Effect of Tetramethylpyrazine on Neuroplasticity after Transient Focal Cerebral Ischemia Reperfusion in Rats

Lin, Junbin; Hao, Chizi; Gong, Yu; Zhang, Ying; Li, Ying; Feng, Zhihe; Xu, Xiangdong; Huang, Hailong; Liao, Weijing

doi:10.1155/2021/1587241

Cited by 12 publications

(8 citation statements)

References 49 publications

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“…SYN exists widely in nerve endings in the central and peripheral nervous system and is speci cally distributed in presynaptic vesicle membranes. It is considered a marker protein of presynaptic terminals and has been extensively used to quantify the number, density, and distribution of synapses [28,29]. Therefore, our ndings suggest that high-frequency rTMS may modify synaptic structure by increasing SYN levels in TBI rats.…”

Section: Discussionmentioning

confidence: 75%

Repetitive transcranial magnetic stimulation promotes neural functional recovery via upregulation of synaptic plasticity-related proteins in rats with traumatic brain injury

Qian

et al. 2021

Preprint

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Background Repetitive transcranial magnetic stimulation (rTMS) has become a popular approach for the treatment of traumatic brain injury (TBI). This study aimed to assess the efficacy and underlying mechanism of rTMS in TBI model rats. Methods Forty-five rats were randomized into SHAM, TBI, and rTMS (TBI and rTMS therapy) groups. Moderate TBI was established using Feeney's weight-dropping method. High-frequency rTMS (20 Hz) was administered to the damaged area in the rTMS group for two weeks. Neural function was assessed by modified neurological severity score (MNSS) at 3, 9, and 16 days after TBI. Synaptic ultrastructure was observed by transmission electron microscopy and levels of synaptic plasticity-related proteins (BDNF, TrkB, NMDAR1, P-CREB, and SYN) were assessed by immunohistochemistry, Western blotting, and real-time PCR. Results The rTMS group showed a lower MNSS than the TBI group at 16 days (P < 0.05). Compared to the TBI group, the postsynaptic density (PSD) was increased, the width of the synaptic cleft was decreased, and the synaptic active zone was lengthened in the rTMS group (all P < 0.05). Compared with the sham group, protein levels and mRNA expression of BDNF, TrkB, NMDAR1, and P-CREB were increased in the TBI group (P < 0.05) and further upregulated after rTMS treatment (P < 0.05). In addition, rTMS partially reversed downregulation of SYN (P < 0.05). Conclusions Taken together, these findings support that rTMS improves neural functional recovery in TBI rats. The possible mechanism is that rTMS modulates synaptic structural plasticity by reducing loss of SYN and alters synaptic functional plasticity by increasing cortical levels of BDNF, TrkB, NMDAR1, and P-CREB.

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Section: Discussionmentioning

confidence: 75%

Repetitive transcranial magnetic stimulation promotes neural functional recovery via upregulation of synaptic plasticity-related proteins in rats with traumatic brain injury

Qian

et al. 2021

Preprint

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“…A total of 20 bioactive phytochemicals of CR were obtained from a recent study using UHPLC-MS/MS ( Wang et al, 2020 ). In addition, TMP, a main bioactive phytochemical of CR, was also included ( Zhu et al, 2021 ; Lin et al, 2021 ). The chemical structures in canonical SMILES format were extracted from the PubChem database ( https://pubchem.ncbi.nlm.nih.gov/ ) ( Kim et al, 2016 ).…”

Section: Methodsmentioning

confidence: 99%

A Tau Pathogenesis-Based Network Pharmacology Approach for Exploring the Protections of Chuanxiong Rhizoma in Alzheimer’s Disease

Zeng

Qiu

et al. 2022

Front. Pharmacol.

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Alzheimer’s disease (AD) is the most common cause of neurodegenerative dementia and one of the top medical concerns worldwide. Currently, the approved drugs to treat AD are effective only in treating the symptoms, but do not cure or prevent AD. Although the exact causes of AD are not understood, it is recognized that tau aggregation in neurons plays a key role. Chuanxiong Rhizoma (CR) has been widely reported as effective for brain diseases such as dementia. Thus, we explored the protections of CR in AD by a tau pathogenesis–based network pharmacology approach. According to ultra-HPLC with triple quadrupole mass spectrometry data and Lipinski’s rule of five, 18 bioactive phytochemicals of CR were screened out. They were shown corresponding to 127 tau pathogenesis–related targets, among which VEGFA, IL1B, CTNNB1, JUN, ESR1, STAT3, APP, BCL2L1, PTGS2, and PPARG were identified as the core ones. We further analyzed the specific actions of CR-active phytochemicals on tau pathogenesis from the aspects of tau aggregation and tau-mediated toxicities. It was shown that neocnidilide, ferulic acid, coniferyl ferulate, levistilide A, Z-ligustilide, butylidenephthalide, and caffeic acid can be effective in reversing tau hyperphosphorylation. Neocnidilide, senkyunolide A, butylphthalide, butylidenephthalide, Z-ligustilide, and L-tryptophan may be effective in promoting lysosome-associated degradation of tau, and levistilide A, neocnidilide, ferulic acid, L-tryptophan, senkyunolide A, Z-ligustilide, and butylidenephthalide may antagonize tau-mediated impairments of intracellular transport, axon and synaptic damages, and neuron death (especially apoptosis). The present study suggests that acting on tau aggregation and tau-mediated toxicities is part of the therapeutic mechanism of CR against AD.

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“…The brain tissues were collected and fixed in 2.5% phosphate-buffered glutaraldehyde for 24 h at room temperature. Then, the tissue samples were prepared for TEM examination routinely ( 24 ). Briefly, the samples were post-fixed in 1% osmium tetroxide and then dehydrated with ethanol and acetone in a graded series.…”

Section: Methodsmentioning

confidence: 99%

Saccharina japonica Ethanol Extract Ameliorates Depression/Anxiety-Like Behavior by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Dextran Sodium Sulfate Induced Ulcerative Colitis Mice

Dong

Lin

et al. 2021

Front. Nutr.

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Saccharina japonica is a common marine vegetable in East Asian markets and has a variety of health benefits. This study was focused on the anti-depressant/anxiety effects of Saccharina japonica ethanol extract (SJE) on dextran sodium sulfate (DSS)-induced mice and its potential mechanism in their brain. Male C57BL/6 mice were treated with mesalazine and various doses of SJE (1, 2, and 4 g/kg body weight) for 2 weeks, followed by DSS treatment at the second week. The DSS-induced mice showed depression/anxiety-like behavior, which included shorter path length in the open field test and longer immobility time in the tail suspension test. L-SJE alleviated the depression-like behaviors. In the DSS-induced mice, reduced synaptic plasticity activated microglia, increased proinflammatory cytokines, decreased anti-inflammatory cytokine, and increased expression levels of Toll-like receptors-4, nuclear factor kappa-B, NOD-like receptors 3, apoptosis-associated speck-like protein, and Caspase-1 were observed, most of which were alleviated by SJE treatment. Furthermore, all the SJE groups could significantly enhance superoxide dismutase activity, while the L-SJE treatment decreased the contents of malondialdehyde, and the H-SJE treatment inhibited apoptosis. All these results showed that the SJE might serve as a nutritional agent for protecting the brain in ulcerative colitis mice.

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Effect of Tetramethylpyrazine on Neuroplasticity after Transient Focal Cerebral Ischemia Reperfusion in Rats

Cited by 12 publications

References 49 publications

Repetitive transcranial magnetic stimulation promotes neural functional recovery via upregulation of synaptic plasticity-related proteins in rats with traumatic brain injury

Repetitive transcranial magnetic stimulation promotes neural functional recovery via upregulation of synaptic plasticity-related proteins in rats with traumatic brain injury

A Tau Pathogenesis-Based Network Pharmacology Approach for Exploring the Protections of Chuanxiong Rhizoma in Alzheimer’s Disease

Saccharina japonica Ethanol Extract Ameliorates Depression/Anxiety-Like Behavior by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Dextran Sodium Sulfate Induced Ulcerative Colitis Mice

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