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Indian Journal of Pharmacology logoLink to Indian Journal of Pharmacology
. 2026 Jul 1;58(4):457–467. doi: 10.4103/ijp.ijp_1191_25

Rice bran extract ameliorates experimental colitis by modulating gut dysbiosis and toll-like receptor 4/nuclear factor kappa β signaling

Hagar M Shendy 1,2,✉, Omneya Galal 3, Walaa Wadie 1, Nourtan F Abdeltawab 4, Amr Helal 5, Mohamed T Khayyal 1, Sarah S Mohamed 1
PMCID: PMC13412436  PMID: 42583981

Abstract

OBJECTIVES:

Gut dysbiosis is widely recognized to serve as crucial role in the etiology of inflammatory bowel disease (IBD). This research evaluates the ability of a stabilized rice bran extract (RBE) to modulate positively microbial dysbiosis in an experimentally induced IBD model.

MATERIALS AND METHODS:

Rats were given 5% dextran sulfate sodium (DSS) in drinking water during a week to cause colitis. RBE was administered to the rats with a daily dosage of 100 mg/kg, 1 week before feeding them with DSS and continued during DSS treatment. Fecal samples were then collected to assess alterations in the chosen microbial phyla, while colon samples were processed for histological and biochemical assessment.

RESULTS:

The colonic expression of toll-like receptor 4 (TLR4), nuclear factor kappa β (NF-κB), tumor necrosis factor alpha, and interlukin-17 (IL-17) was significantly elevated when DSS induced colitis, resulting in significant histopathological damage and a decrease in the amount of IL-10. Furthermore, DSS caused the colonic tight junction (TJ) protiens mRNA expression to drop dramatically. All undesirable changes induced by DSS tended to be reversed by RBE. Moreover, RBE beneficially modulated the gut microbiota by restoring various bacteria to their normal levels.

CONCLUSIONS:

The current research demonstrated the potential protective effect of RBE against colonic inflammation through modulating microbiota dysbiosis, TJ protein dysfunction, and TLR4/NF-κB signaling.

Keywords: Colitis, DSS, dysbiosis, microbiota, rice bran, tight junction

Introduction

Inflammatory bowel disease (IBD) is mostly caused by gut microbiota. Where there is a noticeable decline in healthy gut microbiome, phyla like Firmicutes with a corresponding increase in Proteobacteria have been observed.[1] Chemically-induced colitis was also shown to lower the abundance of Firmicutes but to raise that of Proteobacteria and Actinobacteria.[2,3] It is therefore reasonable to assume that restoration of the disturbed microbiota balance may offer a promising therapeutic approach to treat IBD.

Rice bran extract (RBE) was found to have anti-inflammatory as well as antioxidant effects[4] in addition to a potential nutraceutical effect that could be of value for the avoidance of oxidative stress and mitochondrial disorders.[5] Tocopherols, tocotrienols, and oryzanols – a blend of ferulic acid esters of triterpene alcohol and phytosterols – are the primary constituents of rice bran. It has been demonstrated that an RBE-supplemented diet may help reduce inflammation linked to metabolic diseases.[6]

Despite the extensive investigation of rice bran as a dietary component, the effects of RBE on colonic inflammation and gut dysbiosis remain poorly defined. Notably, most previous studies have focused on its general anti-inflammatory or antioxidant actions, without clearly delineating its role in restoring gut microbial homeostasis during colitis. Indeed, published research has revealed conflicting results about the effectiveness of RBE in experimental colitis. While some authors showed that an aqueous suspension of RBE failed to ameliorate experimentally induced colitis,[7,8] others documented its ability to ameliorate it.[9] Similarly, the impact of RBE on gut microbiota composition is controversial; some reports indicated an increase in Enterobacteriaceae following RBE treatment in dextran sulfate sodium (DSS)-induced colitis,[8] whereas others showed a favorable modulation of gut microbial profiles, including a reduction in Enterobacteriaceae abundance.[10] Given these discrepancies, the current research designed to assess the effects of a stabilized RBE on gut dysbiosis and colonic inflammatory alterations in a DSS-induced colitis rat model.

Materials and Methods

Animals

Adult male Wistar rats that were developed in-house and weighed between 150 and 200 g each were acquired from the animal facility housing at Cairo University’s Faculty of Pharmacy. They were housed for 7 days at a temperature of 22°C ± 2°C with a 12-h light/dark cycle and constant humidity before being used in experiments. They were allowed free access to water and fed a normal pellet diet. The Ethical Committee for Animal Experimentation at Cairo University’s Faculty of Pharmacy authorized the study (Permit number: PT-3017).

Drugs and chemicals

Heat stabilized Egyptian RBE was provided from Health Tech. (Cairo, Egypt). The standardized amount of gamma-oryzanol in the extract was 2%. Prior to usage, the extract was diluted in 0.6% dimethyl sulfoxide (DMSO).[11,12,13] The source of DSS (molecular weight 37–40 kD) was TdB Consultancy in Uppsala, Sweden. The other compounds were the highest quality available for analysis.

Experimental design

Rats were randomly placed into the following four groups of eight rats each:

  • a) Normal group: rats were given 0.6% DMSO (RBE vehicle) orally for 14 days

  • b) Group that received RBE treatment: rats were given (100 mg/Kg) of RBE orally for 14 days[14]

  • c) DSS control group: rats drank water containing 5% (w/v) DSS for 7 days[15]

  • d) DSS/RBE treated group: After receiving RBE treatment for a week, rats were given DSS in their drinking water for the next week.

Rats were sacrificed by cervical dislocation under light anesthesia 1 day after receiving the final drug/vehicle treatment. The colons and caeca were completely removed. The colon length was calculated, then 10 cm removed and rinsed in ice-cold saline, decontaminated of any undesirable leftover tissue, dried up on filter paper, and also measured in weight. After that, the colon sample was split longitudinally into two segments: the first was homogenized in ice-cold phosphate-buffered saline to produce 10% homogenates and the other segment was fixed in 10% formalin for histological examination. A part of these homogenates was used for the determination of cytokine-related parameters using the enzyme-linked immunosorbent assay (ELISA) and the other Western blot analysis was used for assessing the expression of tight junction (TJ) proteins (occludin, claudin-1, and ZO-1).

Ceca were rapidly collected into plastic containers and sealed. Some of the feces were removed from them and used for the determination of total culturable fecal bacteria, while the rest of the fecal content was preserved at −20°C and later employed for microbial genomic DNA separation, a step toward determining the abundance of microbial phyla utilizing culture-independent techniques.

Determination of cytokine related parameters

Colon homogenate was tested for toll-like receptor 4 (TLR4), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-17, and IL-10 using the appropriate rat-specific ELISA kits bought from CUSABIO (Houston, USA; Cat. Nos. CSB-E15822r, CSB-E11987r, CSB-E07451r, and MB764911, respectively). In addition, NF-κB levels were assessed using a kit from MyBioSource (Catalog No. MBS287521). The entire technique was conducted in compliance with the manufacturer’s protocols, utilizing the biotin-labeled antibody sandwich principle.[16,17] Detection involved biotin-labeled antibodies applied at a 2-fold dilution, with the exception of IL-10, where test samples were pre-diluted at a ratio of 1:2 with sample dilution buffer. Colon homogenates were quantified for protein levels using a Bradford Protein Assay Kit (SK3041) that was supplied by BIOBASIC INC (Markham Ontario L3R8T4 Canada).

Determination of tight junction proteins expression

The amount of ZO-1, claudin-1, and occludin proteins was quantified, in compliance with the manufacturer’s guidelines, by using certain primary antibodies for Western blot technique against ZO-1, claudin-1, and occludin (Thermo Fisher Scientific, Cat. (61–7300), (71–7800) and (40–4700), respectively. Following protein transfer to membranes, nonspecific binding sites were blocked using Tris-buffered saline with Tween-20 (TBST; 20 mM Tris-HCl, pH 7.5, 150 mM NaCl, 0.1% Tween-20) supplemented with 3% bouvin serum albumin (BSA) for 1 h at the room temperature. Membranes were then incubated overnight at 4°C with the appropriate primary antibodies. After washing with TBST, membranes were incubated for 1 h at the room temperature with an Horseradish Peroxidase (HRP)-conjugated secondary antibody (goat antirabbit immunoglobulin G-HRP, Novus Biologicals). Protein bands were subsequently visualized and imaged utilizing stain-free blot technology and ChemiDoc TM imager.[18] After normalization of beta-actin protein expression, the data were reported in arbitrary values.

Determination of abundance of microbial phyla

For the determination of the relative abundance of the microbial phyla, both relative proportions of total culturable fecal bacteria and culture-independent methods were applied.

Determination of culturable bacteria

Samples of the fecal contents from the cecum were rapidly collected into plastic containers, sealed, and put on ice for the enumeration of microbial populations. 100 mg of mixed fecal contents were vortexed with 900 μL of sterile saline and tenfold serial dilutions (10−1–10−12) were made in sterile saline for aerobic and anaerobic bacterial enumeration. Different culture media plates of De Man, Rogosa and Sharpe agar, reinforced clostridia medium agar, Wilkins-Chalgren agar, MacConkey agar, Salmonella/Shigella agar, and nutrient agar also mannitol salt agar were inoculated with 0.01 mL of the samples. For each culture medium, 12 dilutions of the samples were incubated aerobically or anaerobically at 37°C for 24 or 48 h as appropriate for each culture medium. Following that, the bacteria were categorized as to genus level, based on colony appearance and fermentation end-product formation compared to appropriate controls.

Determination of microbial phyla using genomic DNA

As a first step in this regard, quantification of genomic DNA concentration in the samples had to be determined. This was achieved using a special DNA extraction kit to eliminate interference by any traces of DSS in the samples (Quick DNA fecal microbe prep kit, Zymo Research Corp., CA, USA), applying the instructions provided by the manufacturer. DNA levels were assessed by evaluating the absorbance at 260 nm using an Implen nanophotometer P-330 (Implen GmbH, Munich, Germany)

The intestinal microbiota was determined using specific primers that target 16S ribosomal ribonucleic acid (rRNA) gene of some microbial genera by Real Time-PCR. qPCR procedures were conducted using QuantiNova SYBR Green PCR Kit (Qiagen, Hilden, Germany) on a Rotor Gene real-time PCR machine (Qiagen, Hilden, Germany) as previously described by Mohamed et al.[19] Standard curves were then generated for Escherichia coli, Clostridium leptum, and Bifidobacterium bifidum applying the previously described procedure by Mohamed et al.[19]

The primer sequences targeting the 16s rRNA gene for the analyzed microbial phyla, along with their corresponding annealing temperatures,[20,21] are provided below in the Following Table.[19]

Microbial phyla 16srRNA Gene Primer sequence 5`–3` Annealing temperature (C°)
Firmicutes phylum ATG TGG TTT AAT TCG AAG CA 60
Actinobacteria phylum CGA GGC CTA TCA GCT TGT TG 57
Proteobacteria phylum CAT GAC GTT ACC CGC AGA AGA AG 63
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Histopathological examination of the colon

Slices (5 μm) of colonic tissue samples fixed in 10% formalin solution and embedded in Paraplast were then stained with hematoxylin and eosin and blindly evaluated with a high-definition imaging system. The histological damage was evaluated on a scale of 0 (normal) to 3 (severe) using the following five criteria:

Epithelial necrosis, inflammatory infiltration of the lamina propria, inflammatory infiltration of the submucosa, crypt dilation, and submucosal edema. The overall histology score for each rat was calculated by adding the scores of the five histological parameters. After that, the data were observed using a box plot.[15]

Statistical analysis

One-way analysis (analysis of variance) and Tukey’s multiple comparisons test were used to assess all of the data, except for the overall histology scores. The mean ± standard error of the mean (SEM) was then used to present the data. Overall histology scores were expressed as median and assessed by applying the Kruskal–Wallis test, afterward using Dunn’s test as a post hoc test. Graph Pad Prism software (GraphPad Prism Version[8.0.1](San Diego,CA,USA)) (version 8.0.1) was used for the statistical analysis, with P ≤ 0.05 as the significance threshold.

Results

The RBE group was evaluated concurrently with the other groups and exhibited biochemical and histological findings comparable to the normal control group, Accordingly, comparisons were made with respect to the normal control group.

Effect on body weight change, colon length, and colon weight

Animals with colitis observed an 80% decrease in body weight [Figure 1a], a result that RBE treatment prevented. In addition, colon length decreased by almost 30% as a result of DSS-induced colitis [Figure 1b]. However, the ratio of colon weight to colon length has increased [Figure 1c]. These changes were effectively mitigated by treatment with RBE.

Figure 1.

Figure 1

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Effect of rice bran extract on body weight change as well as colonic gross inflammatory change in rats with dextran sodium sulfate-induced colitis. (a) Body weight change (g), (b) colon length (cm), and (c) colon weight/colon length (g/cm). Data are expressed as means ± standard error of the mean (n = 8) and compared using one-way analysis of variance followed by Tukey’s post hoc test, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract

Effect on colonic inflammatory mediators

DSS caused a 2–3-fold increase in the colonic values of the pro-inflammatory mediators TNF-α and IL-17, as well as a 3–4-fold increase in the colonic values of TLR4 and NF-κB. These impacts were significantly lowered following RBE treatment [Figures 2, 3b and c]. Moreover, the expression of the anti-inflammatory marker IL-10 decreased by 44% when colitis was induced an effect that was also reversed following RBE treatment [Figure 3a].

Figure 2.

Figure 2

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Effect of rice bran extract on colonic levels of toll-like receptor 4 (TLR4) and nuclear factor kappa-β (NF-κB) in rats with dextran sodium sulfate-induced colitis. (a) Colonic TLR4 content, (b) colonic NF-κB level. Data are expressed as means ± standard error of the mean (n = 8) and compared using one-way analysis of variance followed by Tukey’s post hoc test, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract, TLR4: Toll like receptor 4, NF-κβ: Nuclear factor kappa-β

Figure 3.

Figure 3

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Effect of rice bran extract on pro- and anti-inflammatory cytokines levels in colonic tissue of rats with dextran sodium sulfate-induced colitis. (a) Interlukin-10 (IL-10), (b) IL-17, and (c) tumor necrosis factor alpha. Data are expressed as means ± standard error of the mean (n = 8) and compared using one-way analysis of variance followed by Tukey’s post hoc test, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract, IL: Interleukin, TNF-α: Tumor necrosis factor alpha

Effect on colonic tight junction protein expression

The degree of TJ protein expression namely claudin-1, occludin, and ZO-1 was markedly reduced in the colonic tissues of DSS-treated rats. Treatment with RBE significantly restored the colonic expression of claudin-1, occludin, and ZO-1 proteins through increasing their levels by 4-, 2-, and 3-fold, respectively, compared with the DSS group [Figure 4].

Figure 4.

Figure 4

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Effect of rice bran extract on colonic tight junction proteins expression in rats with dextran sodium sulfate-induced colitis. (a) Western blot bands, (b) Claudin-1, (c) Occludin and (d) ZO-1 protein expression measured by western blot technique. Data are expressed as means ± standard error of the mean (n = 3) and compared using one-way analysis of variance followed by Tukey’s post hoc test, **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract

Effect on colonic histopathological changes

Histological examination of colonic tissue slices from normal and RBE groups demonstrated normal colon wall morphological characteristics, including intact intestinal crypts with a large number of goblet cells and intact covering epithelium with a normal submucosa and an outer muscular surface [Figure 5a and b]. DSS control group showed marked disorganized morphology of intestinal mucosa, submucosa edema, severe loss of goblet cells, remarkable dysplastic changes of intestinal crypts, and hyperchromatic elongated nuclei [Figure 5c]. RBE treatment provided significant preservation against DSS-induced histological alterations [Figure 5d]. Moreover, DSS-induced colitis resulted in a significant elevation of the total histology score; this increase was effectively prevented by treatment with RBE [Figure 5e].

Figure 5.

Figure 5

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Effect of rice bran extract therapy on colonic histopathological changes in rat with dextran sodium sulphate (DSS)-induced colitis. (a-d) Representative hematoxylin and eosin photomicrographs of all experimental groups; Normal, RB, DSS, and DSS + RB groups. Magnifications: ×400. Black arrows demonstrate mature goblet cells while red arrows indicate Mild persistent records of mucosal inflammatory cells infiltrates. Stars demonstrate mild submucosal edema Arrowheads represent intestinal crypts lining epithelium bearing overcrowded, hyperchromatic elongated nuclei. (e) Total histology score, data are expressed as box plots of the median of at least six animals. * versus normal, # versus DSS (Kruskal–Wallis test followed by Dunn’s test as a post hoc test, P < 0.05). DSS: Dextran sulfate sodium, RBE: Rice bran extract

Effect on gut dysbiosis

With regard to the effect of DSS-induced colitis on the bacterial flora, it was found that colitis was characterized with a reduction in abundance of total aerobic and anaerobic bacteria. In addition, DSS induced a decrease in Gram-negative lactose fermenters as E. coli and Lactobacilli as well as Salmonella-shigella genus while inducing a decrease in Staphylococci. RBE administration corrected these abnormalities [Figure 6].

Figure 6.

Figure 6

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Effect of rice bran extract treatment on the growth of intestinal bacteria species. (a) Total aerobic bacterial counts, (b) Total anerobic bacterial counts, (c) Gram-negative lactose fermenters (Escherichia coli), (d) Lactobacilli, (e) Salmonella-shigella, and (f) Staphylococcus aureus. Data are expressed as means ± standard error of the mean (n = 8) and compared using one-way analysis of variance followed by Tukey’s post hoc test, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract

The population of Firmicutes and Actinobacteria phyla dramatically decreased in the intestine of DSS-induced colitis group, while Proteobacteria phylum was increased in the intestine as a consequence of DSS-induced colitis. RBE treatment guarded against these abnormalities [Figure 7].

Figure 7.

Figure 7

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Effect of rice bran extract on genomic DNA concentration of intestinal bacterial phyla. (a) Firmicutes phyla, (b) Actinobacteria, (c) Proteobacteria. Data are expressed as means ± standard error of the mean (n = 8) and compared using the one-way analysis of variance followed by Tukey’s post hoc test **P ≤ 0.01, ***P ≤ 0.001. DSS: Dextran sulfate sodium, RBE: Rice bran extract

Discussion

The current research evaluates the effectiveness of a stabilized RBE in modulating intestinal barrier disruption and gut dysbiosis induced by DSS in rats. RBE alleviated the induced colonic inflammatory changes, decreased the colonic level of pro-inflammatory cytokines (TNF-α and IL-17), also increased the colonic level of anti-inflammatory cytokine IL-10 by suppressing TLR4/NF-ĸB signaling pathway.

DSS administration resulted in marked body weight loss, colon shortening, colon edema, as well as histopathological inflammatory changes, an effect that was previously observed by several authors.[15,19,22,23,24] Treatment with RBE effectively ameliorated DSS caused body weight loss, colon shrinking, colon weight/colon length rise with a marked reduction of total histology score. Along the same lines, rice bran-supplemented diet ameliorated DSS-induced weight loss and colon length reduction.[9] Moreover, supplementation with enzyme-treated rice fiber or fermented rice bran showed promising effects in the animal models of colitis.[25,26]

The intestinal barrier serves as the primary boundary of defensive system against harmful bacteria and other exogenous toxins and it is critical for preventing colonic inflammation.[27] Intestinal TJ proteins form an apical junctional complex that blocks the intercellular gap and modulates selective paracellular permeability. In fact, altered TJ proteins expression and damaged intestinal barrier are reported in IBD patients.[28] In the present study, expression of proteins (ZO-1, occluding and claudin-1) was lowered in the colonic tissues of DSS rats, as compared to normal control, revealing a disrupted intestinal barrier. However, treatment with RBE enhanced the expression of TJ proteins and aided in the restoration of the intestinal barrier integrity. Rice bran supplementation was previously shown to enhance the expression of TJ proteins in the inflamed colonic mucosa.[29,30] Indeed, various compounds were previously shown to ameliorate DSS-induced colitis by improving intestinal barrier.[31,32]

The intestinal barrier serves as a mediator for the exchange of information between the commensal gut bacteria and the host’s immune system, thereby preserving the equilibrium of the gut environment.[33] Moreover, the intestinal microbiota achieves a state of balance among the intestinal membrane by overcoming pathogen colonization and inflammatory processes to maintain the intestinal integrity. The interplay between intestinal barriers and gut microbiota has been the focus of many IBD studies, showing that dysfunction of intestinal barrier leads to pathogen invasion and mucosal dysbiosis.[33,34] Dysbiosis has the potential to further disrupt the integrity of the intestinal barrier, as certain pathogens possess the ability to modify TJ molecules, thereby increasing the permeability of the intestines.[35]

The microbiota ecosystem composition in the DSS-induced colitis group diverged from that in the normal group. DSS reduced the proportion of Firmicutes that are present and Actinobacteria phyla even though increasing the abundance Proteobacteria phyla, an effect that align with the previous study of Mohamed et al.[19] Induction of colitis by DSS led to a marked increase in Lactobacillus and Staphyllococus genus (from Firmicutes phylum.), decrease in Actinobacteria phylum, as well as decrease in E. coli and Salmonella-shigella genus (from Proteobacteria phylum). Feces in the intestinal lumen may comprise near to 1 × 1011 bacteria per gram, with E. coli representing the most abundant species. Commensal E. coli decreased mortality and enhanced colitis healing process in IBD with DSS-induced colitis. E. coli has the ability to alleviate intestinal inflammation and damage epithelium.[36] Furthermore, an increase in harmful species as Enterococcus, staphylococus, shigella and salmonella might affect microbial populations as well as the intestinal mucosa in patients with IBD patients.[37,38]

Treatment with RBE modulated the DSS-induced changes in the bacteria’s proportions decreasing the growth of the pro-inflammatory bacteria Proteobacteria, whereas the levels of Actinobacteria and Firmicutes were increased. RBE significantly inhibited E. coli, Staphylococci, Salmonella, and Shigella species, pointing out the ability of RBE to mitigate microbial dysbiosis. In the same context, RBE was found to favorably alter the gut microbial composition reducing Enterobacteriaceae family.[10] On the other hand, Shibayama et al.[8] showed an increase in Bacteroides acidifaciens and Enterobacteriaceae with rice bran treatment in DSS mice. Contrary to these findings, other researchers have documented that rice bran did not exhibit any impact on the A high-fat diet induces alterations in the gut microbiome of obese rats. specifically at the phylum and genus levels.[39]

The pattern-recognition receptors, TLRs, primarily act as sensors of microbiota and are crucial for the development of inflammatory and immune reactions. TLRs are expressed by immunological cells, including B cells, macrophages, dendretic cells, and neutrophils. As well as non-immunological cells, like epithelial cells.[40] They exhibit direct recognition of ligands originating from commensal microbiota or pathogenic microbes. TLR4, the first identified TLR in mammalian system, pertains to its recognition of bacterial lipopolysaccharide specifically found in gram-negative bacteria. Upon activation of toll-like receptor-4, NF-κB pathway is stimulated, resulting in the generation of proinflammatory cytokines.[41] TLR4 expression is upregulated in intestinal epithelia of patients with active ulcerative colitis causing massive inflammatory cascades.[42,43] Along the same lines, DSS control animals showed intestinal dysbiosis with marked increase in colonic levels of Toll like receptor-4, NF-κ-B and TNF-α Administration of RBE reduced the DSS-induced elevation in TLR4, which might be related to gut microbiota regulation. This was associated with a decrease in NF-κB and TNF-α levels in colonic tissues.

The overproduction of pro-inflammatory cytokines has been extensively documented in IBD patients. TNF-α and IL-17 have been described as key molecules in IBD pathogenesis as they promote recruitment of inflammatory cells to mucosa of the intestine via enhancing synthesis of chemo-attractants and adhesion molecules.[44] T helper cell (Th) 17-related cytokine was found to be increased in mice that given DSS to induce colitis, with a marked drop in regulatory T cell (Treg)-related cytokine IL-10 levels, indicating a significant Treg/Th17 imbalance in colitis. This observation aligns with the current research findings, as the induction of colitis resulted in an elevation of TNF-α and interleukin-17 levels, while concurrently lowering interleukin-10 levels. However, it is evident that this disruption was effectively alleviated through the administration of RBE treatment, pointing out to its anti-inflammatory properties that were previously documented by several authors.[4,45] In fact, regulating the Treg/Th17 balance was considered as one of the anti-inflammatory mechanisms involved in colitis.[46]

Conclusions

The present study has shown the prospective safeguarding impact of a stabilized RBE in mitigating colonic inflammation by means of regulating dysbiosis in the gut microbiota and dysfunction of TJ proteins. RBE reduced pro-inflammatory cytokines (TNF-α and interlukin-17) and raised anti-inflammatory cytokine IL-10 via inhibiting the toll like receptor-4/NF-κ-B signaling pathway.

Author contribution

H. M.: Conceptualization and methodology. O. G: Conceptualization. W. W: Conceptualization, data curation and editing. N. F.: Conceptualization, methodology and data curation. A. H: Conceptualization. M. T.: Conceptualization data review and revising manuscript. S. S.: methodology, data curation and editing.

Data availability

The original information confirming this research will be made accessible on request.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.

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