Autophagy Is Activated in Injured Neurons and Inhibited by Methylprednisolone After Experimental Spinal Cord Injury

Chen, Hsien Chih; Fong, Tsorng Harn; Lee, Ai Wei; Chiu, Wen Ta

doi:10.1097/brs.0b013e318221e859

Cited by 79 publications

(68 citation statements)

References 29 publications

(21 reference statements)

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“…Recently, it has been reported that autophagy has a key role in injured spinal cord tissue. 6,30,31 In this study, we report that autophagy is activated at the injury site after SCI. LC3B expression is increased, beginning at 4 h and peaking at 7 days after SCI.…”

Section: Discussionmentioning

confidence: 96%

G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice

Guo

Liu

Zhang

et al. 2015

Laboratory Investigation

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Granulocyte colony-stimulating factor (G-CSF) was investigated for its capacity to induce autophagy and related neuroprotective mechanisms in an acute spinal cord injury model. To accomplish this goal, we established a mouse spinal cord hemisection model to test the effects of recombinant human G-CSF. The results showed that autophagy was activated after spinal cord injury and G-CSF appears to induce a more rapid activation of autophagy within injured spinal cords as compared with that of non-treated animals. Apoptosis as induced in mechanically injured neurons with G-CSF treatment was enhanced after inhibiting autophagy by 3-methyladenine (3-MA), which partially blocked the neuroprotective effect of autophagy as induced by G-CSF. In addition, G-CSF inhibited the activity of the NF-κB signal pathway in neurons after mechanical injury. We conclude that G-CSF promotes autophagy by inhibiting the NF-κB signal pathway and protects neuronal structure after spinal cord injury. We therefore suggest that G-CSF, which rapidly induces autophagy after spinal cord injury to inhibit neuronal apoptosis, may thus provide an effective auxiliary therapeutic intervention for spinal cord injury.

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Section: Discussionmentioning

confidence: 96%

G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice

Guo

Liu

Zhang

et al. 2015

Laboratory Investigation

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“…6,7 The protective effects of VCE against apoptotic cell death are well described in the literature. 8,9 Some studies also demonstrated associations of VCE with the expression of autophagy.…”

Section: Introductionmentioning

confidence: 88%

“…Recently, we demonstrated that after a spinal cord contusion injury in rats, levels of LC3-II, a marker of autophagy, were elevated in neurons near the lesion epicenter. 6 Liu et al, 13 provided the time course of apoptosis after a contusion injury. By 4 h, apoptosis was detected in neurons within the lesion area, and this neuronal apoptosis peaked at 8 h. A second wave of apoptotic cells, identified as oligodendrocytes, was detected throughout the white matter at 7 days, associated with degenerating axons.…”

Section: Vce Treatment Inhibits Apoptosis and Enhances Autophagymentioning

confidence: 99%

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Effects of the combined administration of vitamins C and E on the oxidative stress status and programmed cell death pathways after experimental spinal cord injury

et al. 2013

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Study Design: Experimental, controlled, animal study. Objectives: To assess the effects of vitamins C and E (VCE) treatment on oxidative stress and programmed cell deaths after rat spinal cord injury (SCI), as well as functional recovery. Setting: Taiwan. Methods: Fifty-four Sprague-Dawley rats were used for the experimental procedure. In the sham group, laminectomy at T10 was performed, followed by impactor contusion of the spinal cord. In the control group, only a laminectomy was performed without contusion. Oxidative stress status was assessed by measuring the spinal cord tissue content of superoxide dismutase (SOD) and gluthatione peroxidase (GSH-Px) activities. We also evaluated the effects of combined VCE treatment using western blot to analyze expression of cleaved caspase-3 and microtubule-associated protein light chain 3 (LC3), and the Basso, Beattie and Bresnahan (BBB) scale to evaluate functional outcomes. Results: Combined treatment of VCE significantly counteracted the effects of spinal cord contusion on oxidative stress represented by activities of SOD and GSH-Px (Po0.05). The VCE treatment also significantly enhanced LC3-II expression and decreased cleaved caspase-3 compared with the sham (Po0.05). Furthermore, BBB scores significantly improved in the VCE-treated group compared with the sham group (on day 14 and 28 after SCI; Po0.05). Conclusions: The combined administration of VCE was clearly capable of modulating the antioxidant effects, and of reducing apoptosis and increasing autophagy at the lesion epicenter leading to an improved functional outcome. Use of such clinically ready drugs could help earlier clinical trials in selected cases of human SCIs.

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“…injection of 30 mg/kg b.w. [13,15,23,28,41] or multiple i.v. injections within 24 h [43], or 30 mg/kg b.w.…”

Section: Introductionmentioning

confidence: 99%

Original article Subdural infusion of dexamethasone inhibits leukomyelitis after acute spinal cord injury in a rat model

Kwiecień¹,

Jarosz²,

Urdzíková³

et al. 2015

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A b s t r a c t Trauma in spinal cord injury often results in massive damage to the white matter and in damage to myelin that results in a severe phagocyte-rich infiltration apparently directed at removing immunologically toxic myelin debris. In the epidural balloon crush injury to the rat cranial thoracic spinal cord, the dorsal column was crushed, which at one week post-op resulted in its obliteration by a severe infiltration by a virtually pure population of macrophages that internalized all damaged myelin. A week-long subdural infusion of dexamethasone, a stable synthetic corticosteroid, resulted in remarkable inhibition of the macrophage infiltration of the crush cavity and in the lack of removal of myelin debris by phagocytosis. In this study we demonstrated that spinal cord injury results in a severe inflammatoryresponse directed at massively damaged myelin, and we inhibited this response with a subdural infusion of a powerful anti-inflammatory drug, dexamethasone.

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Autophagy Is Activated in Injured Neurons and Inhibited by Methylprednisolone After Experimental Spinal Cord Injury

Cited by 79 publications

References 29 publications

G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice

G-CSF promotes autophagy and reduces neural tissue damage after spinal cord injury in mice

Effects of the combined administration of vitamins C and E on the oxidative stress status and programmed cell death pathways after experimental spinal cord injury

Original article Subdural infusion of dexamethasone inhibits leukomyelitis after acute spinal cord injury in a rat model

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