Bupleurum chinense Polysaccharide Improves LPS-Induced Senescence of RAW264.7 Cells by Regulating the NF- κ B Signaling Pathway

Mengran Xu; Shengyang Sun; Junhong Ge; Ye Shen; Tan Li; Xin Sun

doi:10.1155/2020/7060812

Bupleurum chinense Polysaccharide Improves LPS-Induced Senescence of RAW264.7 Cells by Regulating the NF- κ B Signaling Pathway

Evid Based Complement Alternat Med. 2020 Dec 15:2020:7060812. doi: 10.1155/2020/7060812. eCollection 2020.

Authors

Mengran Xu^{1

2}, Shengyang Sun^{2

3}, Junhong Ge^{2

3}, Ye Shen^{2

3}, Tan Li^{2

3}, Xin Sun^{1

2}

Affiliations

¹ College of Pharmacy, Jilin Medical University, Jilin, China.
² Jilin Provincial Laboratory of Molecular Geriatrics, Jilin, China.
³ College of Medicine, Beihua University, Jilin, China.

Abstract

Macrophages are important inflammatory cells that play a vital role in inflamm-aging. Bupleurum chinense polysaccharide (BCP), an effective component of the Bupleurum chinense herb, exerts multiple beneficial pharmacological effects, such as improving immunity and antioxidant activity. However, the effects of BCP on macrophage-aging and inflamm-aging are yet to be established. In this study, we examined the effects of BCP on proliferation, inflammatory cytokines, β-galactosidase (SA-β-gal), senescence-associated heterochromatin foci (SAHF), reactive oxygen species (ROS), mitochondrial membrane potential, p53, p16, and p65/NF-κB signaling proteins in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. BCP significantly inhibited production of interleukin-1α (IL-1α), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), reduced the expression of SA-β-gal and formation of SAHF, as well as ROS level, and stabilized the mitochondrial membrane potential in RAW264.7 cells stimulated with LPS. Furthermore, BCP inhibited the expression of aging-related genes, p53 and p16, suppressed phosphorylation of p65 protein, and enhanced the expression of I-κBα protein through the NF-κB signaling pathway in LPS-stimulated RAW264.7 cells. Accordingly, we conclude that BCP effectively suppresses inflamm-aging by reducing inflammatory cytokine levels and oxidative stress production following activation of the NF-κB signaling pathway in RAW264.7 cells stimulated with LPS. Our collective findings support the utility of BCP as a novel pharmaceutical agent with potential anti-inflamm-aging effects.