Spinal cord injury (SCI) is a devastating
condition causing the
loss of sensory and motor functions. SCI pathology is multifaceted,
encompassing inflammation, scarring, neuronal damage, and vascular
and tissue remodeling. The dynamics of SCI rapidly transform from
acute, sub-acute, and chronic phases. The rapidly changing environment
necessitates the real-time monitoring of disease severity. Therefore,
in this study, we used the IVIS spectrum, a noninvasive fluorescence
imaging modality, to monitor the disease pathology in live animals.
We used near-infrared fluorescence imaging agents including Angiosense
750 EX, a probe that detects vascular changes, and Cat B 680 FAST,
a probe that detects inflammation at various day points post injury
(DPI), that is, DPI-1, DPI-14, and DPI-28. We quantified the pathophysiological
changes after SCI using IVIS in live animals. As a result, we observed
distinct differences in the disease progression between injured and
sham mice. Moreover, live imaging showed a good correlation with behavioral
studies, protein expression, and immunohistological analysis. Hence,
the goal of this study was to introduce a new optical imaging modality
that offers a determination of disease severity and the advantage
of accelerated imaging of the correlated biomarkers in a real-time
and dynamic manner. This study concluded that Cat B 680 Fast and Angiosense
750 EX could be used to assess the disease severity after SCI. Furthermore,
our study suggests that the noninvasive fluorescence optical imaging
modality offers a unique approach in monitoring neuroinflammatory
diseases in live animals.
The extracellular matrix (ECM) is a protein-and-carbohydrate meshwork that supports a variety of biological structures and processes, from tissue development and elasticity to the preservation of organ structures. ECM composition is different in each organ. It is a remarkably dynamic 3-dimensional structure that's constantly changing to maintain tissue homeostasis. This review aims to describe the involvement of ECM components in the remodeling process of spinal cord injury (SCI) and intervertebral disc degeneration (IVDD). Here, we have also described the current ECM-based therapeutic targets, which can be explored for ECM remodeling SCI is a neurological condition with intense influences resulting from a trauma inflicted on the spinal cord. SCI leads to damage to the intact ECM that leads to regeneration failure. IVDD mainly occurs due to aging and trauma. Various ECM components enable fragmentation of the disc and are thereby involved in disc degeneration. ECM manipulation can be used as an adjunct treatment in SCI and IVDD. Current treatment approaches for SCI and IVDD are conservative and unsatisfactory. Targeting ECM remodeling as an adjunct therapy may result in better disease outcomes.
De cits in the neuronal connection that succumbs to the impairment of sensory and motor neurons are the hallmarks of spinal cord injury (SCI). Secondary pathogenesis, which initiates after the primary mechanical insult to the spinal cord, depicts a pivotal role in producing in ammation, lesion formation and ultimately causes brotic scar formation in the chronic period. This brotic scar formed acts as a major hindrance in facilitating axonal regeneration and is one of the root causes of motor impairment. Cascade of secondary events in SCI begins with injury-induced blood spinal cord barrier rupture that promotes increased migration of neutrophils, macrophages, and other in ammatory cells at the injury site to initiate the secondary damages. This phenomenon leads to the release of matrix metalloproteinase, cytokines and chemokines, reactive oxygen species, and other proteolytic enzymes at the lesion site. These factors assist in the activation of TGF-β1 signalling pathway, which further leads to excessive proliferation of perivascular broblast, followed by deposition of collagen and bronectin matrix, which are the main components of the brotic scar. Subsequently, this scar formed inhibits the propagation of action potential from one neuron to adjacent neurons. Ethamsylate, an anti-hemorrhagic drug, has the potential to maintain early hemostasis as well as restores capillary resistance. Therefore, we hypothesized that ethamsylate, by virtue of its anti-hemorrhagic activity, reduces hemorrhagic ischemiainduced neuronal apoptosis, maintains the blood spinal cord barrier integrity, and decreases secondary damage severity, thereby reduce the extent of brotic scar formation, and demonstrates a neuroprotective role in SCI.
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