Protective effects of DL-3-n-butylphthalide in the lipopolysaccharide-induced mouse model of Parkinson's disease

Jiang, Mujun; Chen, Yu‐Hua; Li, Li; Xu, Lan; Líu, Hao; Qu, Xiaolong; Xu, Jing; Ge, Bobo; Qu, Hongdang

doi:10.3892/mmr.2017.7352

Cited by 16 publications

(8 citation statements)

References 34 publications

(35 reference statements)

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“…The MAPK pathways which played an important role in microglial activation were reported to be regulated by NBP in several neurological diseases (Kaminska et al, 2009; Lu et al, 2012; Bhatia et al, 2016; Jiang et al, 2017; Yan R. Y. et al, 2017). Thus we speculated that the protective role of NBP might be associated with the regulation of MAPK pathways.…”

Section: Resultsmentioning

confidence: 99%

Dl-3-n-Butylphthalide Exerts Dopaminergic Neuroprotection Through Inhibition of Neuroinflammation

Chen

et al. 2019

Front. Aging Neurosci.

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Microglia-mediated neuroinflammation contributes to multiple neurodegenerative disorders, including PD. Therefore, the regulation of microglial activation probably has the therapeutic potential. This study is aimed to determine whether NBP could suppress microglial activation and protect dopaminergic neurons from excessive neuroinflammation. In the present study, MPTP-induced PD model was established to explore the neuroprotective and anti-inflammatory effect of NBP. We assessed motor deficits, dopaminergic neurodegeneration and microglial activation in PD mice. In vitro , the anti-inflammatory activity of NBP was confirmed by cell viability assay of SH-SY5Y cells after being treated with conditioned medium from LPS-stimulated BV-2 cells and from 1-Methyl-4-phenylpyridinium iodide (MPP + )-stimulated BV-2 cells. The expression of pro-inflammatory molecules was determined by RT-PCR, Western Blot and ELISA assay. The generation of NO and ROS were also assessed. The involvement of signaling pathways such as MAPK, NF-κB, and PI3k/Akt were further investigated by Western Blot and immunofluorescence assay. The neuroprotective effect of NBP was demonstrated in vivo as shown by the improvement of dopaminergic neurodegeneration, motor deficits and microglial activation in MPTP-induced mouse model of PD. The expression of pro-inflammatory mediators was also reduced by NBP administration. In vitro , NBP also protected dopaminergic neurons from neurotoxicity induced by activated microglia. NBP pretreatment not only reduced pro-inflammatory molecules, but also suppressed NO release and ROS generation in BV-2 cells. Further mechanism research suggested that the inactivation of MAPK, NF-κB and PI3K/Akt may involve in anti-neuroinflammation role of NBP. In conclusion, our results revealed that NBP exerted dopaminergic neuroprotection through inhibition of microglia-mediated neuroinflammation, suggesting the promising therapeutic effect of NBP for PD.

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Section: Resultsmentioning

confidence: 99%

Dl-3-n-Butylphthalide Exerts Dopaminergic Neuroprotection Through Inhibition of Neuroinflammation

Chen

et al. 2019

Front. Aging Neurosci.

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“…Following the establishment of intracranial LPS injections to model PD, Qin et al. (2007) demonstrated for the first time that systemic administration of a single dose of LPS via an intraperitoneal (i.p) injection induced self-sustained neuroinflammation and specific degeneration of dopaminergic neurons in the SN, and these findings were confirmed by later studies ( Chen et al., 2017 ; Jiang et al., 2017 ; Liu et al., 2008 ; Qin et al., 2013 ). Subsequently, He et al.…”

Section: Lps Models Of Pd: An Overviewmentioning

confidence: 88%

“… Abbreviation s : TH, tyrosine hydroxylase; SN, substantia nigra; OB, olfactory bulb; LC, locus coeruleus; NE, noradrenaline; α-syn, α-synuclein. Reference s : 1 ( Chen et al., 2017 ); 2 ( Wang et al., 2015c , Wang et al., 2015b , Wang et al., 2015a ); 3 ( He et al., 2016b , He et al., 2016a ); 4 ( Fu et al., 2015 ); 5 ( Bao et al., 2018 ); 6 ( Hritcu and Ciobica, 2013 ); 7 ( Hritcu and Gorgan, 2014 ); 8 ( Zheng et al., 2013b , Zheng et al., 2013a ); 9 ( Choi et al., 2009 ); 10 ( Hunter et al., 2007 ); 11 ( Hunter et al., 2017 ); 12 ( Zheng et al., 2013b , Zheng et al., 2013a ); 13 ( Zhang and Xu, 2018 ); 14 ( Khan et al., 2018 ); 15 ( Badshah et al., 2016 ); 16 ( Beier et al., 2017 ), 17 ( Bodea et al., 2014 ), 18 ( Qin et al., 2007 ); 19 ( Qin et al., 2013 ); 20 ( Zheng et al., 2013b , Zheng et al., 2013a ); 21 ( Liu et al., 2008 ); 22 ( Reinert et al., 2014 ); 23 Kelly et al., 2014 ; 24 ( Jiang et al., 2017 ); 25 ( Zheng et al., 2013b , Zheng et al., 2013a ), 26 ( Song et al., 2018 ); 27 ( Chen et al...…”

Section: Lps Models Of Pd: An Overviewmentioning

confidence: 99%

Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

Deng

Corrigan

Zhai

et al. 2020

Brain, Behavior, & Immunity - Health

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Parkinson’s disease (PD) is one of the most common neurodegenerative movement disorders which is characterised neuropathologically by progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the presence of Lewy bodies (made predominately of α-synuclein) in the surviving neurons. Animal models of PD have improved our understanding of the disease and have played a critical role in the development of neuroprotective agents. Neuroinflammation has been strongly implicated in the pathogenesis of PD, and recent studies have used lipopolysaccharide (LPS), a component of gram-negative bacteria and a potent activator of microglia cells, to mimic the inflammatory events in clinical PD. Modulating the inflammatory response could ameliorate PD associated complications and thus, it is essential to understand the extent to which LPS models reflect human PD. This review will outline the routes of administration of LPS such as stereotaxic, systemic and intranasal, their ability to recapitulate neuropathological markers of PD, and mechanisms of LPS induced toxicity. We will also discuss the ability of the models to replicate motor symptoms and non-motor symptoms of PD such as gastrointestinal dysfunction, olfactory dysfunction, anxiety, depression and cognitive dysfunction.

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“…While the current study was focused on the effects of QG on muscle and motor performance, our results should evoke further consideration of effects of QG supplementation on the brain. Relevant to this point, in recent studies of mouse models of Parkinson's disease [37,38], treatment with epigallocatechin gallate, a phytochemical found in green tea, was reported to rescue deficits in rotarod performance and striatal dopamine levels induced by central injection of a neurotoxin (MPTP), whereas DL-3-n-butylphthalide, a phytochemical extracted from grape seed, also rescued deficits in rotarod performance and midbrain dopamine neurons reduced by injections with an inflammatory toxin (LPS).…”

Section: Discussionmentioning

confidence: 98%

Quercetin Glycosides Improve Motor Performance and Muscle Weight in Adult Mice

Kanzaki¹,

Takemoto²,

Ono³

et al. 2019

J Nutr Food Sci

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Male C57BL/6J (B6) mice aged 24 weeks were provided two concentrations (1.5 or 3.0 g/L) of quercetin glycosides (QG) in drinking water over the subsequent 24 weeks. The objective was to determine if QG could improve motor function during early stages of aging. No sustained significant differences in body composition or food intake were noted to confirm the safety of QG treatment. Treated mice had significantly improved performance in grip strength and rotarod tests but not in treadmill performance. The functional benefits were reflected in muscle morphology with increased wet weights of a selected group of muscles (quadratus femoris, gastrocnemius, tibialis anterior, and soleus) in treated mice. Thus, it would appear that long-term oral treatment with QG can safely and effectively improve selected elements of motor performance and increase muscle mass during the early stages of aging.

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Protective effects of DL-3-n-butylphthalide in the lipopolysaccharide-induced mouse model of Parkinson's disease

Cited by 16 publications

References 34 publications

Dl-3-n-Butylphthalide Exerts Dopaminergic Neuroprotection Through Inhibition of Neuroinflammation

Dl-3-n-Butylphthalide Exerts Dopaminergic Neuroprotection Through Inhibition of Neuroinflammation

Lipopolysaccharide animal models of Parkinson’s disease: Recent progress and relevance to clinical disease

Quercetin Glycosides Improve Motor Performance and Muscle Weight in Adult Mice

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