Neurological research · 2015
Esculentoside A suppresses Aβ(1-42)-induced neuroinflammation by down-regulating MAPKs pathways in vivo.
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Yang Hui, Wang Sulei, Yu Linjie, Zhu Xiaolei, Xu Yun
Аннотация
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.
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.