Artemisinin Facilitates Motor Function Recovery by Enhancing Motoneuronal Survival and Axonal Remyelination in Rats Following Brachial Plexus Root Avulsion

Chen, Shuangxi; Wu, Lin; He, Bing; Zhou, Guijuan; Xu, Yan; Zhu, Geng; Xie, Jingui; Chen, Shuangqin; Yao, Lan; Huang, Jianghua; Wu, Honglu; Xiao, Zijian

doi:10.1021/acschemneuro.1c00120

Cited by 9 publications

(11 citation statements)

References 55 publications

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“…In previous studies, we revealed the effects of artemisinin, berberine and neuregulin-1 on motor function recovery after BPRA [9,14,15]. In the current study, we demonstrated that NAG treatment combined with nerve reimplantation contributed to better functional recovery after BPRA via increasing motoneuron survival, accelerating motor axonal remyelination and reducing muscle atrophy, which may be associated with the inhibition of in ammatory response and the pyroptosis pathway.…”

Section: Discussionsupporting

confidence: 59%

“…As shown in Fig. 1A, the surgical procedures on rats were performed based on previously described methods [9,14]. Rats were anesthetized by intraperitoneal injection of 10% chloral hydrate at a dose of 5 µL/g.…”

Section: Brachial Plexus Avulsion-re-implantation Surgerymentioning

confidence: 99%

“…The Terzis grooming test was performed to evaluate the motor function of the affected forelimbs as previously described in the literature [3,9,15]. Water was sprayed on the head of the rat from multiple directions to elicit a grooming reaction, and the rat was placed in a glass cylinder.…”

Section: Terzis Grooming Testmentioning

confidence: 99%

“…Koliatsos et al demonstrated that ventral root avulsion causes 80% motor neuron retrograde death within the rst 2 weeks after it occurs [8]. Promoting the survival of the injured motor neurons is a prerequisite for functional motor recovery after BPRA [9]. Accordingly, the exploration of novel medical approaches is essential to accelerate the survival of motoneurons combined with reimplantation surgery during BPRA treatment.…”

Section: Introductionmentioning

confidence: 99%

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Acetylglutamine facilitates motor recovery after brachial plexus root avulsion in ratsby promoting motoneuronal survival and axonal remyelination

Chen

et al. 2023

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Background: Brachial plexus root avulsion (BPRA) is a disabling peripheral nerve injury that induces substantial death of motoneurons, degeneration of motor axons and de-innervation of biceps muscles, leading toloss of upper limb motor function. Acetylglutamine (N-acetyl-L-glutamine, NAG) has been proved to exert neuroprotective and anti-inflammatory effects in various disorders in the nervous system. Hence, the present study focused on the effect of NAG on motor recovery after BPRA in rats and the underlying mechanisms. Methods: Adult male Sprague Dawley rats were subject to BPRA and reimplantation surgery andsubsequently treated with NAG or saline. Behavioral tests were conducted to evaluate motor function recovery and mechanical pain threshold of the affected forelimb. The morphological appearance of the spinal cord, musculocutaneous nerve, and biceps brachii was assessed by histological staining. Quantitative real-time PCR was utilized to measure the mRNA levels of remyelination and regenerstion indicators on myocutaneous nerves. The protein levels of inflammatory and pyroptotic indicators in the anterior horn of the spinal cord were measured using Western blot analysis. Results: Our results indicated NAG could significantly accelerate recovery of motor function in the injured forelimbs, enhance motoneuronal survival in the anterior horn of the spinal cord, inhibit the expression of proinflammatory cytokines and pyroptosis pathway, facilitate axonal remyelination in the myocutaneous nerve and alleviate atrophy of biceps brachii. Additionally, NAG attenuated neuropathic pain following BPRA. Conclusion: NAG promotes functional motor recovery by enhancing motoneuronal survival and axonal remyelination and inhibiting the pyroptosis pathway after BPRA in rats, laying the foundation for NAG to be a novel strategy for BPRA treatment.

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Section: Discussionsupporting

confidence: 59%

Section: Brachial Plexus Avulsion-re-implantation Surgerymentioning

confidence: 99%

Section: Terzis Grooming Testmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acetylglutamine facilitates motor recovery after brachial plexus root avulsion in ratsby promoting motoneuronal survival and axonal remyelination

Chen

et al. 2023

Preprint

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“…Tissue preparation was performed according to the previous publications [6,8,9,49]. For western blot analysis, mice were sacrificed after anaesthesia by isoflurane.…”

Section: Tissue Preparationmentioning

confidence: 99%

Mitochonic acid 5 ameliorates the motor deficits in the MPTP-induced mouse Parkinson’s disease model by AMPK-mediated autophagy

Wan¹,

Gao²,

Tan³

et al. 2022

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Parkinson's disease (PD) is a well-known neurodegenerative disorder characterized by the degeneration of dopaminergic neurons, and oxidative stress and neuroinflammation are also associated with the pathogenesis of PD. Mitochonic acid 5 , an analogue of indole-3-acetic acid, exerts key protective roles in inhibiting apoptosis, oxidative stress and neuroinflammation in multiple diseases. However, whether MA-5 can be beneficial for PD remains unclear. Hence, the aim of this study was to investigate the neuroprotective role of MA-5 in PD. In the current study, MPTP-challenged mice were treated as the in vivo model, and the effect of MA-5 on the motor function, neuronal survival, oxidative stress, neuroinflammation and the underlying mechanisms involved with AMPK and autophagy were determined. We revealed that MA-5 obviously up-regulated the phosphorylation of AMPK and promoted the autophagy (indicated by the increased LC3II/LC3I, parkin, pink and decreased p62) in substantia nigra (SN), ameliorated the motor deficits, up-regulated the expression of TH, suppressed the inflammation (indicated by the decreased protein levels of interleukin (IL)-1β, IL-6, tumour necrosis factor α) in SN in MPTP-induced mice. However, these patterns were reversed after the treatment of Compound C, an inhibitor of AMPK; also, after the application of CSA, an inhibitor of autophagy, MA-5 cannot play against the neurotoxicity of MPTP in mice. These combined results suggest that MA-5 can protect against MPTP-induced neurotoxicity to ameliorate the impaired motor function, which may be modulated via activation of AMPK-induced autophagy.

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Artemisinin upregulates neural cell adhesion molecule L1 to attenuate neurological deficits after intracerebral hemorrhage in mice

2022

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Background and purpose: Intracerebral hemorrhage (ICH) is a subtype of stroke and results in neurological deficits in patients without any effective treatments. Artemisinin (ART), a well-known antimalarial Chinese medicine, exerts multiple essential roles in the central and peripheral nervous system due to its antioxidative and antiinflammation properties. Neural cell adhesion molecule L1 (L1CAM, L1) is considered to be implicated in neural development, functional maintenance, and neuroprotection during disease. However, whether these two essential molecules are neuroprotective in ICH remains unclear.Methods: Therefore, the present study investigated the influence of ART on the recovery of neurological deficits in a mouse model of ICH induced by collagenase and the underlying mechanism.Results: It was revealed that ART is capable of upregulating L1 expression to alleviate brain edema, reduce oxidative stress, and inhibit inflammation to alleviate ICH-induced brain injury to improve the neurological outcome in mice suffering from ICH. Conclusion:These results may lay the foundation for ART to be a novel candidate treatment for ICH. K E Y W O R D S artemisinin (ART), intracerebral hemorrhage (ICH), neural cell adhesion molecule L1, oxidative stress, inflammation 1 INTRODUCTION Intracerebral hemorrhage (ICH), a stroke subtype induced by vascular rupture, is well known for its high rates of mortality and morbidity (Dai et al., 2019). Even if the patients survive, most of them usually live with disabilities (Pinho et al., 2019), including speech impediment, cognitive deficits, and movement disorders (Hallevi et al., 2009), in the following years. Despite ongoing research, therapies for ICH currently This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Artemisinin Facilitates Motor Function Recovery by Enhancing Motoneuronal Survival and Axonal Remyelination in Rats Following Brachial Plexus Root Avulsion

Cited by 9 publications

References 55 publications

Acetylglutamine facilitates motor recovery after brachial plexus root avulsion in ratsby promoting motoneuronal survival and axonal remyelination

Acetylglutamine facilitates motor recovery after brachial plexus root avulsion in ratsby promoting motoneuronal survival and axonal remyelination

Mitochonic acid 5 ameliorates the motor deficits in the MPTP-induced mouse Parkinson’s disease model by AMPK-mediated autophagy

Artemisinin upregulates neural cell adhesion molecule L1 to attenuate neurological deficits after intracerebral hemorrhage in mice

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