Format

Send to

Choose Destination
Eur Rev Med Pharmacol Sci. 2019 Apr;23(8):3533-3541. doi: 10.26355/eurrev_201904_17722.

Probiotic administration of lactobacillus rhamnosus GR-1 attenuates atherosclerotic plaque formation in ApoE-/- mice fed with a high-fat diet.

Author information

1
First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, China. 51422503@qq.com.

Abstract

OBJECTIVE:

To investigate the effect of Lactobacillus rhamnosus GR-1 on atherosclerotic progression in apolipoprotein-E knockout (ApoE-/-) mice fed with a high-fat diet and the underlying mechanisms of its action.

MATERIALS AND METHODS:

Eight-week-old ApoE-/- mice were treated with Lactobacillus rhamnosus GR-1 daily for 12 weeks. ApoE-/- mice in the vehicle group and wild type (WT) mice were treated with normal saline. Serum lipid levels, histopathological analysis of the aorta, oxidative and inflammatory indexes and activation of the nuclear factor-kappa B (NF-κB) signaling pathway were examined.

RESULTS:

Compared to ApoE-/- mice in the vehicle group, no changes in body weight or serum lipid levels were found in ApoE-/- mice treated with Lactobacillus rhamnosus GR-1. However, the administration of GR-1 slowed down the development of atherosclerosis and reduced plaque formation. Additionally, GR-1 attenuated the development of oxidative stress and chronic inflammation in a dose-dependent manner in ApoE-/- mice fed a high-fat diet. Furthermore, in ApoE-/- mice treated with GR-1, GR-1 was demonstrated to have a role in inhibiting the translocation of NF-κB p65 from the cytoplasm to the nucleus and suppressing the degradation of IκB-α.

CONCLUSIONS:

We showed that the administration of GR-1 decreased atherosclerotic lesion size in ApoE-/- mice by reducing oxidative stress and inflammation. Additionally, the NF-κB signaling pathway might mediate these effects.

PMID:
31081110
DOI:
10.26355/eurrev_201904_17722
Free full text

Supplemental Content

Full text links

Icon for European Review for Medical and Pharmacological Sciences
Loading ...
Support Center