Protective effects of hydrogen sulfide in a rat model of traumatic brain injury via activation of mitochondrial adenosine triphosphate–sensitive potassium channels and reduction of oxidative stress

Jiang, Xiaofan; Huang, Yi; Wang, Lin; Gao, Dakuan; Zhou, Fengjiao

doi:10.1016/j.jss.2013.03.067

Cited by 55 publications

(27 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…; Jiang et al . ), we tested these markers in total extracts and subcellular fractions of the TBI samples. Tissue extracts from Ct showed elevated protein oxidation compared to PC, while it was unchanged in areas away from Ct and controls (Fig.…”

Section: Resultsmentioning

confidence: 99%

Characterization of traumatic brain injury in human brains reveals distinct cellular and molecular changes in contusion and pericontusion

Harish

Mahadevan

Pruthi

et al. 2015

Journal of Neurochemistry

View full text Add to dashboard Cite

Traumatic brain injury (TBI) contributes to fatalities and neurological disabilities worldwide. While primary injury causes immediate damage, secondary events contribute to long-term neurological defects. Contusions (Ct) are primary injuries correlated with poor clinical prognosis, and can expand leading to delayed neurological deterioration. Pericontusion (PC) (penumbra), the region surrounding Ct, can also expand with edema, increased intracranial pressure, ischemia, and poor clinical outcome. Analysis of Ct and PC can therefore assist in understanding the pathobiology of TBI and its management. This study on human TBI brains noted extensive neuronal, astroglial and inflammatory changes, alterations in mitochondrial, synaptic and oxidative markers, and associated proteomic profile, with distinct differences in Ct and PC.While Ct displayed petechial hemorrhages, thrombosis, inflammation, neuronal pyknosis, and astrogliosis, PC revealed edema, vacuolation of neuropil, axonal loss, and dystrophic changes. Proteomic analysis demonstrated altered immune response, synaptic, and mitochondrial dysfunction, among others, in Ct, while PC displayed altered regulation of neurogenesis and cytoskeletal architecture, among others. TBI brains displayed oxidative damage, glutathione depletion, mitochondrial dysfunction, and loss of synaptic proteins, with these changes being more profound in Ct. We suggest that analysis of markers specific to Ct and PC may be valuable in the evaluation of TBI pathobiology and therapeutics.

show abstract

Section: Resultsmentioning

confidence: 99%

Characterization of traumatic brain injury in human brains reveals distinct cellular and molecular changes in contusion and pericontusion

Harish

Mahadevan

Pruthi

et al. 2015

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…Such undifferentiated cells can express an incomplete set of glutamate NMDA receptors, and, therefore, those cascade processes that trigger apoptosis in mature neurons in immature cells cannot cause death. On the other hand, it is known that H 2 S is metabolized by mitochondria through participation in the oxidation process of the H 2 S-producing enzymes [13,31]. The stress-induced H 2 S production in mitochondria and a subsequent increase in the ATP production were demonstrated [32].…”

Section: Cbs In the Telencephalon Parenchymamentioning

confidence: 99%

“…We believe that this increase in the number of the CBS+ cells is due to the oxidative stress and the accumulation of ROS, which are neutralized by hydrogen sulfide. The sources of ROS generation in cell include mitochondria, superoxide-producing enzymes, such as xanthine oxide, NADPH oxidase, and hydrogen peroxide-producing enzymes, such as superoxide dismutase [12,13]. ROS acceptors include antioxidants, such as glutathione, as well as enzymes superoxide dismutase and catalase.…”

Section: Cerebellummentioning

confidence: 99%

“…The use of monoclonal antibodies against cystathionine β-synthase (CBS) in immunohistochemical (IHC) detection of the H 2 S-producing complexes in the brain of juvenile trout showed an increase in hydrogen sulfide production in different parts of the brain and CBS induction in the radial glia cells after the damage of the optic nerve [11]. It was shown that the toxic and/or neuroprotective effects of hydrogen sulfide depended on concentration: lower concentrations play a physiological role, while very high concentrations cause cell death [12,13]. Although hydrogen sulfide is considered a gasotransmitter, there is uncertainty about the total concentration of this volatile gas or highly active anionic particles (SH-) in both plasma and central nervous system tissues [14].The progress in studies of the hydrogen sulfide biology has led to a conclusion that polysulfides are more significant sources of intermediate sulfhydration of proteins than H 2 S [3].…”

mentioning

confidence: 99%

See 1 more Smart Citation

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Пущина¹,

Вараксин²,

Обухов³

2020

Neuroprotection - New Approaches and Prospects

View full text Add to dashboard Cite

The H 2 S-producing systems were studied in trout telencephalon, tectum, and cerebellum at 1 week after eye injury. The results of ELISA analysis have shown a 1.7-fold increase in the CBS expression at 1 week post-injury, as compared to the intact trout. In the ventricular and subventricular regions of trout telencephalon, CBS+ cells, as well as neuroepithelial and glial types, were detected. As a result of injury, the number of CBS+ neuroepithelial cells in the pallial and subpallial periventricular regions of the telencephalon increases. In the tectum, a traumatic damage leads to an increase in the CBS expression in radial glia with a simultaneous decrease in the number of CBS immunopositive neuroepithelial cells detected in intact animals. In the cerebellum, we revealed neuroglial interrelations, in which H 2 S is probably released from the astrocyte-like cells with subsequent activation of the neuronal NMDA receptors. The organization of the H 2 S-producing cell complexes suggests that the amount of glutamate produced in the trout cerebellum and its reuptake is controlled with the involvement of astrocyte-like cells, reducing its excitotoxicity. We believe that the increase in the number of H 2 S-producing cells constitutes a response to oxidative stress, and the overproduction of H 2 S neutralizes the reactive oxygen species.2 completely clarified thus far. H 2 S, like nitric oxide (NO), is known to mediate posttranslational modification of proteins by adding additional sulfur to reactive cysteine residues. This modification, referred to as S-sulfhydration, is required to activate or inactivate many classes of proteins, including the ion channels, such as the ATP-dependent potassium channels, TRPV3, TRPV6, TRPM [6], enzymes, and the transcription factors NF-kB and Nrf2 [7]. Modulation of ion channels, as well as the inflammatory and the antioxidant transcription factors, using H 2 S after traumatic brain injury, can play a significant role in reducing edema and inflammation [8].Recently, the involvement of H 2 S in cerebral ischemia, traumatic brain injury (TBI), and decrease in reactive oxygen species in the H 2 S-dependent mechanisms has been studied using different models [8][9][10]. The use of monoclonal antibodies against cystathionine β-synthase (CBS) in immunohistochemical (IHC) detection of the H 2 S-producing complexes in the brain of juvenile trout showed an increase in hydrogen sulfide production in different parts of the brain and CBS induction in the radial glia cells after the damage of the optic nerve [11]. It was shown that the toxic and/or neuroprotective effects of hydrogen sulfide depended on concentration: lower concentrations play a physiological role, while very high concentrations cause cell death [12,13]. Although hydrogen sulfide is considered a gasotransmitter, there is uncertainty about the total concentration of this volatile gas or highly active anionic particles (SH-) in both plasma and central nervous system tissues [14].The progress in studies of the hydrogen sulfide biology h...

show abstract

“…Overexpression of AQP4 in the gray matter of the spinal cord indicates that AQP4 might play an important role in regulating the water balance of the spinal cord. Inward rectifier potassium channel 4.1 (Kir4.1) participates in not only the formation of action potentials, but also water transportation, in brain tissues 5 . The expression of Kir4.1 in rats with focal cerebral ischemia/reperfusion positively correlated …”

Section: ■ Introductionmentioning

confidence: 99%

Effects of aquaporin 4 and inward rectifier potassium channel 4.1 on medullospinal edema after methylprednisolone treatment to suppress acute spinal cord injury in rats

Liu

et al. 2018

Acta Cir. Bras.

View full text Add to dashboard Cite

Effects of aquaporin 4 and inward rectifier potassium channel 4.1 on medullospinal edema after methylprednisolone treatment to suppress acute spinal cord injury in rats 1 9-Experimental SurgeryActa Cir Bras. 2018;33(2):175-184 AbstractPurpose: To investigate the effects of aquaporin 4 (AQP4) and inward rectifier potassium channel 4.1 (Kir4.1) on medullospinal edema after treatment with methylprednisolone (MP) to suppress acute spinal cord injury (ASCI) in rats. Methods: Sprague Dawley rats were randomly divided into control, sham, ASCI, and MPtreated ASCI groups. After the induction of ASCI, we injected 30 mg/kg MP via the tail vein at various time points. The Tarlov scoring method was applied to evaluate neurological symptoms, and the wet-dry weights method was applied to measure the water content of the spinal cord. Results:The motor function score of the ASCI group was significantly lower than that of the sham group, and the spinal water content was significantly increased. In addition, the levels of AQP4 and Kir4.1 were significantly increased, as was their degree of coexpression. Compared with that in the ASCI group, the motor function score and the water content were significantly increased in the MP group; in addition, the expression and coexpression of AQP4 Conception, design, intellectual and scientific content of the study; acquisition of data; manuscript writing; critical revision. IIAttending Doctor, Department of Orthopaedics, China-Japan Union Hospital, Jilin University, Changchun, China. Acquisition of data, manuscript writing. IIIProfessor, Department of Orthopaedics, China-Japan Union Hospital, Jilin University, Changchun, China. Scientific content of the study, acquisition of data, manuscript writing. IV Professor, Department of Orthopaedics, China-Japan Union Hospital, Jilin University, Changchun, China. Acquisition of data. V Professor, Department of Orthopaedics, China-Japan Union Hospital, Jilin University, Changchun, China. Intellectual, scientific, conception and design of the study; critical revision. 175Effects of aquaporin 4 and inward rectifier potassium channel 4.1 on medullospinal edema after methylprednisolone treatment to suppress acute spinal cord injury in rats Li Y et al.

show abstract

Protective effects of hydrogen sulfide in a rat model of traumatic brain injury via activation of mitochondrial adenosine triphosphate–sensitive potassium channels and reduction of oxidative stress

Cited by 55 publications

References 44 publications

Characterization of traumatic brain injury in human brains reveals distinct cellular and molecular changes in contusion and pericontusion

Characterization of traumatic brain injury in human brains reveals distinct cellular and molecular changes in contusion and pericontusion

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Effects of aquaporin 4 and inward rectifier potassium channel 4.1 on medullospinal edema after methylprednisolone treatment to suppress acute spinal cord injury in rats

Contact Info

Product

Resources

About