Ginsenoside Rb1 ameliorates hippocampal neuroinflammation in rats after intracerebral hemorrhage by inactivating the TLR4/NF-kB pathway.

Purpose: This work elucidated the therapeutic effect and mechanism of ginsenoside Rb1 on intracerebral hemorrhage (ICH).

Methods: ICH rat models were treated by ginsenoside Rb1. Modified neurological deficit score, and Y-maze and Morris water-maze tests were performed on rats. Hippocampal neuronal damage was observed by Nissl staining. Rat primary astrocytes were exposed to ginsenoside Rb1, Hemin, and lipopolysaccharide (LPS). TNF-α, IL-1β, and IL-6 levels were assessed via enzyme-linked immunosorbent assay. TLR4/NF-kB pathway activity was appraised by Western blot. Immunofluorescence staining was for hippocampal glial fibrillary acidic protein (GFAP) expression and P65 protein location in hippocampus and astrocytes.

Results: In rats after ICH, ginsenoside Rb1 ameliorated neurological impairment and hippocampal neuronal damage; improved learning and memory ability; reduced brain water content; decreasedhippocampal TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and declined hippocampal GFAP expression. In rat primary astrocytes exposed to Hemin, ginsenoside Rb1 declined TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and hindered P65 protein entry into nucleus. However, these functions of ginsenoside Rb1 on the Hemin-induced astrocytes were abolished by LPS.

Conclusion: Ginsenoside Rb1 has promising future for clinical ICH treatment, which exerts therapeutic effect on ICH by ameliorating hippocampal neuroinflammation via inactivating the TLR4/NF-kB pathway.