Purslane (Portulacae oleracea L.) polysaccharide relieves cadmium-induced colonic impairments by restricting Cd accumulation and inhibiting inflammatory responses.

This study aimed to assess the protective effects of purslane polysaccharide (PP) on colonic impairments in mice exposed to cadmium (Cd). C57BL/6 mice were administered with PP (200-800 mg/kg/day) by gavage for 4 weeks after treatment with 100 mg·L-1 CdCl2. PP significantly reduced Cd accumulation in the colon tissue and promoted the excretion of Cd in the feces. PP could reduce the expression levels of inflammatory factors (tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6) and inhibit the activation of the TLR4/MyD88/NF-κB signaling pathway. In addition, the results of 16S rRNA analysis revealed that PP significantly increased the abundance of probiotics (Lactobacillus), while decreased the abundance of pathogenic bacteria (Lachnospiraceae_NK4A136_group). Following the augmentation of beneficial intestinal bacteria, the treatment with PP led to an increase in the levels of intestinal microbial metabolites, specifically short-chain fatty acids (SCFAs). The SCFAs are known for their anti-inflammatory properties, immune-regulatory effects, and promotion of intestinal barrier function. Additionally, the results suggested that PP effectively impeded the enterohepatic circulation by inhibiting the FXR-FGF15 axis in the intestines of Cd-exposed mice. In summary, PP mitigated the toxic effects of Cd by limiting its accumulation and suppressing inflammatory responses in colon.

Rice hull insoluble dietary fiber alleviated experimental colitis induced by low dose of dextran sulfate sodium in cadmium-exposed mice.

Cadmium (Cd), an important toxic environmental pollutant, can invade the gastrointestinal tract and induce the occurrence of gastrointestinal diseases. This study aimed to investigate the protective effect of rice hull insoluble dietary fiber (RHF) on Cd-promoted colitis induced by low dose of dextran sulfate sodium. Administration of RHF attenuated inflammation by limiting Cd accumulation and regulating intestinal immune homeostasis in colitis mice with Cd exposure. RHF could maintain the structure of the gut barrier by increasing mucin secretion and intestinal tight connectivity in mice. Subsequently, RHF repressed the colonic inflammation mediated by the TLR4/MyD88/NF-κB pathway, and inhibited the transcription regulation of inflammatory cytokines. Furthermore, RHF showed an enhancement of a variety of probiotics, such as Eubacterium and Faecalibaculum. RHF also inhibited the growth of pathogenic bacteria, including Erysipelatoclostridium, Helicobacter and Bacteroides. The growth of beneficial bacteria was also accompanied by reversing the decline in short-chain fatty acids, supporting the initial potentiality of RHF as a prebiotic in cases of damage by Cd exposure in colitis mice. Importantly, RHF also remained resistant to Cd toxicity in colitis mice when the gut microbiota was depleted by antibiotics. We suggest that RHF could be used as a novel dietary supplement strategy against Cd-exacerbated colitis.

Purslane (Portulacae oleracea L.) attenuates cadmium-induced hepatorenal and colonic damage in mice: Role of chelation, antioxidant and intestinal microecological regulation.

BACKGROUND: Cadmium (Cd) is a representative pernicious metal, which has high biological toxicity. Its precaution through dietary administration is considered an important strategy. Considering that Portulaca oleracea L. (Por.L) has antioxidant, anti-inflammatory and other high medicinal value, and purslane insoluble dietary fiber (PIDF) has good binding property to metal ions, they could be good methods for Cd-induced biotoxicity therapy. PURPOSE: To investigate the beneficial effects of Por.L or PIDF against Cd-induced subchronic toxicity and identify its underlying mechanisms. STUDY DESIGN AND METHODS: C57BL/6 male mice (n = 12) were received 100 mg l-1 CdCl2 in water for 8 weeks. Mice were divided into four groups: Control, Cd-treated, 8% Por.L + Cd, and 8% PIDF + Cd. Histological evaluation, inductively coupled plasma-mass spectrometry, western blotting analysis, quantitative real time-PCR, gas chromatography-mass spectrometry and 16S rDNA analysis were used in the study. RESULTS: Por.L treatment was able to inhibit inflammation and accumulation of Cd, enhance the activity of antioxidant enzymes, increase beneficial bacterial species of Akkermansia and Faecalibaculum and suppress the production of inflammatory cytokines in the colon, such as TNF-α, IL-6, IL-1ß and IFN-γ. PIDF mainly relieved the toxicity of Cd by increasing the production of short chain fatty acids with anti-inflammatory functions and repressing the liver and kidney inflammation mediated by the TLR4/ MyD88/NF-κB pathway. CONCLUSION: Our study has demonstrated that the antagonistic-Cd effects of Por.L might be mediated via chelation, antioxidation, regulation of intestinal microecology. Thus, our study provides a novel insight into Por.L as a promising function food for the anti-Cd biotoxicity. Por.L supplement could be considered as a potential coping strategy to alleviate hazardous effects in Cd-exposed humans.

Comparative Study on the Protective Effect of Chlorogenic Acid and 3-(3-Hydroxyphenyl) Propionic Acid against Cadmium-Induced Erythrocyte Cytotoxicity: In Vitro and In Vivo Evaluation.

The metabolism of chlorogenic acid (CGA) through the intestinal tract was studied. As cadmium is a well-known toxic heavy metal, this study was carried out to investigate the comparative protective effect of CGA and its representative intestinal metabolite (3-(3-hydroxyphenyl) propionic acid, HPPA) against Cd-induced erythrocyte cytotoxicity in vitro and in vivo. We found that CGA and its intestinal metabolite appreciably prevented erythrocyte hemolysis, osmotic fragility, and oxidative stress induced by Cd. Also, we found that HPPA had a stronger protective ability than CGA against Cd-induced erythrocyte injury in vivo, such as increasing the ratio of protein kinase C from 7.7% (CGA) to 12.0% (HPPA). Therefore, we hypothesized that CGA and its microbial metabolite had protective effects against Cd-induced erythrocyte damage via multiple actions including antioxidation and chelation. For humans, CGA supplementation may be favorable for avoiding Cd-induced biotoxicity.