Esculentoside A suppresses Aβ_1–42-induced neuroinflammation by down-regulating MAPKs pathways in vivo

Abstract

Introduction:

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous studies have demonstrated that EsA exerts strong anti-inflammatory effects in peripheral immune inflammation. This study is to determine whether EsA is effective in inflammation-related neurodegenerative diseases, such as Alzheimer's disease (AD).

Methods:

Male C57BL/6(B6) mice were divided into three groups of six mice as follows: (1) control group; (2) AD model group (Aβ_1–42-induced AD mice with saline); (3) EsA group (Aβ_1–42-induced AD mice with EsA, 5 mg/kg/day, i.p. for 15 days). Behavioural testing was performed after 15 days of EsA treatment. Real time PCR and Western blot were used to assess the level of inflammation factors and mitogen-activated protein kinases (MAPKs). Immunostaining was used to determine the level of activated microglia and astrocyte.

Results:

The results showed that EsA attenuated memory deficits in Aβ_1–42-induced AD mice. Esculentoside A decreased the pro-inflammatory factors and microglia and astrocyte activation in the hippocampi of Aβ_1–42-induced AD mice. Moreover, Aβ_1–42 activated phosphorylation of ERK, JNK and p38 MAPKs in the hippocampi of mice in the AD model group, while EsA significantly decreased the phosphorylation levels.

Conclusion:

These findings indicate that EsA provides protective effects against neuroinflammation triggered by β-amyloid.

Keywords:

• Alzheimer's disease
• Beta-amyloid
• Esculentoside A
• Neuroinflammation
• MAPKs pathways