Damage to intestinal epithelial cells is present in obesity and other diseases because of inflammatory and oxidative processes. This damage compromises the gastrointestinal barrier, killing enterocytes, altering intestinal permeability, and eliciting abnormal immune responses that promote chronic inflammation. Recent evidence shows that spirulina is a potent natural agent with antioxidant and anti-inflammatory properties. Objectives: This study was conducted to evaluate the effect of spirulina aqueous extract (SPAE) on the alterations of the intestinal epithelium induced by lipid micelles (LMs) and/or inflammation induced by lipopolysaccharides (LPSs) in the Caco-2 cell line. Methods: In the current research, we assessed the protective actions of SPAE against cytotoxicity, oxidative stress, inflammation, and epithelial barrier perturbation by using an in vitro model, the intestinal Caco-2 cells, treated with LPSs and/or LMs. We also performed an in silico molecular docking analysis with spirulina’s bioactive compound, phycocyanobilin. Results: Our results showed that SPAE has no cytotoxic effect on Caco-2 cells. On the contrary, it improved cell viability and exhibited anti-inflammatory and antioxidant actions. SPAE also protected against endoplasmic reticulum stress and tight junction proteins, thus improving the epithelial barrier. The in silico study revealed a strong binding affinity of the phycocyanobilin compound with human SOD and NADPH oxidase and a good binding affinity towards COX-2 and iNOS. Conclusions: Taken together, these findings demonstrate the beneficial actions of SPAE on Caco-2 cells, suggesting it may be useful in preserving the epithelial intestinal barrier in human conditions involving oxidative stress and inflammation such as obesity.

Background and Objectives: Obesity is currently a major health problem due to fatty acid accumulation and excess intake of energy, which leads to an increase in oxidative stress, particularly in the liver. The main goal of this study is to evaluate the protective effects of spirulina (SP) against cafeteria diet (CD)-induced obesity, oxidative stress, and lipotoxicity in rats. Materials and Methods: The rats were divided into four groups and received daily treatments for eight weeks as follows: control group fed a standard diet (SD 360 g/d); cafeteria diet group (CD 360 g/d); spirulina group (SP 500 mg/kg); and CD + SP group (500 mg/kg, b.w., p.o.) according to body weight (b.w.) per oral (p.o.). Results: Our results show that treatment with a CD increased the weights of the body, liver, and abdominal fat. Additionally, severe hepatic alteration, disturbances in the metabolic parameters of serum, and lipotoxicity associated with oxidative stress in response to the CD-induced obesity were observed. However, SP treatment significantly reduced the liver alteration of CD feed and lipid profile disorder associated with obesity. Conclusions: Our findings suggest that spirulina has a marked potential therapeutic effect against obesity and mitigates disturbances in liver function parameters, histological alterations, and oxidative stress status.

The cafeteria diet (CD), designed as an experimental diet mimicking the obesogenic diet, may contribute to the pathogenesis of inflammatory bowel diseases (IBD). This study delves into the influence of spirulina (SP) on obesity associated with colitis in Wistar rats. The amino acids composition of SP was analyzed using HPLC-FLD. Animals were equally separated into eight groups, each containing seven animals and treated daily for eight weeks as follows: Control diet (SD), cafeteria diet (CD) group, CD + SP (500 mg/kg) and SD + SP. Ulcerative colitis was provoked by rectal injection of acetic acid (AA) (3 % v/v, 5 ml/kg b.w.) on the last day of treatment in the following groups: SD + AA, SD + AA + SP, CD + AA, and CD + AA + SP. Findings revealed that UC and/or CD increased the abdominal fat, weights gain, and colons. Moreover, severe colonic alteration, perturbations in the serum metabolic parameters associated with an oxidative stress state in the colonic mucosa, defined by overproduction of reactive oxygen species (ROS) and increased levels of plasma scavenging activity (PSA). Additionally, obesity exacerbated the severity of AA-induced UC promoting inflammation marked by the overexpression of pro-inflammatory cytokines. Significantly, treatment with SP provided notable protection against inflammation severity, reduced histopathological alterations, attenuated lipid peroxidation (MDA), and enhanced antioxidant enzyme activities (CAT, SOD, and GPX) along with non-enzymatic antioxidants (GSH and SH-G). Thus, the antioxidant effects and anti-inflammatory proprieties of SP could be attributed to its richness in amino acids, which could potentially mitigate inflammation severity in obese subjects suffering from ulcerative colitis. These results imply that SP hold promise as a therapeutic agent for managing of UC, particularly in individuals with concomitant obesity. Understanding SP's mechanisms of action may lead novel treatment strategies for inflammatory bowel diseases and hyperlipidemia in medical research.

Background and Objectives: Urtica dioica, a source of bioactive functional compounds, provides nutritional and gastrointestinal therapeutic benefits. This study attempted to investigate the prophylactic coloprotective action of an aqueous extract of Urtica dioica (AEUD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). Materials and Methods: Phenolic compounds, total sugar, and mineral levels were determined in AEUD. Then, AEUD at different doses (50, 100, and 200 mg/kg, BW, p.o.) and mesalazine (MESA) as a standard treatment (100 mg/kg, BW, p.o.) were given orally for 21 days. Acute colitis was induced by administering drinking water with 5% (w/v) DSS for 7 days. Body weight variation, fecal occult blood, and stool consistency were determined daily. The severity of colitis was graded according to colon length, disease activity index (DAI), histological evaluations, and biochemical alterations. Rats orally administered DSS regularly developed clinical and macroscopic signs of colitis. Results: Due to its richness in phenolic and flavonoid compounds (247.65 ± 2.69 mg EAG/g MS and 34.08 ± 0.53 mg EQt/g MS, respectively), AEUD markedly ameliorated DAI, ulcer scores, colon length shortening, colonic histopathological changes, and hematological and biochemical modifications. Taken together, AEUD treatment notably (p < 0.01) suppressed DSS-induced UC by reducing oxidative stress via lowering MDA/H₂O₂ production and stimulating the effect of enzyme antioxidants as well as attenuating inflammation by decreasing CRP levels by 79.5% between the DSS and DSS + AEUD-50 groups compared to the MESA group (75.6%). Conclusions: AEUD was sufficient to exert a coloprotective effect that might be influenced by its bioactive compounds’ anti-inflammatory and antioxidant capabilities.

Background and Objectives:Urticadioica, a source of bioactive functional compounds, provides nutritional and gastrointestinal therapeutic benefits.The recent study attempted to investigate the prophylactic coloprotective action of aqueous extract of Urticadioica (AEUD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). Materials and Methods: Phenolic compounds, total sugar, and mineral levels were determined in AEUD. Then, AEUD at different doses (50, 100, and 200 mg/kg, BW, p.o.) and Mesalazine (MESA), as a standard treatment (100 mg/kg, BW, p.o.), were given orally for 21 days. Acute colitis was induced by administering drinking water with 5% (w/v) DSS for 7 days. Body weight variation, fecal occult blood, and stool consistency were determined daily. The severity of colitis was graded by colon length, disease activity index (DAI), histological evaluations, and biochemical alterations. Rats orally administered with DSS regularly developed clinical and macroscopic signs of colitis.Results: Due to its richness in phenolic and flavonoid compounds (247.65±2.69 mg EAG/g MS and 34.08±0.53 mg EQt/g MS, respectively),AEUD markedly ameliorated DAI, ulcer scores, colon length shortening, colonic histopathological changes, and hematological and biochemical modifications. Taken together, AEUD-treatment suppressed notably (p< .01) DSS-induced UC by reducing oxidative stress via lowering MDA/H2O2 generation and stimulating effect of enzyme antioxidants as well as attenuating inflammation by decreasing CRP levels by 79.5% between DSS and DSS+AEUD-50 groups compared to MESA-group (75.6%).Conclusions: AEUD was sufficient to exert its coloprotectiveeffect which might be influenced by its bioactive compounds’ anti-inflammatory and antioxidant capabilities.

Obesity is associated with chronic intestinal inflammation, oxidative stress, and disruption of epithelial barrier integrity. Phycocyanin (PHY), a bioactive pigment from Spirulina platensis , is known for its antioxidant and anti‐inflammatory activities. This study was conducted to evaluate the protective effect of PHY on the disruption of the intestinal epithelium induced by repeated lipid micelles (LM) and/or inflammation induced by lipopolysaccharides (LPS) in the Caco‐2 cell line. Firstly, we evaluated the protective actions of PHY against cytotoxicity, oxidative stress imbalance, inflammatory response, and epithelial barrier alteration through an in vitro model, the intestinal Caco‐2 cells, treated with LPS and/or LM. We also conducted an in silico molecular docking with PHY. In vitro, PHY was not cytotoxic to Caco‐2 cells; instead, it improved cell viability, demonstrated antioxidant and inflammation‐suppressing effects, preserved tight junction organization, and protected against endoplasmic reticulum (ER) stress, thereby maintaining epithelial barrier integrity. In silico analysis revealed strong binding affinity of PHY to antioxidant enzymes (SOD, CAT) and favorable interactions with pro‐inflammatory cytokines (TNF‐α, IL‐6), supporting its regulatory potential. Taken together, these findings indicate that PHY protects Caco‐2 cells, preserving intestinal barrier integrity under oxidative and inflammatory stress, and may serve as a natural therapeutic candidate against obesity‐related gut dysfunction.