Dataset Information

Seawater immersion exacerbates the pathological changes caused by incisive corneal injury in rabbit eyes.

ABSTRACT:

Background

Seawater immersion complicates injuries suffered during maritime conflicts and eye injury is one of most common injuries on the battlefield. This study aimed to delineate the pathophysiological changes in the cornea after corneal injury combined with seawater immersion.

Methods

The left eye of New Zealand White rabbits was injured with firecracker and a 3-mm long whole-layer incision in the center of the cornea parallel to the corneal limbus, followed by seawater immersion. The right eye was used as a control. The histology of the cornea and the inflammatory cytokine/chemokine levels in the aqueous humor were examined on days 1 and 7 after injury. The protein levels of aquaporin 1, 3, and 5 were assessed by immunohistochemical staining 7 days after injury. The expression and activation of nuclear factor κB (NF-κB) were examined by Western blot analysis.

Results

Seawater immersion exacerbated penetrating explosive injury caused progressive tissue damage of the cornea and ocular inflammation, with drastic increases in the expression of cytokines/chemokines in the aqueous humor, which was mediated by the upregulation and activation of NF-κB. Furthermore, corneal protein levels of aquaporin 1, 3, and 5 were significantly increased after incisive injury and seawater immersion.

Conclusions

These data demonstrated that the combination of incisive injury and seawater immersion is a dangerous situation and effective care strategies should be developed for the management of such maritime injuries.

SUBMITTER: Wang YF

PROVIDER: S-EPMC9201191 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Publications

Seawater immersion exacerbates the pathological changes caused by incisive corneal injury in rabbit eyes.

Wang Ying-Fei YF Jia Hong-Zhen HZ Song Yiguo Y

Annals of translational medicine 20220501 10

<h4>Background</h4>Seawater immersion complicates injuries suffered during maritime conflicts and eye injury is one of most common injuries on the battlefield. This study aimed to delineate the pathophysiological changes in the cornea after corneal injury combined with seawater immersion.<h4>Methods</h4>The left eye of New Zealand White rabbits was injured with firecracker and a 3-mm long whole-layer incision in the center of the cornea parallel to the corneal limbus, followed by seawater immers ...[more]

PMID: 35722388

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Project description:Traumatic brain injury (TBI) is a major cause of death and disability in naval warfare. Due to the unique physiochemical properties of seawater, immersion in it exacerbates TBI and induces severe neural damage and complications. However, the characteristics and underlying mechanisms of seawater-immersed TBI remain unclear. Mitochondrial dysfunction is a major cause of TBI-associated brain damage because it leads to oxidative stress, decrease in energy production, and apoptosis. Thus, the present study aimed to further elucidate the current understanding of the pathology of seawater-immersed TBI, particularly the role of mitochondrial dysfunction, using a well-defined rat model of fluid percussion injury and a stretch injury model comprising cultured neurons. The biochemical and pathological markers of brain-related and neuronal injuries were evaluated. Histological analysis suggested that seawater immersion enhanced brain tissue injury and induced a significant increase in apoptosis in rats with TBI. Additionally, lactate dehydrogenase release occurred earlier and at higher levels in stretched neurons at 24 h after seawater immersion, which was consistent with more severe morphological changes and enhanced apoptosis. Furthermore, seawater immersion induced more rapid decreases in mitochondrial membrane potential, adenosine triphosphate (ATP) content, and H+-ATPase activity in the cortices of TBI rats. In addition, the immunochemical results revealed that seawater immersion further attenuated mitochondrial function in neurons exposed to stretch injury. The increases in neuronal damage and apoptosis triggered by seawater immersion were positively correlated with mitochondrial dysfunction in both in vivo and in vitro models. Thus, the present findings strengthen the current understanding of seawater-immersed TBI. Moreover, because seawater immersion aggravates mitochondrial dysfunction and contributes to post-traumatic neuronal cell death, it is important to consider mitochondria as a therapeutic target for seawater-immersed TBI.

Dataset Information

Seawater immersion exacerbates the pathological changes caused by incisive corneal injury in rabbit eyes.

Background

Methods

Results

Conclusions

Publications

Seawater immersion exacerbates the pathological changes caused by incisive corneal injury in rabbit eyes.

Similar Datasets

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