Gypenosides Attenuate Lipopolysaccharide‐Induced Neuroinflammation and Memory Impairment in Rats

Abstract

Neuroinflammation is deliberated a major factor in various neurodegenerative diseases. Gypenosides (GPS) have pharmacological properties with multiple beneficial effects including anti-inflammatory, antioxidative, and protective properties. In the present study, whether GPS could improve cognitive dysfunction and chronic inflammation caused by injecting lipopolysaccharide (LPS) in the hippocampus was investigated. Effects of GPS on inflammatory factors in the hippocampus and the downstream mechanisms of these effects were also examined. Induction of LPS into the lateral ventricle caused inflammatory reactions and memory impairment on the rats. Every day treatment of GPS (25, 50, and 100 mg/kg) for 21 consecutive days attenuated spatial recognition, discrimination, and memory deficits. GPS treatment significantly decreased proinflammatory mediators such as interleukin-6 (IL-6), interleukin-1β (IL-1β), and nuclear factor-kappaB (NF-κB) levels in the brain. Furthermore, GPS reduced LPS-induced elevated levels of inducible nitric oxide synthase (iNOS) and toll-like receptor 4 (TLR4) mRNA and inhibition of brain-derived neurotrophic factor (BDNF) mRNA level. Collectively, these results showed that GPS may improve cognitive function and provide a potential therapy for memory impairment caused by neuroinflammation. Based on these, GPS may be effective in inhibiting the progress of neurodegenerative diseases by improving memory functions due to its anti-inflammatory activities and appropriate modulation of NF-κB/iNOS/TLR4/BDNF.

Dietary Supplementation of the Antioxidant Curcumin Halts Systemic LPS-Induced Neuroinflammation-Associated Neurodegeneration and Memory/Synaptic Impairment via the JNK/NF-κB/Akt Signaling Pathway in Adult Rats

“…Moreover, according to recent studies, LPS given intraperitoneally can activate astrocytes and microglial cells, inducing the processes of astrogliosis and microgliosis, respectively. Activation of both astrocytes and microglia induces neurotoxicity, neuroinflammation, and the production of ROS by stimulating proinflammatory mediators [7, 12–16]. Badshah et al demonstrated the systemic administration of LPS to adult mice at a dose of 250 μ g/kg for 1 week-induced neuronal cell death by increasing the expression of caspase-3 and poly [ADP-ribose] polymerase 1 (PARP-1), triggering the mitochondrial apoptotic pathway [1].…”

Lipopolysaccharide and inflammatory cytokines levels decreased after sleeve gastrectomy in Chinese adults with obesity

“…Bariatric surgery promotes remission of diabetes mellitus and improves insulin resistance compared with medical intervention, but the mechanism is not very clear. It has been proposed that some potential mechanisms may be involved in the carbohydrate metabolism, including intestinal microflora metabolism [14], bile acid physiology [15] and a reduction in LPS level after surgery [5,6]. LPS, a component of the outer membrane of gramnegative bacteria, is formed by a phosphoglycolipid or lipid A that is covalently linked to a hydrophilic heteropolysaccharide [16].…”

“…LPS acts on target tissues such as adipose, skeletal muscle, and liver. These tissues have specific receptors which interact with LPS and induce the secretion of inflammatory cytokines and negatively regulate insulin signaling [5,6]. Two LPS-pathway proteins, including cluster of differentiation 14 (CD14) and LPSbinding protein (LBP), are widely used as indirect measures of response to the LPS endotoxin in numerous experimental studies [7].…”

Neuromodulatory Activity of Dietary Phenolics Derived from Corchorus olitorius L.

“…injection of 250 µg/kg/day LPS starting day 6, and CO control group received i.p. injection of 100 mg/kg/day Co for 12 consecutive days (Lee, Shim, & Lee, ).…”