1,25-Dyhydroxyvitamin D3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy

Jang, Wooyoung; Kim, Hee-Ju; Li, Huan; Jo, Kyung-Wook; Lee, Moon Kyu; Song, Sun Hong; Yang, Hyun Ok

doi:10.1016/j.bbrc.2014.07.081

Cited by 93 publications

(63 citation statements)

References 39 publications

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“…9 In addition, similar therapeutic effects were confirmed in an in vitro model of Parkinson's disease. 10 Therefore, calcitriol treatment reduces Effects of calcitriol on SCI K-l Zhou et al the level of cell apoptosis in many diseases. Previous studies have shown that Bcl2 exerts an antiapoptotic effect, 15 whereas Bax participates in the induction of apoptosis; 16 activation of C-caspase3 is seen as a hallmark of apoptotic cell death, acting as the final executor of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

“…9 In addition, calcitriol has been reported to upregulate the level of cellular autophagy. 10 However, its relevance to promotion of functional recovery after SCI in rats has not been reported. In the present study, the effects of calcitriol on SCI and the underlying mechanism of action were explored.…”

Section: Introductionmentioning

confidence: 99%

Effects of calcitriol on experimental spinal cord injury in rats

Jin

et al. 2016

Spinal Cord

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“…Recently, many studies of PD models have demonstrated roles for vitamin D in neuronal cell differentiation and neuroprotection via various mechanisms [17,18,19,20,21]. Therefore, vitamin D may be neuroprotective against PD-related degenerative processes in the dorsal motor vagal system and enteric nervous system, indicating that vitamin D plays an important role in gastric dysmotility in PD.…”

Section: Discussionmentioning

confidence: 99%

“…However, several studies have demonstrated an additional role for vitamin D in neuroprotection through various mechanisms, including antioxidation, neuronal calcium regulation, immunomodulation, enhanced nerve conduction, detoxification and autophagy [16,17,18,19,20,21]. Furthermore, vitamin D has recently been suggested to be involved in the pathogenesis and progression of PD [22], and recently, we reported that vitamin D levels were associated with orthostatic hypotension in PD patients [23].…”

Section: Introductionmentioning

confidence: 99%

Low Serum Vitamin D Levels May Contribute to Gastric Dysmotility in de novo Parkinson's Disease

Kwon

Jo²,

Lee³

et al. 2016

Neurodegener Dis

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Background and Objectives: Gastrointestinal dysfunction is a common non motor symptom in Parkinson's disease (PD). However, the potential association between vitamin D and gastroparesis in PD has not been previously investigated. The aim of this study was to compare vitamin D levels between drug-naive de novo PD patients with normal gastric emptying and those with delayed gastric emptying. Methods: Fifty-one patients with drug-naive de novo PD and 20 age-matched healthy controls were enrolled in this study. Gastric emptying time (GET) was assessed by scintigraphy, and gastric emptying half-time (T_1/2) was determined. The PD patients were divided into a delayed-GET group and a normal-GET group. Results: The serum 25-hydroxyvitamin D₃ levels were decreased in the delayed-GET group compared with the normal-GET and control groups (11.59 ± 4.90 vs. 19.43 ± 6.91 and 32.69 ± 4.93, respectively, p < 0.01). In the multivariate model, the serum 25-hydroxyvitamin D₃ level was independently associated with delayed gastric emptying in PD patients. Conclusions: Vitamin D status may be an independent factor for gastric dysmotility in PD. Although the underlying mechanism remains to be characterized, vitamin D status may play a role in the pathogenesis of delayed gastric emptying in drug-naive PD.

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“…Yapılan deneysel nörodejenerasyon modellerinde vitamin D 3 'ün nöroprotektif olduğu gösterilmiştir (14)(15)(16)(17). Yapılan çalışmalarda vitamin D 3 'ün immün sistem ve beyin fonksiyonlarını da düzenlediğine yönelik bilimsel kanıtlar elde edilmiştir (18).…”

Section: Introductionunclassified

Therapeutic effects of vitamin D3 on motor functions following experimental spinal cord injury

Çelik¹,

Mutevelizade²,

Harman³

et al. 2015

tnd

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Amaç: Akut spinal kord yaralanması (SKY) sonrası nörolojik hasar, primer mekanik yaralanma ile olduğu kadar sekonder olarak doku hasarına yol açan hücre ölümü aktivasyon kaskatlarından da kaynaklanmaktadır. Bu çalışmada vitamin D 3 'ün sıçanlarda oluşturulan deneysel SKY sonrasında motor fonksiyonlar üzerindeki iyileştirici etkinliği araştırıldı. Gereç ve Yöntem:Bu çalışma Sağlık Bakanlığı Haydarpaşa Numune Eğitim ve Araştırma Hastanesi'nde yapıldı. Çalışmada 3 grupta, 7'şer adet olmak üzere toplam 21 adet Spraque-Dawley cinsi sıçan kullanıldı. İlk gruba sadece laminektomi yapıldı (kontrol grubu). İkinci gruba laminektomi yapılıp omurilik yaralanması oluşturuldu (travma grubu). Üçüncü gruba laminektomi yapılıp omurilik yaralanması oluşturuldu ve 1., 3., 5., 7. günlerde intraperitoneal olarak 1 mcg/kg/gün dozunda vitamin D 3 enjeksiyonu yapıldı (vitamin D 3 grup). Deneklerin fonksiyonel iyileşmeleri cerrahi işlem sonrası 1., 7., 14. ve 21. günlerde eğik düzlem testi, Drummond ve Moore motor fonksiyon skoru ile değerlendirildi. Kontrol, travma ve vitamin D 3 uygulanan gruplardaki doku parçaları hematoksileneozin (HE) boyası ile boyanıp ışık mikroskobunda incelendi. Bulgular: Vitamin D 3 grubunda eğik düzlem testi sonuçları ve motor fonksiyon skorları travma grubu ile karşılaştırıldığında 1., 2. ve 3. haftalarda anlamlı olarak daha yüksek bulundu. Objective: Spinal cord injuries are frequently encountered and is a major health problem due to the severe disability they cause. The neurological damage of acute spinal cord trauma triggers primary mechanisms of injury and cell death activation cascades leading to tissue damage. The aim of this study was to investigate the therapeutic effects of vitamin D 3 in a rat model of spinal cord injury. Materials and Methods:The study was performed at Haydarpaşa Numune Training Hospital, İstanbul, Turkey. Twenty-one Spraque-Dawley rats were randomly assigned to the following study groups: the control group, undergoing laminectomy procedure; trauma group, undergoing spinal cord injury after laminectomy; and trauma plus vitamin D 3 group, undergoing spinal cord injury after laminectomy and subsequent administration of vitamin D 3 on days 1, 3, 5, 7 intraperitoneally with a dosage of 1 mcg/kg/day. The functional outcome was evaluated by using inclined plane test and Drummond and Moore motor function

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1,25-Dyhydroxyvitamin D3 attenuates rotenone-induced neurotoxicity in SH-SY5Y cells through induction of autophagy

Cited by 93 publications

References 39 publications

Effects of calcitriol on experimental spinal cord injury in rats

Effects of calcitriol on experimental spinal cord injury in rats

Low Serum Vitamin D Levels May Contribute to Gastric Dysmotility in de novo Parkinson's Disease

Therapeutic effects of vitamin D3 on motor functions following experimental spinal cord injury

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