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BMC Complement Altern Med. 2015 Dec 15;15:434. doi: 10.1186/s12906-015-0958-z.

Ashwagandha attenuates TNF-α- and LPS-induced NF-κB activation and CCL2 and CCL5 gene expression in NRK-52E cells.

Author information

1
Department of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, MA 415 Medical Sciences Building, One Hospital Drive, 65212, Columbia, MO, USA.
2
Department of Biochemistry, University of Missouri, Columbia, USA.
3
Division of Animal Sciences, University of Missouri, Columbia, USA.
4
Department of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, MA 415 Medical Sciences Building, One Hospital Drive, 65212, Columbia, MO, USA. parrishar@health.missouri.edu.

Abstract

BACKGROUND:

The aging kidney is marked by a chronic inflammation, which may exacerbate the progression of renal dysfunction, as well as increase the susceptibility to acute injury. The identification of strategies to alleviate inflammation may have translational impact to attenuate kidney disease.

METHODS:

We tested the potential of ashwaganda, sutherlandia and elderberry on tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) induced chemokine (CCL2 and CCL5) expression in vitro.

RESULTS:

Elderberry water-soluble extract (WSE) was pro-inflammatory, while sutherlandia WSE only partially attenuated the TNF-α-induced changes in CCL5. However, ashwaganda WSE completely prevented TNF-α-induced increases in CCL5, while attenuating the increase in CCL2 expression and NF-κB activation. The same pattern of ashwagandha protection was seen using LPS as the pro-inflammatory stimuli.

CONCLUSIONS:

Taken together, these results demonstrate the ashwaganda WSE as a valid candidate for evaluation of therapeutic potential for the treatment of chronic renal dysfunction.

PMID:
26667305
PMCID:
PMC4678649
DOI:
10.1186/s12906-015-0958-z
[Indexed for MEDLINE]
Free PMC Article

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