Ursolic acid alleviates early brain injury after experimental subarachnoid hemorrhage by suppressing TLR4-mediated inflammatory pathway

Zhang, Tingting; Su, Jingyuan; Guo, Bingyu; Zhu, Tingzhun; Wang, Kaiwen; Liu, Xiaoming

doi:10.1016/j.intimp.2014.10.009

Cited by 46 publications

(36 citation statements)

References 23 publications

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“…Ersahin et al (2010), Zhang et al (2014b) have reported the involvement of neutrophil infiltration, represented by MPO activity, in oxidative brain injury after SAH. Several pro-inflammatory mediators, such as TNF-α, IL-1β, IL-6 and ICAM-1, participate in the development of diverse brain/ spinal cord injuries and of EBI and delayed vasospasm after SAH (Bastien and Lacroix, 2014;Chen et al, 2014a;Hong et al, 2012;Larysz-Brysz et al, 2012) and also mediate BBB disruption secondary to the SAH insult (Borowicz et al, 2003;Cohen et al, 1996;Ryuto et al, 1996;Sozen et al, 2009;Tzeng et al, 2013;Zhang et al, 2014aZhang et al, , 2014b. Therefore, neutrophil infiltration and the release of pro-inflammatory mediators are possible targets for the treatment of EBI after SAH.…”

Section: Discussionmentioning

confidence: 99%

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Tian

Guo

et al. 2015

Brain Research

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Section: Discussionmentioning

confidence: 99%

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Tian

Guo

et al. 2015

Brain Research

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“…Buchanan et al reported that TLR4 is expressed in various cell types in the CNS, including microglia cells, astrocytes, neurons, and cerebral vascular cells [10]. It has also been reported that tamoxifen, apigenin, melatonin and ursolic acid have neuroprotective effects in EBI following SAH by inhibiting TLR4/NF-κ B signaling pathway, which indicated that TLR4/NF-κ B pathway is involved in EBI following SAH [15,16,32,33]. In Ma et al's study, there is a biphasic change in TLR4 expression in both mRNA and protein: an initial peak (2-6 hours) and a sustained elevation (12-48 hours) in rats after SAH [12].…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Intervention Modulates Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats: Possible Involvement of TLR4/NF-κ B-Mediated Signaling Pathway

Líu

Yang

Pan

et al. 2016

Cell Physiol Biochem

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Background/Aims: Previous studies have proved that the activation of TLR4/NF-κ B signaling pathway is involved in inflammatory processes in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Hyperbaric oxygen (HBO) intervention has successfully been used to treat several animal models of tissue injury via its anti-inflammation property. This study was undertaken to investigate the influence of HBO administration on the TLR4/NF-κ B signaling pathway in rats at the early stage of SAH. Methods: Male Sprague-Dawley rats (n = 150) were randomly divided into 5 groups: the sham, the sham + 2.8 atmospheres absolute (ATA) HBO group, the SAH group, the SAH + 2.0ATA HBO group, the SAH + 2.8ATA HBO group. Each group (n = 30) was randomly subdivided into three subgroups that were examined at the following time points: 24 h, 48 h and 72 h post-injury. HBO (100% O2, 2.0ATA or 2.8ATA for 90mins) was initiated 12 h after injury. Neurological deficit, brain edema and blood-brain barrier (BBB) permeability were assessed to evaluate the development of EBI. The expressions of TLR4, NF-κ B and pro-inflammatory cytokines in the cortical were determined by real time polymerase chain reaction (RT-PCR), western blot, immunohistochemistry, or enzyme-linked immunosorbent assay (ELISA). Results: Our study showed that treatment with HBO significantly decreased the expressions of TLR4, NF-κ B and the downstream inflammatory agents, such as TNF-α, IL-6, IL-1β and ICAM-1, and also improved brain edema, blood-brain barrier permeability and neurologic function. Conclusions: These findings indicate that HBO treatment may result in abatement of the development of EBI after SAH, possibly through suppression of TLR4/NF-κ B signaling pathway.

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“…Ursolic acid (UA) is the anti-hepatitis active ingredient extracted from the Caprifoliaceae plant Sambucus chinensis. It is a pentacyclic triterpenoid extensively distributed in the nature (12). Typically, it exists in the free form or binds with sugar to form glycoside in plants like Sambucus chinensis, Fructus crataegus, Arbutus menziesii, Prunella vulgaris, glossy privet fruit, plantain herb, Incarvillea arguta, and oldenlandia diffusa (13,14).…”

Section: Ursolic Acid Alleviates Inflammation and Against Diabetes-inmentioning

confidence: 99%

Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway

Yan

et al. 2018

Mol Med Report

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Ursolic acid (UA) is a triterpenoid isolated from Chinese herbal medicine. It is extensively distributed in the plant kingdom in at least 63 Chinese herbal medicines of 26 families. UA has multiple bioactivities, including anti‑viral hepatitis, antitumor, anti‑oxidation, anti‑bacterium and anti‑inflammation. The aim of this in vitro study was to examine the effects of UA on diabetes‑induced nephropathy and its possible mechanism. In mice with diabetes‑induced nephropathy, UA increased the body weight, reduced kidney/body weight index, protected kidney cells, alleviated inflammation [tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 levels] and kidney cell damage. It was also indicated that UA suppressed Toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 and nuclear factor‑κB protein expression in mice with diabetes‑induced nephropathy. The inhibition of TLR4 increased the anti‑inflammation of UA on inflammation in rat with diabetes‑induced nephropathy through the TLR4 signaling pathway. In conclusion, UA alleviates inflammation and inhibits diabetes‑induced nephropathy through a TLR4‑mediated inflammatory pathway. The present findings indicated that UA may be a possible therapeutic agent against diabetic nephropathy.

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Ursolic acid alleviates early brain injury after experimental subarachnoid hemorrhage by suppressing TLR4-mediated inflammatory pathway

Cited by 46 publications

References 23 publications

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Hyperbaric Oxygen Intervention Modulates Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats: Possible Involvement of TLR4/NF-κ B-Mediated Signaling Pathway

Ursolic acid alleviates inflammation and against diabetes‑induced nephropathy through TLR4‑mediated inflammatory pathway

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