Ginsenosid Rg1 verhindert PTBS-ähnliches Verhalten bei Mäusen. Durch die Förderung synaptischer Proteine wird Kir4.1 reduziert und TNF-α im Hippocampus
Zhengrong Zhang1 & Zhujin Song2 & Fengming Shen1 & Pan Xie1 & Juan Wang1 & Ai-song Zhu2 & Guoqi Zhu1
Received: 24 September 2020 / Accepted: 16 November 2020 / Published online: 19 November 2020
Abstract
Ginsenoside Rg1 is efficient to prevent or treat mental disorders. However, the mechanisms underlying the effects of ginsenoside Rg1 on post-traumatic stress disorder (PTSD) are still not known. In this study, single-prolonged stress (SPS) regime, as well as injection of lipopolysaccharide (LPS), was used to produce PTSD-like behaviors in C57 mice, and the effects of ginsenoside Rg1 (10, 20, 40 mg/kg/d, ip, for 14 days) on PTSD-like behaviors were evaluated. Our results showed that ginsenoside Rg1 promoted fear extinction and prevented depression-like behaviors in both LPS and SPS models. Importantly, ginsenoside Rg1 alleviated LPS- or SPS-stimulated expression of pro-inflammatory cytokines (IL-1βand TNF-α), activation of astrocytes and microglia, and reduction of hippocampal synaptic proteins (PSD95, Arc, and GluA1). Ginsenoside Rg1 also reduced the increase of hippocampal Kir4.1 and GluN2A induced by PTSD regime. Importantly, reducing hippocampal astroglial Kir4.1 expression promoted fear extinction and improved depression-like behaviors in LPS-treated mice. Additionally, intracerebroventricular injection of TNF-α caused an impairment of fear extinction and promoted Kir4.1 expression in the hippocampus. Together, our study reveals novel protective effects of ginsenoside Rg1 against PTSD-like behaviors in mice, likely via promoting synaptic proteins, reducing Kir4.1 and TNF-αin the hippocampus.
Keywords
Ginsenoside Rg1 . PTSD . Fear extinction . Kir4.1 . Inflammation . Synaptic
