Protective effects of icariin on brain dysfunction induced by lipopolysaccharide in rats

Guo, Jinghong; Li, F.; Wu, Qin; Gong, Qihai; Lu, Yuan‐Fu; Shi, Jing‐Shan

doi:10.1016/j.phymed.2010.03.007

Cited by 77 publications

(51 citation statements)

References 23 publications

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“…An acute, intense inflammatory response triggers T1DM It has therefore been hypothesized that anti-inflammatory agents may be an effective clinical treatment for patients with T1DM. A number of in vivo and in vitro studies have confirmed the anti-inflammatory effect of icariin, including in the brain, heart, bones and airways (22,23,(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50). The present study demonstrated that icariin prevents viability loss in rat pancreatic β cells, as well as suppressing cytokine-induced NO production and apoptosis activation.…”

Section: Discussionsupporting

confidence: 77%

Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling

Zhong

2018

Exp Ther Med

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Abstract. The loss of insulin secretion in type I diabetes mellitus (T1DM) is caused by autoimmune-mediated destruction of insulin-producing pancreatic β-cells. Inflammatory cytokines and immune cell infiltration activate oxidative and endoplasmic reticulum (ER) stress, resulting in reduced β-cell viability. The current pharmacological agents used to control blood glucose have a limited effective duration and are accompanied by strong side effects. Blocking the inflammatory and immune responses that cause the β-cell damage has been investigated as a novel therapeutic approach to control T1DM. Icariin is a flavonoid component of Chinese medicinal herbs that has anti-inflammatory effects in vitro and in vivo. The results of the present study revealed that icariin abrogates the pro-apoptotic effect of inflammatory cytokines and significantly suppresses the activation of nuclear factor (NF)-κB in rat pancreatic β-cell lines. The present study may provide a basis for the potential use of icariin as a therapeutic agent for T1DM.

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Section: Discussionsupporting

confidence: 77%

Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling

Zhong

2018

Exp Ther Med

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“…The survival of hippocampal progenitors has been shown to decrease following co-culture with microglial cells activated by LPS (2), substantially preventing neuronal differentiation and significantly increasing glial differentiation (3). An LPS injection into the lateral ventricle has been shown to cause deficits in the ability of spatial learning as regards the Morris water maze test (4). Chronic neuroinflammation is a hallmark of several neurological disorders associated with cognitive loss and LPS-induced brain inflammation deteriorates hippocampusdependent cognitive deficits (5).…”

Section: Introductionmentioning

confidence: 99%

Treadmill and wheel exercise alleviate lipopolysaccharide-induced short-term memory impairment by enhancing neuronal maturation in rats

Kim

Park

et al. 2012

Molecular Medicine Reports

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Abstract. Lipopolysaccharide (LPS) is an endotoxin derived from Gram-negative bacteria, which induces brain inflammation. LPS-induced brain inflammation deteriorates hippocampus-dependent cognitive deficits. In the present study, we investigated the effects of forced treadmill exercise and voluntary wheel exercise on short-term memory in relation to neuronal maturation in LPS-induced brain inflammation of rats. Brain inflammation in rats was induced by an injection of LPS into the cerebral ventricle. Short-term memory was evaluated using a step-down avoidance task. Cell proliferation in the hippocampal dentate gyrus was determined by 5-bromo-2'-deoxyuridine (BrdU), a marker of new cells, immunohistochemistry. Western blot analysis for the determination of doublecortin (DCX), a marker of immature neurons and neuronal nuclear antigen (NeuN), a marker of mature neurons, was performed. In the present study, LPS-induced brain inflammation impaired short-term memory by increasing DCX expression and suppressing NeuN expression. These results suggest that LPS-induced brain inflammation disturbs neuronal maturation. The number of BrdU-positive cells in the hippocampal dentate gyrus was increased by LPS injection. This increase in the number of BrdU-positive cells can be ascribed to the increase in the number of of immature neurons following LPS injection. On the other hand, forced treadmill exercise and voluntary wheel exercise improved brain inflammation-induced short-term memory impairment by suppressing DCX expression and increasing NeuN expression, enhancing neuronal maturation. Forced treadmill exercise and voluntary wheel exercise showed similar efficacy. From these results, it can be inferred that forced treadmill exercise and voluntary wheel exercise may improve memory function deteriorated by brain inflammation.

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“…Learning and memory deficits in the rats were induced by bilateral intracranial injection (right and left side) of LPS, according to the procedures described previously (Guo et al 2010;Lim et al 2008). Fifty micrograms of LPS dissolved in 10-ml cerebrospinal fluid (CSF) (Sigma-Aldrich Co., St. Louis, MO, USA) was microinjected into the lateral ventricle of the rat brains in all lesion groups.…”

Section: Lesion Generation and Lps Administrationmentioning

confidence: 99%

“…Stained sections were randomly chosen from equal levels of serial sections along the rostralÁcaudal axis. The TNF-a-, IL-1b-, and COX-2-immunopositive cells were only counted when their densities reached a defined darkness above the background level (Guo et al 2010). Distinct brown spots for TNF-a, IL-1b, and COX-2 were observed in the cytoplasms and in the membranes of the cone-shaped cells of the hippocampus.…”

Section: Immunohistochemistry For Proinflammatory Markersmentioning

confidence: 99%