Obovatol attenuates LPS-induced memory impairments in mice via inhibition of NF-κB signaling pathway

Choi, Dong‐Young; Lee, Jae Woong; GuiHua, Lin; Lee, Yong Kyung; Lee, Yeon Hee; Choi, Im Seop; Han, Sang Bae; Cho, Jungsook; Kim, Young Hee; Kim, Ki Ho; Oh, Ki‐Wan; Hong, Jin Tae; Lee, Moon Soon

doi:10.1016/j.neuint.2011.11.005

Cited by 81 publications

(47 citation statements)

References 44 publications

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“…Additionally, post-extinction training administration of LPS did not affect consolidation of extinction memory. This is consistent with a previous study showing that LPS impaired training and probe sessions in the Morris water maze task (Choi et al, 2012). …”

Section: Discussionsupporting

confidence: 93%

Candesartan ameliorates impaired fear extinction induced by innate immune activation

Quiñones

Maldonado

Velázquez

et al. 2016

Brain, Behavior, and Immunity

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Patients with post-traumatic stress disorder (PTSD) tend to show signs of a relatively increased inflammatory state suggesting that activation of the immune system may contribute to the development of PTSD. In the present study, we tested whether activation of the innate immune system can disrupt acquisition or recall of auditory fear extinction using an animal model of PTSD. Male adolescent rats received auditory fear conditioning in context A. The next day, an intraperitoneal injection of lipopolysaccharide (LPS; 100 μg/kg) prior to auditory fear extinction in context B impaired acquisition and recall of extinction. LPS (100 μg/kg) given after extinction training did not impair extinction recall suggesting that LPS did not affect consolidation of extinction. In contrast to cued fear extinction, contextual fear extinction was not affected by prior injection of LPS (100 μg/kg). Although LPS also reduced locomotion, we could dissociate the effects of LPS on extinction and locomotion by using a lower dose of LPS (50 μg/kg) which impaired locomotion without affecting extinction. In addition, 15 hrs after an injection of 250 μg/kg LPS in adult rats, extinction learning and recall were impaired without affecting locomotion. A sub-chronic treatment with candesartan, an angiotensin II type 1 receptor blocker, prevented the LPS-induced impairment of extinction in adult rats. Our results demonstrate that activation of the innate immune system can disrupt auditory fear extinction in adolescent and adult animals. These findings also provide direction for clinical studies of novel treatments that modulate the innate immune system for stress-related disorders like PTSD.

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Section: Discussionsupporting

confidence: 93%

Candesartan ameliorates impaired fear extinction induced by innate immune activation

Quiñones

Maldonado

Velázquez

et al. 2016

Brain, Behavior, and Immunity

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“…Previous studies revealed that 4-O-methylhonokiol potently inhibited neuroinflammatory responses and was associated with cognitive enhancement in AD animal models. The antiinflammatory activity was mediated by diminishing NF-jB signaling pathway (Lee et al 2012a (Schuehly et al 2011). They suggest that the effects of the compound on CB 2 receptors are associated with anti-neuroinflammatory effects, since the receptors are primarily associated with a broad range of inflammatory processes (Gertsch & Anavi-Goffer 2012).…”

Section: Magnolia Extract 4-o-methylhonokiol and Obovatolmentioning

confidence: 99%

“…In particular, 4-O-methylhonokiol ameliorated memory impairment in several different animal models including a systemic LPS-induced dementia model (Lee et al 2012a), presenilin 2 mutant transgenic mice (Lee et al 2011a), and Tg2576 mice . Obovatol blocked Ab aggregation and enhanced learning and memory in Tg2576 mice by blocking neuroinflammatory responses and Ab production (Choi et al 2012a, b).…”

Section: Magnolia Extract 4-o-methylhonokiol and Obovatolmentioning

confidence: 99%

Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents

et al. 2015

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Alzheimer's disease (AD) is the most common form of dementia. It is characterized by beta-amyloid (Aβ) peptide fibrils, which are extracellular depositions of a specific protein, and is accompanied by extensive neuroinflammation. Various studies have demonstrated risk factors that can affect AD pathogenesis, and they include accumulation of Aβ, hyperphosphorylation of tau protein, and neuroinflammation. Among these detrimental factors, neuroinflammation has been highlighted by epidemiologic studies suggesting that use of anti-inflammatory drugs could significantly reduce the incidence of AD. Evidence suggests that astrocytes, microglia, and infiltrating immune cells from periphery might contribute to or modify the process of neuroinflammation and neurodegeneration in AD brains. In addition, recent data indicate that microRNAs may affect neuroinflammatory responses in the brain. This article focuses on supportive evidence that neuroinflammation plays a critical role in AD development. In addition, we depict putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment. We also discuss pathogenic mechanisms by which astrocytes, microglia, T cells and microRNA participate in AD and the neuroprotective mechanisms of anti-inflammatory drugs.

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“…Astrocytes show abnormal morphology and protein expression by perinatal hypothyroidism [24,37,38]. LPS exposure also affects the developing brain [5][6][7]. Thus, we initially hypothesized that LPS may further induce adverse effects under hypothyroid conditions and the signal pathway may be at least partly A. p38 MAPK inhibitor rescued LPS-induced T4-regulated D2 activity.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular proliferation, differentiation and migration are also affected [13,14]. Such abnormalities are also seen after perinatal LPS exposure [3][4][5][6][7][8].…”

Section: Semi-quantitative Rt-pcrmentioning

confidence: 99%

The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

Iwasaki

Shimokawa

et al. 2013

Endocr J

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Obovatol attenuates LPS-induced memory impairments in mice via inhibition of NF-κB signaling pathway

Cited by 81 publications

References 44 publications

Candesartan ameliorates impaired fear extinction induced by innate immune activation

Candesartan ameliorates impaired fear extinction induced by innate immune activation

Involvement of inflammation in Alzheimer’s disease pathogenesis and therapeutic potential of anti-inflammatory agents

The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

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