antibiotic cocktail was applied to deplete the gut microbiota, and the gut microbiota-mediated effect was confirmed by FMT. Furthermore, CSR treatment increased the gut microbiota diversity and composition, and raised the metabolic productions of pyruvate and adenosine, which probably involve in gut microbiota mediated protective effect. In conclusion, CSR ameliorates colonic inflammation in a gut microbiota-dependent manner. The underlying protective mechanism is associated with the rectified Treg/Th1 and Treg/Th17 balance, and increased pyruvate and adenosine production. The study provided the solid evidence that CSR might be a promising therapeutic drug for UC.

scholarly journals Polyphenolic Maqui Extract as a Potential Nutraceutical to Treat TNBS-Induced Crohn’s Disease by the Regulation of Antioxidant and Anti-Inflammatory Pathways

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1752
Author(s):  
Tamara Ortiz ◽  
Federico Argüelles-Arias ◽  
Matilde Illanes ◽  
Josefa-María García-Montes ◽  
Elena Talero ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Body Weight Loss ◽  
Trinitrobenzene Sulfonic Acid ◽  
Therapeutic Effects ◽  
Transmural Inflammation ◽  
Microscopic Damage ◽  
Anti Inflammatory

Nutraceuticals include a wide variety of bioactive compounds, such as polyphenols, which have been highlighted for their remarkable health benefits. Specially, maqui berries have shown great antioxidant activity and anti-inflammatory effects on some inflammatory diseases. The objectives of the present study were to explore the therapeutic effects of maqui berries on acute-phase inflammation in Crohn’s disease. Balb/c mice were exposed to 2,4,6-trinitrobenzene sulfonic acid (TNBS) via intracolonic administration. Polyphenolic maqui extract (Ach) was administered orally daily for 4 days after TNBS induction (Curative Group), and for 7 days prior to the TNBS induction until sacrifice (Preventive Group). Our results showed that both preventive and curative Ach administration inhibited body weight loss and colon shortening, and attenuated the macroscopic and microscopic damage signs, as well as significantly reducing transmural inflammation and boosting the recovery of the mucosal architecture and its muco-secretory function. Additionally, Ach promotes macrophage polarization to the M2 phenotype and was capable of down-regulating significantly the expression of inflammatory proteins COX-2 and iNOS, and at the same time it regulates the antioxidant Nrf-2/HO-1 pathway. In conclusion, this is the first study in which it is demonstrated that the properties of Ach as could be used as a preventive and curative treatment in Crohn’s disease.

scholarly journals Ethyl 2-Succinate-Anthraquinone Attenuates Inflammatory Response and Oxidative Stress via Regulating NLRP3 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Burong Feng ◽  
Xiuye Zhao ◽  
Wei Zhao ◽  
Huiwei Jiang ◽  
Zijing Ren ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Cell Activity ◽  
The Body ◽  
Alveolar Wall ◽  
Dependent Manner ◽  
Sod Activity ◽  
Concentration Dependent Manner ◽  
Anti Inflammatory

Aloe-emodin widely possesses antibacterial, anti-inflammatory, antioxidant, antiviral, and anti-infectious properties. This study investigated the effect of ethyl 2-succinate-anthraquinone (Luhui derivative, LHD) on inflammation. In vitro, a THP-1 macrophage inflammation model, made by 100 ng/ml phorbol-12-myristate-13-acetate (PMA) and 1 μg/ml LPS for 24 h, was constructed. The LHD group (6.25 μmol/L, 12.5 μmol/L, 25 μmol/L, 50 μmol/L) had no effect on THP-1 cell activity, and the expression of IL-6 mRNA was down-regulated in a concentration-dependent manner, of which the 25 μmol/L group had the best inhibitory effect. The migration of THP-1 macrophages induced by LPS was decreased by the LHD. Moreover, the LHD suppressed ROS fluorescence expression by inhibiting MDA expression and increasing SOD activity. In vivo, we revealed that the LHD, in different doses (6.25 mg/kg, 12.5 mg/kg, 25 mg/kg, 50 mg/kg), has a protective effect on stress physiological responses by assessing the body temperature of mice. Interestingly, acute lung injury (e.g., the structure of the alveoli disappeared and capillaries in the alveolar wall were dilated and congested) and liver damage (e.g., hepatocyte swelling, neutrophil infiltration, and hepatocyte apoptosis) were obviously improved at the same condition. Furthermore, we initially confirmed that the LHD can down-regulate the expression of NLRP3, IL-1β, and caspase-1 proteins, thereby mediating the NLRP3 inflammasome signaling pathway to produce anti-inflammatory effects. In conclusion, our results indicate that the LHD exerts anti-inflammatory activity via regulating the NLRP3 signaling pathway, inhibition of oxidative stress, and THP-1 macrophage migration.

scholarly journals Dental pulp stem cells overexpressing hepatocyte growth factor facilitate the repair of DSS-induced ulcerative colitis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ning Li ◽  
Yichi Zhang ◽  
Narayan Nepal ◽  
Guoqing Li ◽  
Ningning Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Body Weight ◽  
Stem Cell ◽  
Dental Pulp ◽  
The Other ◽  
Therapeutic Effects ◽  
Colon Injury ◽  
Treatment Groups ◽  
Hepatocyte Growth

Abstract Background Ulcerative colitis (UC) is a chronic and recurrent disease without satisfactory treatment strategies. Dental pulp stem cell (DPSC) transplantation has been proposed as a potential therapy for UC. This study aimed to investigate the therapeutic effects of the rat hepatocyte growth factor (HGF) gene transduced into DPSCs for UC. Methods The therapeutic effects of HGF-DPSCs transplanted intravenously into a rat model of UC induced by 5% dextran sulphate sodium (DSS) were compared with the other treatment groups (LV-HGF group, DPSCs group and GFP-DPSCs group). Immunofluorescence and immunohistochemistry were used to observe the localization and proliferation of HGF-DPSCs at the site of colon injury. The expression levels of inflammatory factors were detected by real-time quantitative PCR (RT-PCR) and western blotting. The oxidative stress markers were detected by ELISA. DAI scores and body weight changes were used to macroscopically evaluate the treatment of rats in each group. Results Immunofluorescence and immunohistochemistry assays showed that HGF-DPSCs homed to colon injury sites and colocalized with intestinal stem cell (ISC) markers (Bmi1, Musashi1 and Sox9) and significantly promoted protein expression (Bmi1, Musashi1, Sox9 and PCNA). Anti-inflammatory cytokine (TGF-β and IL-10) expression was the highest in the HGF-DPSCs group compared with the other treatment groups, while the expression of pro-inflammatory cytokines (TNF-α and INF-γ) was the lowest. Additionally, the oxidative stress response results showed that malondialdehyde (MDA) and myeloperoxidase (MPO) expression decreased while superoxide dismutase (SOD) expression increased, especially in the HGF-DPSCs group. The DAI scores showed a downward trend with time in the five treatment groups, whereas body weight increased, and the changes were most prominent in the HGF-DPSCs group. Conclusions The study indicated that HGF-DPSCs can alleviate injuries to the intestinal mucosa by transdifferentiating into ISC-like cells, promoting ISC-like cell proliferation, suppressing inflammatory responses and reducing oxidative stress damage, which provides new ideas for the clinical treatment of UC.

scholarly journals Role of Luteolin-Induced Apoptosis and Autophagy in Human Glioblastoma Cell Lines

Medicina ◽  
2021 ◽  
Vol 57 (9) ◽  
pp. 879 ◽  
Author(s):  
Hye-Sung Lee ◽  
Bong-Soo Park ◽  
Hae-Mi Kang ◽  
Jung-Han Kim ◽  
Sang-Hun Shin ◽  
...  
Keyword(s):  
Cell Lines ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Glioblastoma Cell ◽  
Related Factors ◽  
Green Pepper ◽  
Real Time Quantitative Pcr ◽  
Anti Inflammatory ◽  
Induced Apoptosis ◽  
Glioblastoma Cell Lines

Background and Objectives: Malignant glioblastoma (GBM) is caused by abnormal proliferation of glial cells, which are found in the brain. The therapeutic effects of surgical treatment, radiation therapy, and chemo-therapy against GBM are relatively poor compared with their effects against other tumors. Luteolin is abundant in peanut shells and is also found in herbs and other plants, such as thyme, green pepper, and celery. Luteolin is known to be effective against obesity and metabolic syndrome. The anti-inflammatory, and anti-cancer activities of luteolin have been investigated. Most studies have focused on the antioxidant and anti-inflammatory effects of luteolin, which is a natural flavonoid. However, the association between the induction of apoptosis by luteolin in GBM and autophagy has not yet been investigated. This study thus aimed to confirm the occurrence of luteolin-induced apoptosis and autophagy in GBM cells and to assess their relationship. Materials and Methods: A172 and U-373MG glioblastoma cell lines were used for this experiment. We confirmed the apoptosis effect of Luteolin on GBM cells using methods such as 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence, Flow cytometry (FACS) western blot, and real-time quantitative PCR (qPCR). Results: In the luteolin-treated A172 and U-373MG cells, cell viability decreased in a concentration- and time-dependent manner. In addition, in A172 and U-373MG cells treated with luteolin at concentrations greater than 100 μM, nuclear fragmentation, which is a typical morphological change characterizing apoptosis, as well as fragmentation of caspase-3 and Poly (ADP-ribose) polymerase (PARP), which are apoptosis-related factors, were observed. Autophagy was induced after treatment with at least 50 μM luteolin. Inhibition of autophagy using 3MA allowed for a low concentration of luteolin to more effectively induce apoptosis in A172 and U-373MG cells. Conclusions: Results showed that luteolin induces apoptosis and autophagy and that the luteolin-induced autophagy promotes cell survival. Therefore, an appropriate combination therapy involving luteolin and an autophagy inhibitor is expected to improve the prognosis of GBM treatment.

scholarly journals Dynamic Evaluation of Compound Ento-PB for the Repair of Mucosal Ulcer in Dogs With Acetic Acid-induced Experimental Colitis 

2020 ◽  
Author(s):  
Jin-hu Chen ◽  
Jian-ting Zhao ◽  
Zheng-yong Yu ◽  
Yi-hao Che ◽  
Yu-jia Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Acetic Acid ◽  
Inflammatory Cytokines ◽  
Mucosal Healing ◽  
Dynamic Monitoring ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Expression Levels ◽  
Cox 2 ◽  
Anti Inflammatory

Abstract Background: Mucosal inflammation and ulcer play important roles in the pathogenesis of ulcerative colitis. As as traditional Chinese medicine compound composed of Periplaneta americana and Taraxacum mongolicum, Ento-PB is always prescribed for the treatment of ulcer and inflammatory diseases. As for the significant role of P. americana in terms of promoting mucosal healing, the compatibility of the anti-inflammatory drug T. mongolicum may enable Ento-PB to simultaneously play anti-inflammatory and promote mucosal healing effects on the treatment of UC. Therefore, this study aimed to evaluate the therapeutic potential and possible mechanism of Ento-PB for UC by establishing an acetic acid-induced colitis model in dogs.Methods: Preliminary identification to the chemical components of compound Ento-PB was carried out through high performance liquid chromatography. A cross-bred dogs model of acetic acid-induced ulcerative colitis was established to evaluate the efficacy of compound Ento-PB. The expression levels of inflammatory cytokines C-reactive protein (CRP), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10) in plasma were measured by carrying out enzyme-linked immunosorbent assay (ELISA).Results: With the extension of treatment time, Ento-PB could effectively improve clinical symptoms of UC cross-bred dogs. Colonoscopy displayed that mucosal redness, swelling and congestion decreased gradually, and obviously repaired after mucosal injury. The intestinal texture was gradually clear, and the colonoscopy score gradually reduced. Histopathological examination revealed that the structure of colon was restored significantly, the infiltration of inflammatory cells was reduced, and the histological score was remarkably reduced. At the same time, the results of dynamic monitoring of inflammatory cytokines in plasma proved that Ento-PB can gradually down-regulate the activity of CRP, iNOS and COX-2, reduce the expression levels of inflammatory cytokines TNF-α and IL-1β, and gradually restore anti-inflammatory and the expression level of cytokine IL-10.Conclusions: Ento-PB reduces the level of pro-inflammatory cytokines in a dose- and time-dependent manner and inflammation, improves colon tissue lesions and the repair of intestinal mucosa after injury, and effectively increases acetic acid-induced colon inflammation in UC cross-bred dogs.

Abstract 16009: Y RNA Fragments Enriched in Exosomes From Cardiosphere-derived Cells Mediate Cardioprotection and Macrophage Polarization

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Linda Cambier ◽  
Geoffrey de Couto ◽  
Ahmed Ibrahim ◽  
Eduardo Marbán
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Noncoding Rna ◽  
Neonatal Rat ◽  
Target Cells ◽  
Therapeutic Effects ◽  
Data Set ◽  
Rna Content ◽  
Rna Fragments ◽  
Anti Inflammatory

Background: Exosomes secreted by cardiosphere-derived cells (CDCs) are critical agents of regeneration and cardioprotection following ischemic injury, mediating the beneficial therapeutic effects of CDCs. Transfer of exosomal RNA to target cells is important for bioactivity. Objective: We sought to determine the RNA content of CDCs-secreted exosomes (CDC-exo), and to assess the contributions of selected small non-coding RNAs to the therapeutic efficacy of CDC-exo. Methods: Using next-generation sequencing (Illumina), we characterized the RNA content of CDC-exo. By direct transfection of fluorescently-labelled oligoribonucleotides, we delivered and tracked selected RNA fragments that are highly enriched in CDC-exo. In order to examine potential cytoprotective effects, neonatal rat ventricular myocytes (NRVMs) were pretreated with each of these fragments or a scrambled control fragment prior to H2O2-induced oxidative stress. Effects on gene expression were assessed by transfection of the fragments into bone marrow-derived macrophages. Results: Several noncoding RNA species were present in CDC-exo. Among these, Y RNAs (either whole or in fragments of the 5’ end) constituted 18% of all hits. From this data set, we selected two highly-enriched Y RNA fragments. Both fragments localized to the cytoplasm of CDC, NRVM and macrophages, and conferred augmented resistance to oxidative stress of NRVM (64.25±31.13% viability vs. 44±26.85%; p=0.06). Additionally, macrophages transfected with Y fragments exhibit rapid, robust polarization to a distinctive gene expression profile notable for upregulation of IL-10 (83.07 vs. 0.59 fold; p<0.0001), an anti-inflammatory cytokine. Conclusions: Here, we demonstrated that abundant noncoding RNA components of CDC-exo, Y RNA fragments, are bioactive components of CDC-exo. Two distinct fragments confer cardioprotection and also induce a strong anti-inflammatory response in macrophages. Although several components of the CDC-exo payload (including miRNA) contribute to functional efficacy, the present findings demonstrate the capacity of Y RNA fragments, an RNA species of previously-unknown function, to elicit therapeutic effects in vitro.

Antioxidative effect of DJ-1 is enhanced in NG108-15 cells by DPMQ induced copper influx

2020 ◽  
Author(s):  
Ting-Yu Chin ◽  
Che-Chuan Wang ◽  
Kuo-Hsing Ma ◽  
Chia-Wei Kuo ◽  
Ming-Kuan Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Nuclear Translocation ◽  
Cellular Level ◽  
Dependent Manner ◽  
Copper Binding ◽  
Antioxidative Effect ◽  
Sod Activity ◽  
Redox Imbalance ◽  
Endogenous Proteins

Disruption of copper homeostasis is closely involved in neurodegenerative disorders. This study examined whether a hybrid copper binding compound, (E)-2-(4-(dimethylamino)phenylimino)methyl)quinolin-8-ol (DPMQ), is able to protect NG108-15 cells against oxidative stress. we found that treatment of cells with rotenone or hydrogen peroxide increased cellular oxidative stress and resulted in mitochondrial dysfunction and apoptosis. The cellular levels of Nrf2 and the Cu2+ chaperone DJ-1 were also decreased. These oxidative detrimental effects were all inhibited when cells were co-treated with DPMQ. DPMQ increased cellular Cu2+ content, DJ-1 protein level, superoxide dismutase (SOD) activity and Nrf2 nuclear translocation under basal state. The activity of SOD decreased under redox imbalance and this decrease was blocked by DPMQ treatment, while the protein level of SOD1 remained unaltered regardless of the oxidative stress and DPMQ treatment. Using endogenous proteins, co-immunoprecipitation showed that DJ-1 bound with SOD1 and Nrf2 individually. The amount of Nrf2, bound to DJ-1, consistently reflected its cellular level, while the amount of SOD1, bound to DJ-1, was potentiated by DPMQ, being greater in basal state than under redox imbalance. Simultaneous inclusion of non-permeable Cu2+ chelator tetrathiomolybdate or triethylenetetramine during DPMQ treatment blocked all aforementioned effects of DPMQ, showing that the dependency of the effect of DPMQ on extracellular Cu2+. In addition, silencing of DJ-1 blocked the protection of DPMQ against oxidative stress. Taken all together, our results suggest that DPMQ stabilizes DJ-1 in a Cu2+ dependent manner, which then brings about SOD1 activation and Nrf2 nuclear translocation; these together alleviate cellular oxidative stress.

scholarly journals P049 A new preclinical rationale for first-line therapy of ulcerative colitis

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S157-S157
Author(s):  
H Thorlacius ◽  
A Bjoerk ◽  
Ö Nordle ◽  
G Hedlund
Keyword(s):  
Ulcerative Colitis ◽  
Activity Index ◽  
Body Weight Loss ◽  
Disease Activity Index ◽  
Therapeutic Effects ◽  
Aminosalicylic Acid ◽  
First Line ◽  
First Line Therapy ◽  
Line Therapy ◽  
Chronic Inflammatory Condition

Abstract Background Ulcerative colitis (UC) is a chronic inflammatory condition with no known medical cure. 5-Aminosalicylic acid (5-ASA [mesalazine]) represents the cornerstone of first-line therapy for mild-to-moderate UC. Sulfasalazine (SASP) is the original agent in this class of drugs. Meta-analyses of patients with mild-to-moderately active UC comparing 5-ASA to placebo showed 5-ASA to be significantly superior to placebo. However, about two-thirds of patients treated with 5-ASA fail to enter clinical remission. It is therefore most important to identify strategies to accelerate and maximise the therapeutic effects of 5-ASA. Therapeutic intervention against NFκB activation is a useful strategy for treatment of UC. The 4-alkanoylaminobenzamide PM0503 inhibits the breakdown of the NFκB inhibitor IκBβ, and SASP/5-ASA inhibits the breakdown of IκBα. This elicited a hypothesis of a possible synergistic action and converging effect on NFκB signalling. In the present study, we investigated the effect of combining SASP/5-ASA with PM0503 in experimental colitis. Methods SASP and PM0503 alone or in combination were administered for 5 days to Balb/c mice with colitis triggered by 5% dextran sulphate sodium (DSS). Blood in the stool, stool consistency and body weight loss were evaluated daily on a 0–4 point scale. The disease activity index (DAI) was calculated by summarising the total score of these three parameters. Results Addition of 5% DSS in the drinking water for 5 days produced reproducible symptoms of colitis. PM0503 was shown to inhibit DSS induced colitis by reducing mean DAI at day 5 from 6.9 in controls to 1.7 (a 75% decrease). Mean DAI recorded with SASP treatment at optimal doses in the same series of experiments was 4.4 (a 36% decrease). Furthermore, and most important, lower doses of PM0503 acted synergistically with SASP in ameliorating DSS-induced disease severity. The combination of PM0503 and SASP using suboptimal doses having minimal beneficial effects as monotherapies, showed more than 50% disease inhibition at day 5. In addition, no toxicity was observed with PM0503 alone or in combination with SASP. Conclusion Our findings offer a preclinical rationale for simultaneous coadministration of PM0503 and a 5-ASA agent such as SASP or 5-ASA as first-line treatment for patients with UC.

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