Baicalin Inhibits TLR2/4 Signaling Pathway in Rat Brain Following Permanent Cerebral Ischemia

Tu, Xian-kun; Yang, Wu; Shu, Shi; Chen, Ye; Wang, Chunhua; Chen, Chunmei; Chen, Zhe

doi:10.1007/s10753-010-9254-8

Cited by 81 publications

(58 citation statements)

References 28 publications

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“…The experimental results also showed that the neuroprotective and antiinflammatory role of baicalin in ischemic stroke might be associated with the inhibition of toll-like receptor 2/4 (TLR2/4) signaling pathway [12]. Similarly, baicalin is also considered to protect brain from cerebral ischemiareperfusion by down-regulating the expression of nucleotide-binding oligomerization domain protein 2 (NOD2) and TNF-a [18].…”

Section: Discussionmentioning

confidence: 97%

“…Recent studies from our laboratory have shown that baicalin reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis [11,12]. In the present study, we, for the first time, explored whether baicalin reduces ischemia-induced brain edema and BBB permeability, and further investigated the effect of baicalin on the expression of MMP-9 and occludin.…”

Section: Introductionmentioning

confidence: 88%

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Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Yang

Liang

et al. 2011

Neurochem Res

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Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic brain edema via disrupting the blood-brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability, then further investigated its potential mechanisms. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 and 12 h after the onset of MCAO. Neuronal damage, brain edema and BBB permeability were measured 24 h following MCAO. Expression of MMP-9 protein and mRNA were determined by western blot and RT-PCR, respectively. Expression of tight junction protein (TJP) occludin was detected by western blot. Neuronal damage, brain edema and BBB permeability were significantly reduced by baicalin administration following focal cerebral ischemia. Elevated expression of MMP-9 protein and mRNA were significantly down-regulated by baicalin administration. In addition, MCAO caused the decreased expression of occludin, which was significantly up-regulated by baicalin administration. Our study suggested that baicalin reduces MCAO-induced neuronal damage, brain edema and BBB permeability, which might be associated with the inhibition of MMP-9 expression and MMP-9-mediated occludin degradation.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 88%

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Yang

Liang

et al. 2011

Neurochem Res

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“…1), a flavonoid isolated from Scutellaria baicalensis is known to have multiple biological functions including anti-oxidant, anti-tumor, antiischemic, and anti-inflammatory properties (Jung et al 2008;Li-Weber 2009). The inhibitory effects of baicalin on inflammation are associated with the inhibition of NF-jB activation, as has been shown in various acute and chronic inflammation models, including severe acute pancreatitis (Xiping et al 2010), air embolism-induced acute lung injury ), cerebral ischemia (Tu et al 2010), and chronic obstructive pulmonary disease (Lixuan et al 2010). Further, in a previous study, we demonstrated that baicalin treatment suppresses the activation of NF-jB and related inflammatory genes in aging kidneys (Kim et al 2006).…”

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confidence: 99%

PPARγ activation by baicalin suppresses NF-κB-mediated inflammation in aged rat kidney

et al. 2011

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Baicalin, a herb-derived flavonoid compound, has beneficial activities, including the modulation of oxidative stress and inflammation. Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-activated transcription factor that plays an important role in regulating nuclear factor-κB (NF-κB)-induced age-related inflammation. We investigated the anti-inflammatory action of baicalin, which depends on its ability to activate PPARγ, and subsequently to suppress NF-κB. We examined baicalin-treated kidney tissue from 24-month-old Fischer 344 aged rats (10 or 20 mg/kg/day for 10 days) and baicalin-fed mice (10 mg/kg/day for 3 days) for in vivo investigations, and used endothelial YPEN-1 cells for in vitro studies. In the baicalin-fed aged rats, there was a marked enhancement of both nuclear protein levels and DNA binding activity of PPARγ, and a decreased expression of NF-κB target genes (VCAM-1, IL-1β, and IL-6) compared with non-baicalin-fed aged rats. Furthermore, to confirm the anti-inflammatory action of PPARγ activated by baicalin, we used lipopolysaccharide (LPS)-treated cells and mice. The results showed that baicalin induced PPARγ-selective activation in YPEN-1 cells, and that the effects of baicalin were blocked by the PPARγ receptor antagonist, GW9662. In addition, baicalin treatment prevented RS generation, NF-κB activation and the expression of pro-inflammatory genes, whereas it increased PPARγ expression in LPS-treated cells and mouse kidney. Our data suggest that baicalin-induced PPARγ expression reduced age-related inflammation through blocking pro-inflammatory NF-κB activation. These results indicate that baicalin is a novel PPARγ activator and that this agent may have the potential to minimize inflammation.

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“…Baicalin, an active ingredient originally isolated from the root of a Chinese herb Huangqin (S. baicalensis Georgi), has been frequently used as an antiinflammatory drug in TCM practice [12][13][14][15]. Our findings suggest that the anti-inflammatory properties of baicalin may result from the inhibition of IL-6, IL-8, and TNF-α expression via preventing signaling NF-κB pathway in HBE16 airway epithelial cells.…”

Section: Discussionmentioning

confidence: 69%

Baicalin Inhibits Lipopolysaccharide-Induced Inflammation Through Signaling NF-κB Pathway in HBE16 Airway Epithelial Cells

Dong

Zhong

Lu³

et al. 2015

Inflammation

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Baicalin, a flavonoid monomer derived from Scutellaria baicalensis called Huangqin in mandarin, is the main active ingredient contributing to S. baicalensis' efficacy. It is known in China that baicalin has potential therapeutic effects on inflammatory diseases. However, its anti-inflammatory mechanism has still not been fully interpreted. We aim to investigate the anti-inflammatory effect of baicalin on lipopolysaccharide (LPS)-induced inflammation in HBE16 airway epithelial cells and also to explore the underlying signaling mechanisms. The anti-inflammatory action of baicalin was evaluated in human airway epithelial cells HBE16 treated with LPS. Airway epithelial cells HBE16 were pretreated with a range of concentrations of baicalin for 30 min and then stimulated with 10 μg/ml LPS. The secretions of interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) in cell culture supernatants were quantified by enzyme-linked immunosorbent assay (ELISA). The messenger RNA (mRNA) expressions of IL-6, IL-8, and TNF-α were tested by quantitative real-time polymerase chain reaction (real-time RT-PCR). Furthermore, Western blotting was used to determine whether the signaling pathway NF-κB was involved in the anti-inflammatory action of baicalin. The inflammatory cell model was successfully built with 10 μg/ml LPS for 24 h in our in vitro experiments. Both the secretions and the mRNA expressions of IL-6, IL-8, and TNF-α were significantly inhibited by baicalin. Moreover, the expression levels of phospho-IKKα/β and phospho-NF-κB p65 were downregulated, and the phospho-IκB-α level was upregulated by baicalin. These findings suggest that the anti-inflammatory properties of baicalin may be resulted from the inhibition of IL-6, IL-8, and TNF-α expression via preventing signaling NF-κB pathway in HBE16 airway epithelial cells. In addition, this study provides evidence to understand the therapeutic effects of baicalin on inflammatory diseases in clinical practice.

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Baicalin Inhibits TLR2/4 Signaling Pathway in Rat Brain Following Permanent Cerebral Ischemia

Cited by 81 publications

References 28 publications

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

PPARγ activation by baicalin suppresses NF-κB-mediated inflammation in aged rat kidney

Baicalin Inhibits Lipopolysaccharide-Induced Inflammation Through Signaling NF-κB Pathway in HBE16 Airway Epithelial Cells

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