Neuroprotective effects of allicin on spinal cord ischemia–reperfusion injury via improvement of mitochondrial function in rabbits

Zhu, Jinwen; Chen, Tao; Guan, Jianzhong; Liu, Wenbo; Liu, Jian

doi:10.1016/j.neuint.2012.06.021

Cited by 44 publications

(21 citation statements)

References 51 publications

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“…These results suggested that allicin may exert protective effects against oxidative stress-induced damage in RPEs. These data further our understanding of the protective effects of allicin against oxidative stress not only with regards to neuroprotection and cardioprotection (14,15,29,32), but also vision protection. Intracellular accumulation of ROS is associated with oxidative stress and RPE dysfunction (33,34).…”

Section: Discussionsupporting

confidence: 54%

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Zhang

Wei

et al. 2016

Molecular Medicine Reports

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Abstract.Retinal pigmented epithelial cell (RPE) oxidative stress is known to have a vital role in the etiology of age-related macular degeneration (AMD). The present study aimed to investigate whether allicin, a natural product with antioxidant activity, was able to protect RPEs (ARPE-19) from hydrogen peroxide (H 2 O 2 )-induced damage, and to determine the underlying mechanisms. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to determine cellular viability, and reactive oxygen species (ROS) were detected using a ROS Assay kit. The results demonstrated that allicin was able to protect ARPE-19 cells from H 2 O 2 -induced damage in a dose-dependent manner. In addition, allicin attenuated oxidative stress by reducing the levels of intracellular ROS and malondialdehyde (MDA), and enhancing the glutathione/glutathione disulfide (GSSG) ratio. With regards to the underlying mechanism, allicin was able to markedly modulate the expression levels of ROS-associated enzymes, including superoxide dismutase, NADPH oxidase 4 and NAD(P)H dehydrogenase quinone 1, and elevate the activity of nuclear factor erythroid 2-related factor 2 in the H 2 O 2 -stimulated ARPE-19 cells. These results suggested that allicin may exert protective effects against H 2 O 2 -induced cytotoxicity in RPEs via ROS regulation.

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Section: Discussionsupporting

confidence: 54%

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Zhang

Wei

et al. 2016

Molecular Medicine Reports

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“…Mitochondria are the special organelles in most cells that generate ATP, for which mitochondria are sometimes called “cellular power factories” [45]. As the mitochondria supply cellular energy, mitochondrial dysfunction may play an important role in a variety of pathological conditions, including SCI [45]. Studies [46-48] have demonstrated that preserving mitochondrial function improved functional recovery after SCI.…”

Section: Discussionmentioning

confidence: 99%

Inhalation of Hydrogen of Different Concentrations Ameliorates Spinal Cord Injury in Mice by Protecting Spinal Cord Neurons from Apoptosis, Oxidative Injury and Mitochondrial Structure Damages

Chen

Cui

Zhai

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hydrogen selectively neutralizes reactive oxygen species (ROS) and ameliorates various ROS-induced injuries. Spinal cord injury (SCI) is a serious injury to the central nervous system, and secondary SCI is closely related to excessive ROS generation. We hypothesized that hydrogen inhalation ameliorates SCI, and the mechanism of action may be related to the protective effects of hydrogen against oxidative stress, apoptosis, and mitochondrial damage. Methods: Mechanically injured spinal cord neurons were incubated with different concentrations of hydrogen in vitro. Immunofluorescence staining and transmission electron microscopy were used to confirm the protective effects of hydrogen. ROS and related proteins were detected with dihydroethidium fluorescence staining, enzyme-linked immunosorbent assays, and western blotting. Terminal deoxynucleotidyl transferase dUTP nick end labeling assays, flow cytometry, and western blotting were used to detect neuronal apoptosis. ATP concentrations, Janus Green B staining, and mitochondrial permeability transition pore (mPTP) status were assessed to investigate mitochondrial damage. RNA sequencing was performed to screen potential target genes of hydrogen application. Hydrogen was administered to mice after spinal cord contusion injury was established for 42 days. The Basso Mouse Scale (BMS) and footprint analyses were used to assess locomotor functions, and immunofluorescence staining of the injured spinal cord segments was performed to detect oxidative stress status. Results: Spinal cord neurons were preserved by hydrogen administration after mechanical injury in a dose-dependent manner. ROS generation, oxidative stress injury-related markers, and the number of apoptotic neurons were significantly reduced after hydrogen treatment. The ATP production and mPTP function in injured neurons were preserved by hydrogen incubation. The expression levels of Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were inhibited by hydrogen treatment. BMS scores and the footprint assessment of mice with SCI were improved by hydrogen inhalation. Conclusions: Hydrogen inhalation (75%) ameliorated SCI in vivo and attenuated neuronal mechanical injuries in vitro, and its protective effect on spinal cord neurons was exerted in a dose-dependent manner. The underlying mechanisms included reducing ROS generation and oxidative stress, inhibiting neuronal apoptosis, and restoring mitochondrial construction and function. Cox8b, Cox6a2, Cox7a1, Hspb7, and Atp2a1 were identified as potential target genes of hydrogen treatment.

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“…Paraplegia is a fatal complication resulting from SCII during thoracic-abdominal aortic aneurysm surgery [1]. Several pathophysiological events, including excitotoxicity (glutamate-mediated), energy failure, inflammation, apoptosis, and oxidative stress, have been implicated in SCIR injury [4,5].…”

Section: Discussionmentioning

confidence: 99%

“…Spinal cord ischemic reperfusion (SCIR) injury is a fatal postoperative complication of thoracicabdominal aortic aneurysm surgery that contributes to paraplegia in about 10 % to 40 % of cases [1]. Paraplegia is a medical condition in which the sensory or motor part of the lower extremities is impaired due to spinal injury, resulting in long-term disability [2].…”

Section: Introductionmentioning

confidence: 99%

Dose-dependent protection of reseveratrol against spinal cord ischemic-reperfusion injury in rats

Su¹,

Zhong²,

Ren³

2016

Trop. J. Pharm Res

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Purpose: To examine the protective effects of resveratrol (RESV) against spinal cord ischemic reperfusion (SCIR) injury. Methods: Forty-eight male rats were divided into six groups: sham-operated (control-I), SCIR-treated (SCIR-II), rats receiving 20 mg/kg of RESV with SCIR (RESV 20+SCIR-III), rats receiving 40 mg/kg of RESV with SCIR (RESV 40+SCIR-IV), rats receiving 60 mg/kg of RESV with SCIR (RESV 60+SCIR-V), and rats receiving 50 mg/kg of methylprednisolone (MP) with SCIR (MP + SCIR-VI), for 7 days prior to IR (pre-treatment) and 7 days after IR (post-treatment). Results: The levels of oxidative markers (TBARS, MPO) and inflammatory markers (IL-1β, IL-6, TNF-α, and NF-p65) were concomitantly suppressed in RESV-treated rats, which showed improved locomotor function. A pronounced increase in the activities of antioxidant enzymes (SOD, CAT and GSH) was noted in the RESV

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Neuroprotective effects of allicin on spinal cord ischemia–reperfusion injury via improvement of mitochondrial function in rabbits

Cited by 44 publications

References 51 publications

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Inhalation of Hydrogen of Different Concentrations Ameliorates Spinal Cord Injury in Mice by Protecting Spinal Cord Neurons from Apoptosis, Oxidative Injury and Mitochondrial Structure Damages

Dose-dependent protection of reseveratrol against spinal cord ischemic-reperfusion injury in rats

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