Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Zhu, Wenjun; L, X; Guo, Aimin; Zhao, Hong; Hy, Luo

doi:10.4238/2011.november.29.9

Cited by 7 publications

(3 citation statements)

References 23 publications

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“…Nogo-66 inhibits activity-dependent axonal growth by binding to the Nogo-66 receptor-1 (NgR1) ( 20 ). In turn, the NgR1 competitive antagonist, NEP1-40 (Nogo-66, residues 1–40), and antibodies against NogoA block this inhibitory effect and improve the neurological outcomes following ischemic stroke in adult rats ( 21 , 22 ). Lysophosphatidic acid (LPA) is a bioactive lipid ( 23 ).…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

et al. 2018

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Electroacupuncture (EA) may stimulate neurogenesis in animal models of ischemic stroke; however, the associated mechanisms are not clear. The present study aimed to evaluate the neurogenesis efficacy of EA on ischemic stroke and the underlying associated mechanisms. A model of middle cerebral artery occlusion (MCAO) was employed as the rat model of brain ischemia and reperfusion. EA treatment at the GV20 (Baihui) and GV14 (Dazhui) acupoints was conducted for 30 min daily following MCAO. Immunofluorescence was performed to measure the number of bromodeoxyuridine (BrdU)/nestin- or BrdU/doublecortin (DCX)-positive cells in the sham, MCAO and MCAO + EA groups. Results indicated that EA stimulation significantly decreased the neurological score and neuronal loss in rats in the MCAO group (both P<0.05). Furthermore, immunostaining assays indicated that BrdU/nestin- and BrdU/DCX-positive cells in EA-treated rats were significantly increased (P<0.05) when compared with the rats in the MCAO group, indicating EA may induce the proliferation and differentiation of endogenous neural stem cells (eNSCs) during cerebral ischemia-reperfusion. In addition, EA treatment significantly enhanced the protein expression levels of plasticity-related gene 5 (PRG5), a critical neurogenesis factor, and significantly decreased the protein expression levels of three neurogenesis inhibiting molecules, NogoA, lysophosphatidic acid and RhoA (all P<0.05). These results suggested that EA promotes the proliferation and differentiation of eNSCs, likely through modulating PRG5/RhoA signaling.

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Section: Introductionmentioning

confidence: 99%

Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

et al. 2018

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“…A number of factors contribute to nerve injury-associated diseases ( 1 – 3 ). Among these, spinal cord injury (SCI)-induced nerve damage is a serious threat to health worldwide ( 4 ). Following SCI, patients experience continuous and often diverse neurological deficits and disability ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Exercise intervention alleviates nerve injury by the suppression of inflammatory mediator expression via the TLR4/NF‑κB signaling pathway

2018

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Spinal cord injury (SCI) may cause changes that have damaging effects on sensation and functionality. However, methods for the significant amelioration of SCI-reduced nerve injury are lacking. Previous studies have indicated that reasonable and effective exercise may promote the recovery of injured nerves. Therefore, the aim of the present study was to investigate the ability of exercise to improve recovery following SCI and the underlying mechanism. A rat model was used to evaluate the effects of two different periods of exercise intervention on recovery following SCI. The exercise intervention comprised 15 or 30 min/day passive walking for 30 days. ELISA measurements were used to analysis the plasma levels of inflammatory cytokines. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were performed to examine the levels of proteins and mRNAs associated with nuclear factor (NF)-κB-related signaling. In addition, histological examination and immunostaining were used to evaluate the neural injury and associated indicators. The results indicated that severe SCI induced a peripheral inflammatory response and increased the expression of inflammatory cytokines. In addition, the SCI-induced nerve injury was associated with increased glial fibrillary acidic protein (GFAP) expression and the upregulation of Toll-like receptor 4 (TLR4)/NF-κB signaling, which may further aggravate the inflammatory responses induced by SCI. However, the exercise intervention decreased SCI-induced GFAP expression and reduced the activation of the TLR4/NF-κB signaling pathway compared with that of SCI model rats that did not exercise. Furthermore, the exercise intervention inhibited the release of inflammatory cytokines into the serum. These results indicate that exercise treatment reduces inflammation and glial activation, and may be beneficial to recovery following SCI.

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“…While amino-Nogo is important in axonal regeneration, sprouting and new network formation (3–5), Nogo-66 inhibits activity-dependent axonal growth by binding to the Nogo-66 receptor-1 (NgR1) (5). In turn, the NgR1 competitive antagonist, NEP1-40 (Nogo-66 residues 1–40), blocks this inhibitory effect (6). Notably, antibodies against Nogo-A improve neurological outcomes following ischemic stroke in adult rats (7).…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture attenuates cervical spinal cord injury following cerebral ischemia/reperfusion in stroke-prone renovascular hypertensive rats

Tan

Chen

Liang

et al. 2014

Experimental and Therapeutic Medicine

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Cerebral ischemia induces injury, not only in the ischemic core and surrounding penumbra tissues, but also in remote areas such as the cervical spinal cord. The aim of the present study was to determine the effects of electroacupuncture (EA) on cervical spinal cord injury following cerebral ischemia/reperfusion in stroke-prone renovascular hypertensive (RHRSP) rats. The results demonstrated that neuronal loss, which was assayed by Nissl staining in the cervical spinal cords of RHRSP rats subjected to transient middle cerebral artery occlusion (MCAO), was markedly decreased by EA stimulation at the GV20 (Baihui) and GV14 (Dazhui) acupoints compared with that in rats undergoing sham stimulation. Quantitative polymerase chain reaction and western blot analysis demonstrated that EA stimulation blocked the MCAO-induced elevated protein expression levels of glial fibrillary acidic protein and amyloid precursor protein in the cervical spinal cord at days 24 and 48. To further investigate the mechanism underlying the neuroprotective role of EA stimulation, the protein expression levels of Nogo-A and Nogo-66 receptor-1 (NgR1), two key regulatory molecules for neurite growth, were recorded in each group. The results revealed that EA stimulation reduced the MCAO-induced elevation of Nogo-A and NgR1 protein levels at day 14 and 28 in RHRSP rats. Therefore, the results demonstrated that EA reduced cervical spinal cord injury following cerebral ischemia in RHRSP rats, indicating that EA has the potential to be developed as a therapeutic treatment agent for cervical spinal cord injury following stroke.

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Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Cited by 7 publications

References 23 publications

Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

Exercise intervention alleviates nerve injury by the suppression of inflammatory mediator expression via the TLR4/NF‑κB signaling pathway

Electroacupuncture attenuates cervical spinal cord injury following cerebral ischemia/reperfusion in stroke-prone renovascular hypertensive rats

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