Inhibitory Effects of Ginsenoside Rb1 on Neuroinflammation Following Systemic Lipopolysaccharide Treatment in Mice

Abstract

Ginsenoside Rb1 (GRb1) is a major ingredient of ginseng and has a wide range of neuroprotection effects. Neuroinflammation is a feature of neurodegenerative conditions and is characterized by microglia activation and the expression of major inflammatory mediators. The present study investigated the modulatory effect of GRb1 on microglia activation, the expression of pro-inflammatory cytokines and cyclooxygenase (COX)-2 in the brain induced by systemic lipopolysaccharide (LPS) treatment in C57BL/6 mice. Systemic LPS treatment induces immediate microglia activation in the brain. Based on this information, GRb1 was administered orally, at doses of 10 and 20 mg/kg, 1 h prior to the LPS (3 mg/kg, intraperitoneally) injection. At a dose of 20 mg/kg GRb1 attenuated Iba1 protein expression and morphological activation of microglia by LPS. GRb1 significantly reduced the upregulation of tumor necrosis factor-α, interleukin (IL)-1β and IL-6 mRNA in the brain tissue at 4 h after LPS injection. In addition, the expression of COX-2 mRNA and protein in the brain tissue were also attenuated at the 20 mg/kg dose of GRb1. These results indicate that GRb1 plays a modulatory role in microglia activation and neuroinflammation. This study shows that GRb1 attenuates microglia activation in the brain using an in vivo animal model.

Xueshuantong injection (lyophilized) combined with salvianolate lyophilized injection protects against focal cerebral ischemia/reperfusion injury in rats through attenuation of oxidative stress

“…Rosmarinic acid has significant neuroprotective effects during cerebral I/R injury, such as attenuated BBB breakdown, decreased infarct volume and reduced HMGB1 expression in ischemic brain tissue. Ginsenoside Rb1 weakens the activity of microglia and decreases the upregulation of brain tissue mRNA of TNF-α and interleukin-1 (IL-1), IL-β, and IL-6 in the brain induced by systemic lipopolysaccharide (LPS) treatment in C57BL/6 mice [50,51] . Ginsenoside Rg1 attenuates BBB disruption by downregulating the expression of aquaporin 4 induced via ischemic stroke in animals [52] .…”

Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

“…Rb1 attenuates microglial activation, reducing the expression of pro‐inflammatory cytokines associated with the immune response including tumor necrosis factor‐α (TNF‐α) and interleukin (IL)‐1β with lipopolysaccharides (LPS). However, the mechanism and significance of Rb1‐related neuroinflammation and cell death are largely obscure . Microglial activation and the associated production of pro‐inflammatory cytokines has been linked to neuronal death and several neurodegenerative disease states in clinical studies .…”

“…However, the mechanism and significance of Rb1-related neuroinflammation and cell death are largely obscure. 9 Microglial activation and the associated production of pro-inflammatory cytokines has been linked to neuronal death and several neurodegenerative disease states in clinical studies. 10 Bacterial meningitis also produces microglial activation and the release of inflammatory cytokines as well as microglial cell death due to infection.…”

Bridging Type 2 Diabetes and Alzheimer's Disease: Assembling the Puzzle Pieces in the Quest for the Molecules With Therapeutic and Preventive Potential

“…This compound promotes GLP‐1 release, thus enhancing glucose‐stimulated insulin secretion by β‐cells through the activation of cAMP/PKA/CREB signaling in vitro, which has been pointed out as a key mechanism involved in its antidiabetic activity . Moreover, it significantly attenuates neuroinflammation, Aβ‐induced neurotoxicity, and tau hyperphosphorylation in cortical neurons …”