Neuroprotection by co-treatment and post-treating with calcitriol following the ischemic and excitotoxic insult in vivo and in vitro

Kajta, Małgorzata; Makarewicz, Dorota; Ziemińska, Elżbieta; Jantas, Danuta; Domin, Helena; Lasoń, Władysław; Kutner, Andrzej; Łazarewicz, Jerzy W.

doi:10.1016/j.neuint.2009.03.010

Cited by 67 publications

(51 citation statements)

References 57 publications

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“…Calcitriol has been shown to provide neuroprotection against ischaemia-reperfusion injury by decreasing the level of oxidative stress in the rat hippocampus. 22 In the present study, we found that SOD activity and GSH content were markedly increased in the calcitriol group compared with controls, whereas the MDA level was decreased. Therefore, we verified that calcitriol suppresses oxidative stress in the damaged SCI.…”

Section: Discussionsupporting

confidence: 55%

Effects of calcitriol on experimental spinal cord injury in rats

Jin

et al. 2016

Spinal Cord

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Study design: Experimental, controlled, animal study. Objectives: To evaluate the effects of calcitriol on oxidative stress, apoptosis, autophagy and locomotor recovery in rats after spinal cord injury (SCI). Setting: China. Methods: Ninety female rats were randomly divided into three groups. Laminectomy only was performed in the control group. The SCI group received laminectomy as well as spinal cord compression injury. In the calcitriol group, SCI rats received an intraperitoneal injection of calcitriol (2 μg kg − 1 day − 1 ). Oxidative stress was assessed by the tissue superoxide dismutase (SOD) activity and the contents of glutathione (GSH) and malondialdehyde (MDA). The extent of apoptosis was assessed by immunohistochemistry for C-caspase3, TUNEL staining and western blotting for C-caspase3, Bax and Bcl2. Transmission electron microscopy was used to examine autophagosomes in the injured spinal cord of calcitriol-treated rats. Autophagy was detected by western blotting for LC3-II, Beclin1 and p62. Histological changes were assessed by haematoxylin and eosin staining and Nissl staining. Functional recovery was reflected by the Basso, Beattie and Bresnahan locomotion rating scale and the inclined plane test. Results: With calcitriol treatment, oxidative stress was decreased, SOD activity and GSH content were increased and MDA content was decreased. Moreover, apoptosis was inhibited in the SCI plus calcitriol group. However, a higher level of autophagy was detected in the lesions of the calcitriol group compared with the SCI group. Histological damage and neuron loss after SCI were reduced in calcitrioltreated rats, and functional recovery was significantly promoted in the calcitriol group compared with controls. Conclusions: Calcitriol promotes locomotor recovery after SCI by reducing oxidative stress and inhibiting apoptosis, as well as promoting autophagy.

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Section: Discussionsupporting

confidence: 55%

Effects of calcitriol on experimental spinal cord injury in rats

Jin

et al. 2016

Spinal Cord

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“…In the gerbil model of global forebrain ischemia we used a simple and reliable method of counting the surviving neurons for the assessment of ischemia-induced loss of neurons in CA1 [16,17]. Also, the methods of evaluating brain damage induced by hypoxia-ischemia by measuring weight deficit of the ischemic hemispheres and counting the apoptotic neurons in the immature rat brain have been proven in our previous studies [16][17][18]30,41].…”

Section: Discussionmentioning

confidence: 99%

Original article Delayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia

Makarewicz¹,

Sulejczak²,

Duszczyk³

et al. 2014

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A b s t r a c t Introduction: In vitro experiments have demonstrated that preconditioning primary neuronal cultures by temporary application of NMDA receptor antagonists induces long-term tolerance against lethal insults.In the present study we tested whether similar effects also occur in brain submitted to ischemia in vivo and whether the potential benefit outweighs the danger of enhancing the constitutive apoptosis in the developing brain. Material and methods: Memantine in pharmacologically relevant doses of 5 mg/kg or (+)MK-801 (3 mg/kg) was administered i.p. 24, 48, 72 and 96 h before 3-min global forebrain ischemia in adult Mongolian gerbils or prior to hypoxia/ ischemia in 7-day-old rats. Neuronal loss in the hippocampal CA1 in gerbils or weight deficit of the ischemic hemispheres in the rat pups was evaluated after 14 days. Also, the number of apoptotic neurons in the immature rat brain was evaluated. Results: In gerbils only the application of (+)MK-801 24 h before ischemia resulted in significant prevention of the loss of pyramidal neurons. In rat pups administration of (+)MK-801 at all studied times before hypoxia-ischemia

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“…These proapoptotic effects appear to be concentration-dependent. At least in vitro, high doses of calcitriol increase apoptosis, while lower doses are antiapoptotic [12]. …”

Section: Vitamin D and The Developing Brainmentioning

confidence: 99%

“…Studies of therapeutic vitamin D administration to improve the outcomes in adults with ischemic stroke have yet to demonstrate clear benefit. These data do not rule out a role for vitamin D in neonatal ischemic disorders, however, as animal studies of cerebral ischemia have demonstrated an increasing effect of calcitriol administration correlating with younger age [12]. During development, vitamin D influences the brain via its effects on neurotrophic factors [13-16], and animal studies have shown vitamin D deficiency to be a risk factor for abnormal brain development [13].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D and Its Role in Neonatal Hypoxic-Ischemic Brain Injury

Stessman

Peeples

2018

Neonatology

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Emerging evidence has demonstrated that vitamin D plays an important role in many adult neurologic disorders, but is also critical in neuronal development and pruning in the neonatal and pediatric populations. Neonates are at a particularly high risk of vitamin D deficiency, in part due to the high prevalence of maternal deficiency during pregnancy. Several preclinical studies have demonstrated that infants born to vitamin D-deficient mothers are at a high risk of developing neonatal brain injury, and recent clinical studies have shown that neonates with hypoxic-ischemic encephalopathy (HIE) tend to be vitamin D-deficient. There are limited data, however, on whether additional prenatal or postnatal supplementation may alter the prevalence or severity of neonatal HIE. This review examines the current data supporting the neuroprotective role of vitamin D, with a focus on how these findings may be translated to neonates with HIE.

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Neuroprotection by co-treatment and post-treating with calcitriol following the ischemic and excitotoxic insult in vivo and in vitro

Cited by 67 publications

References 57 publications

Effects of calcitriol on experimental spinal cord injury in rats

Effects of calcitriol on experimental spinal cord injury in rats

Original article Delayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia

Vitamin D and Its Role in Neonatal Hypoxic-Ischemic Brain Injury

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