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Publication : Kefir peptides alleviate particulate matter &lt;4 μm (PM<sub>4.0</sub>)-induced pulmonary inflammation by inhibiting the NF-κB pathway using luciferase transgenic mice.

First Author  Chen HL Year  2019
Journal  Sci Rep Volume  9
Issue  1 Pages  11529
PubMed ID  31395940 Mgi Jnum  J:285906
Mgi Id  MGI:6387725 Doi  10.1038/s41598-019-47872-4
Citation  Chen HL, et al. (2019) Kefir peptides alleviate particulate matter <4 mum (PM4.0)-induced pulmonary inflammation by inhibiting the NF-kappaB pathway using luciferase transgenic mice. Sci Rep 9(1):11529
abstractText  Kefir peptides, generated by kefir grain fermentation of milk proteins, showed positive antioxidant effects, lowered blood pressure and modulated the immune response. In this study, kefir peptide was evaluated regarding their anti-inflammatory effects on particulate matter <4 mum (PM4.0)-induced lung inflammation in NF-kappaB-luciferase(+/+) transgenic mice. The lungs of mice under 20 mg/kg or 10 mg/kg PM4.0 treatments, both increased significantly the generation of reactive oxygen species (ROS) and inflammatory cytokines; increased the protein expression levels of p-NF-kappaB, NLRP3, caspase-1, IL-1beta, TNF-alpha, IL-6, IL-4 and alpha-SMA. Thus, we choose the 10 mg/kg of PM4.0 for animal trials; the mice were assigned to four treatment groups, including control group (saline treatment), PM4.0 + Mock group (only PM4.0 administration), PM4.0 + KL group (PM4.0 + 150 mg/kg low-dose kefir peptide) and PM4.0 + KH group (PM4.0 + 500 mg/kg high-dose kefir peptide). Data showed that treatment with both doses of kefir peptides decreased the PM4.0-induced inflammatory cell infiltration and the expression of the inflammatory mediators IL-lbeta, IL-4 and TNF-alpha in lung tissue by inactivating NF-kappaB signaling. The oral administrations of kefir peptides decrease the PM4.0-induced lung inflammation process through the inhibition of NF-kappaB pathway in transgenic luciferase mice, proposing a new clinical application to particulate matter air pollution-induced pulmonary inflammation.
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