Neurogenesis and Proliferation of Neural Stem/Progenitor Cells Conferred by Artesunate via FOXO3a/p27Kip1 Axis in Mouse Stroke Model

Zhang, Kaiyuan; Yang, Yang; Ge, Hongfei; Wang, Ju; Lei, Xuejiao; Chen, Xuezhu; Wan, Feng; Feng, Hua; Tan, Liang

doi:10.1007/s12035-021-02710-5

Cited by 39 publications

(17 citation statements)

References 36 publications

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“…In CNS, our previous research demonstrated artesuante could alleviate SAH animals BBB damage and promote SAH mice neurological function recover [37]. Furthermore, artesunate could promote NSPCs proliferation and neurogenesis of MCAO mice and improve their neurological function [18,19]. In this study, our results demonstrated artesunate could alleviate the inhibitory effect of cadmium on the proliferation and neurogenesis of NSPCs in vitro (Fig.…”

Section: Discussionsupporting

confidence: 56%

“…What's more, artesunate alleviated AD phenotypes in amyloid precursor protein/presenilin mice, reducing Aβ deposition and reversing de cits in memory and learning function [17]. And our recent reports suggested artesunate could promote NSPCs proliferation and differentiation in ischemic stroke and improve neurological function of stroke mice [18,19]. However, whether the artesunate could reduce the in uence of cadmium on the proliferation and neurogenesis of NSPCs and whether artesunate could thereafter improve the memory and learning of chronic cadmium exposure mice were still unknown.…”

Section: Introductionmentioning

confidence: 99%

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Artesunate Mitigates Cognitive Deficits by Promoting Hippocampal Neural Stem/Progenitor Cells Proliferation and Neurogenesis in Cadmium-Exposed Mice

Zhong

Yang

Mao

et al. 2022

Preprint

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Cadmium is a toxic heavy metal which could cause central nervous system damage and cognitive dysfunction. However, the effective therapy strategy for cadmium-caused cognitive dysfunction had not been established. In present study, we investigated the therapeutic effect of artesunate on cadmium induced cognitive deficits and neural stem/progenitor cells (NSPCs) proliferation as well as neurogenesis inhibition. Male mice were injected with cadmium chloride (1mg/Kg) for 4weeks, followed with 4 weeks of artesunate (50mg/Kg). Cadmium chloride and artesunate were used to treat NSPCs in vitro. Subsequently, the learning and memory function of mice were detected by Y-maze and Morris water maze tests and NSPCs proliferation and neurogenesis were examined by western blots and immunofluorescence. The results showed cadmium impaired mice cognitive severity. And cadmium significantly inhibited the proliferation and neurogenesis of NSPCs in hippocampi and in vitro. Moreover, cadmium reduced the expression of phosphorylated AKT. However, artesunate reversed the cadmium-induced cognitive deficits as well as the inhibition of NSPCs proliferation and neurogenesis. Additionally, artesunate increased the phosphorylation of AKT in hippocampi and NSPCs. Our data manifested artesunate could reverse cadmium-induced mice cognitive deficits and reduce the inhibition of cadmium on NSPCs proliferation and neurogenesis via PI3K-AKT pathway.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Artesunate Mitigates Cognitive Deficits by Promoting Hippocampal Neural Stem/Progenitor Cells Proliferation and Neurogenesis in Cadmium-Exposed Mice

Zhong

Yang

Mao

et al. 2022

Preprint

Self Cite

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“…In addition, three MAPK pathways, including ERK1/2, JNK, and p38 in DRGs of DM rats are activated [39][40][41][42]. As the most important nuclear transcription factor of the JNK/SAPK signal transduction pathway, C-Jun has been confirmed closely related to neuronal apoptosis under pathological conditions [43][44][45][46]. Zhuang et al [47] detected the expression of c-Jun in DRG after spinal nerve injury (SNL) and found that c-Jun expression in L5 DRG is upregulated, suggesting that c-Jun is a marker of the molecular level of peripheral nerve injury [41].…”

Section: Related Workmentioning

confidence: 99%

[Retracted] Lidocaine Ameliorates Diabetic Peripheral Neuropathy in Streptozotocin‐Induced Diabetic Rats through Modulating the c‐Jun Signaling Pathway

Luo

Wu²,

Wu³

et al. 2022

Contrast Media & Molecular Imaging

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As one of the common complications of diabetes mellitus (DM), Diabetic Peripheral Neuropathy (DPN) threatens human lives seriously. Emerging evidences have confirmed the protective effects of lidocaine on DPN. However, the possible role and underlying mechanisms of lidocaine in DPN have not been clarified. In this study, the potential role of lidocaine in DPN is explored, and the possible mechanisms are investigated. The rat DPN model is constructed through administration of streptozotocin (STZ, 60 mg/kg). All rats are randomly divided into four groups, including the control group, DPN group, lidocaine (3.78 mg/time) group, and lidocaine combined with the SP600125 (15 mg/kg) group. Mechanical threshold, thermal latency, and blood glucose of rats before and after treatment are detected, and Nerve Conduction Velocity (NCV) is assessed. Moreover, qRT-PCR and western blot assays are carried out to determine the expressions of the c-Jun signaling pathway. The experimental results demonstrate that lidocaine remarkably downregulates the mRNA and protein expressions of the c-Jun signaling pathway in serum and DRGs induced with DPN. Besides, lidocaine combined with SP600125 can obtain better effects than lidocaine alone. It is clearly evident that lidocaine has a certain therapeutic effect on DPN.

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“…Male SD rats (n = 125) weighing 320-350 g were randomly divided into the following five groups: sham, vehicle (ICH) and artesunate groups (20, 50 and 70 mg/ kg). 26,27 Rats without motor function injury (n = 4) or that died (n = 12) were excluded from the study. In the artesunate group, rats received artesunate at 20, 50 or 70 mg/kg (A3731, Sigma, USA) via intraperitoneal injection for three consecutive days before ICH induction, while rats in the vehicle group received a 0.5 ml 1% DMSO injection.…”

Section: Establishment Of An Ich Animal Model and Groupingmentioning

confidence: 99%

Artesunate alleviates intracerebral haemorrhage secondary injury by inducing ferroptosis in M1‐polarized microglia and suppressing inflammation through AMPK/mTORC1/GPX4 pathway

Xie

Liang

Gao

et al. 2023

Basic Clin Pharma Tox

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Intracerebral haemorrhage (ICH) is a catastrophic subtype of stroke with severe morbidity and mortality. However, little progress has been made in the subsequent secondary injury. Artesunate, a water-soluble semi-synthetic derivative of artemisinin, exhibits remarkable pharmacological effects on anti-neuroinflammation. However, the effects of artesunate on ICH remain unknown.In the present study, haemoglobin (Hb) treatment in BV2 cell and collagenase type IV intracerebroventricular injection in Sprague-Dawley rats were used to establish in vitro and in vivo ICH models, respectively. For in vivo, the neurological scores, haematoma volume, brain oedema, inflammatory factors and iron deposition were evaluated. Besides, lipopolysaccharide (LPS) was used in in vitro to polarize BV2 cell to M1 phenotype. Cell viability, cellular reactive oxygen species (ROS), Fe 2+ concentration, and lipid peroxidation levels, ferroptosis-associated proteins and mRNA, morphological of mitochondria were measured in vitro. Additionally, the AMP-activated protein kinase (AMPK)/mammalian/mechanistic target of rapamycin (mTOR) pathway were measured by western blot and immunofluorescence staining. The present in vivo results indicated that artesunate significantly ameliorated neurological deficits, haematoma volume and brain oedema in ICH rats. Besides, artesunate suppressed the M1-microglia relative inflammatory factors and up-regulated iron deposition. For in vitro, artesunate significantly selectively decreased the viability of LPS-stimulated BV2 cell. Furthermore, ROS and lipid peroxidation levels were up-regulated. And the glutathione peroxidase 4 (GPX4) were silenced via the AMPK/mTORC1 axis. Our finding supports that artesunate ameliorates the ICH secondary injury both in vitro and in vivo by inducing ferroptosis in microglia and further inhibiting inflammation mainly through the Guanfeng Xie and Yubing Liang contributed equally to this work.

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Neurogenesis and Proliferation of Neural Stem/Progenitor Cells Conferred by Artesunate via FOXO3a/p27Kip1 Axis in Mouse Stroke Model

Cited by 39 publications

References 36 publications

Artesunate Mitigates Cognitive Deficits by Promoting Hippocampal Neural Stem/Progenitor Cells Proliferation and Neurogenesis in Cadmium-Exposed Mice

Artesunate Mitigates Cognitive Deficits by Promoting Hippocampal Neural Stem/Progenitor Cells Proliferation and Neurogenesis in Cadmium-Exposed Mice

[Retracted] Lidocaine Ameliorates Diabetic Peripheral Neuropathy in Streptozotocin‐Induced Diabetic Rats through Modulating the c‐Jun Signaling Pathway

Artesunate alleviates intracerebral haemorrhage secondary injury by inducing ferroptosis in M1‐polarized microglia and suppressing inflammation through AMPK/mTORC1/GPX4 pathway

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