Effect of Praeruptorin C on 3-nitropropionic acid induced Huntington’s disease-like symptoms in mice

Wang, Lu; Wang, Jing; Yang, Le; Zhou, Shimeng; Guan, Shao-yu; Yang, Liu-kun; Shi, Qingqing; Zhao, Ming; Yang, Qi

doi:10.1016/j.biopha.2016.11.111

Cited by 44 publications

(33 citation statements)

References 41 publications

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“…Levels of glutamate and GABA in the BLA were detected by reverse-phase high-performance liquid chromatography (HPLC, Agilent Technologies 1260 Infinity, Santa Clara, CA, USA) according to previously reported methods [24,25]. 2, 4-dinitrofluorobenzene (DNFB) was used for pre-column derivatization.…”

Section: Determination Of Glutamate and Gaba Levelsmentioning

confidence: 99%

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Sun

Yang

et al. 2020

Mol Brain

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Anxiety disorder is highly prevalent worldwide and represents a chronic and functionally disabling condition, with high levels of psychological stress characterized by cognitive and physiological symptoms. Scopoletin (SP), a main active compound in Angelica dahurica, is traditionally used for the treatment of headache, rhinitis, pain, and other conditions. Here, we evaluated the effects of SP in a mouse model of complete Freund's adjuvant (CFA)-induced chronic inflammation anxiety. SP (2.0, 10.0, 50.0 mg/kg) administration for 2 weeks dose-dependently ameliorated CFA-induced anxiety-like behaviors in the open field test and elevated plus maze test. Moreover, we found that SP treatment inhibited microglia activation and decreased both peripheral and central IL-1β, IL-6, and TNF-α levels in a dose-dependent manner. Additionally, the imbalance in excitatory/inhibitory receptors and neurotransmitters in the basolateral nucleus after CFA injection was also modulated by SP administration. Our findings indicate that the inhibition of the nuclear factor-kappa B and mitogen-activated protein kinase signaling pathways involving antiinflammatory activities and regulation of the excitatory/inhibitory balance can be attributed to the anxiolytic effects of SP. Moreover, our molecular docking analyses show that SP also has good affinity for gamma-aminobutyric acid (GABA) transaminase and GABA A receptors. Therefore, these results suggest that SP could be a candidate compound for anxiolytic therapy and for use as a structural base for developing new drugs.

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Section: Determination Of Glutamate and Gaba Levelsmentioning

confidence: 99%

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Sun

Yang

et al. 2020

Mol Brain

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“…Furthermore, several studies also reported up-regulation of BDNF levels by other neuroprotectants in the 3-NP-treated animals. Thus, 3-NP-induced deficits in motor behaviors can be reversed by Praeruptorin C, an effective component in the root of Peucedanum praeruptorum Dunn that is a traditional Chinese medicine; more importantly, Praeruptorin C up-regulated several proteins, including BDNF, in the striatum of the 3-NP-treated mice [68]. Memantine, a NMDA blocker well known for its protective effect against various neurodegenerative diseases, improved 3-NP-induced motor deficits and concomitantly increased the expression of BDNF in the brains of 3-NP-treated mice [69].…”

Section: Experimental Evidence Supporting Bdnf-mediated Neuroprotementioning

confidence: 99%

More Insight into BDNF against Neurodegeneration: Anti-Apoptosis, Anti-Oxidation, and Suppression of Autophagy

Chen

Hwang

et al. 2017

IJMS

169

117

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In addition to its well-established neurotrophic action, brain-derived neurotrophic factor (BDNF) also possesses other neuroprotective effects including anti-apoptosis, anti-oxidation, and suppression of autophagy. We have shown before that BDNF triggers multiple mechanisms to confer neuronal resistance against 3-nitropropionic acid (3-NP)-induced mitochondrial dysfunction in primary rat cortical cultures. The beneficial effects of BDNF involve the induction of anti-oxidative thioredoxin with the resultant expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) as well as erythropoietin (EPO)-dependent stimulation of sonic hedgehog (SHH). We further revealed that BDNF may bring the expression of sulfiredoxin, an ATP-dependent antioxidant enzyme, to offset mitochondrial inhibition in cortical neurons. Recently, we provided insights into another novel anti-oxidative mechanism of BDNF, which involves the augmentation of sestrin2 expression to endow neuronal resistance against oxidative stress induced by 3-NP; BDNF induction of sestrin2 entails the activation of a pathway involving nitric oxide (NO), cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG), and nuclear factor-κB (NF-κB). Apart from anti-apoptosis and anti-oxidation, we demonstrated in our most recent study that BDNF may activate the mammalian target of rapamycin (mTOR) with resultant activation of transcription factor c-Jun, thereby stimulating the expression of p62/sequestosome-1 to suppress heightened autophagy as a result of 3-NP exposure. Together, our results provide in-depth insight into multi-faceted protective mechanisms of BDNF against mitochondrial dysfunction commonly associated with the pathogenesis of many chronic neurodegenerative disorders. Delineation of the protective signaling pathways elicited by BDNF would endow a rationale to develop novel therapeutic regimens to halt or prevent the progression of neurodegeneration.

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“…DE induced by hyperglycemia impairs learning and memory abilities in diabetic patients and animals [6,10], increased the risks of occurrence and progression of neurodegenerative diseases [7]. Our previous study showed that Pra-C improved the behavioral performance in Huntington's disease model mice by regulating neurotransmitter balance [24]. In present study, T2DM model mice show poor ability in and metabolism in physiological and morbid conditions, such as obesity and T2DM.…”

Section: Discussionmentioning

confidence: 53%

“…Monomer composition studies show the anti-inflammatory activity and anti-osteoporosis effects of Pra-C [21,22]. Our previous studies revealed its neuroprotective effect in excitatory toxicity in vitro [23] and behavioral improvement in a Huntington's disease mouse model in vivo [24]. Given its beneficial effects on neuron apoptosis and neurodegenerative model animals, we hypothesize that Pra-C may provide therapeutic benefits for treating cognitive impairment related diseases, such as DE.…”

Section: Introductionmentioning

confidence: 85%

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Praeruptorin C alleviates cognitive impairment in Type 2 diabetic mice through restoring PI3K/AKT/ GSK3β pathway

Zhao

Yan

et al. 2020

Preprint

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Diabetic encephalopathy is a common complication of diabetes, leading to cognitive impairment. In this study, we investigated the therapeutic effects of Praeruptorin C (Pra-C), an active component of traditional Chinese herb medicine Peucedanum praeruptorum, on cognitive impairment in a mouse model of type 2 diabetes. Our results showed that Pra-C administration significantly reduced body weight and fasting blood glucose levels, relieved learning and memory behavioral deficits in diabetic model mice. The effects of Pra-C on learning and memory ability were further confirmed by late-phase LTP (L-LTP) facilitation, which was recorded by Med64 electrophysiology recording system. Pra-C also restored the activation of PI3K/AKT/GSK3β signaling pathway in hippocampus of mice suffering from diabetes. Taken together, this study demonstrates that Pra-C alleviates cognitive impairment in diabetic mice by restoring PI3K/AKT/GSK3β activation.

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Effect of Praeruptorin C on 3-nitropropionic acid induced Huntington’s disease-like symptoms in mice

Cited by 44 publications

References 41 publications

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model

More Insight into BDNF against Neurodegeneration: Anti-Apoptosis, Anti-Oxidation, and Suppression of Autophagy

Praeruptorin C alleviates cognitive impairment in Type 2 diabetic mice through restoring PI3K/AKT/ GSK3β pathway

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