AI Article Synopsis

  • Kale is rich in bioactive compounds and may prevent inflammation and gut issues caused by a high-fat diet.
  • A study involving mice showed that those fed kale before exposure to a harmful substance (DSS) had less inflammation and maintained better gut integrity.
  • The results suggest that kale helps by reducing harmful bacteria and strengthening gut barriers, offering protection against inflammation.

Article Abstract

Kale ( var. acephala), a food rich in bioactive phytochemicals, prevents diet-induced inflammation and gut dysbiosis. We hypothesized that the phytochemicals protect against the lipopolysaccharide (LPS)-induced acute inflammation which results from gut dysbiosis and loss of gut barrier integrity. We designed this study to test the protective effects of the whole vegetable by feeding C57BL/6J mice a rodent high-fat diet supplemented with or without 4.5% kale (0.12 g per 30 g mouse) for 2 weeks before administering 3% dextran sulfate sodium (DSS) via drinking water. After one week, DSS increased the representation of proinflammatory LPS (P-LPS)-producing genera and in colon contents, reduced the representation of anti-inflammatory LPS (A-LPS)-producing taxa from , reduced the expression of tight junction proteins, increased serum LPS binding protein, upregulated molecular and histopathological markers of inflammation in the colon and shortened the colons. Mice fed kale for 2 weeks before the DSS regime had a significantly reduced representation of and and instead had increased and Gram-positive taxa and enhanced expression of tight junction proteins. Downstream positive effects of dietary kale were lack of granuloma in colon samples, no shortening of the colon and prevention of inflammation; the expression of F4/80, TLR4 and cytokines 1L-1b, IL-6, TNF-a and iNOS was not different from that of the control group. We conclude that through reducing the proliferation of P-LPS-producing bacteria and augmenting the integrity of the gut barrier, kale protects against DSS-induced inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10383939PMC
http://dx.doi.org/10.3390/nu15143222DOI Listing

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