Ethamsylate Attenuates Mutilated Secondary Pathogenesis and Exhibits a Neuroprotective Role in Experimental Model of Spinal Cord Injury

Abstract

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.

Ratiometric Fluorescent Probe Promotes Trans-differentiation of Human Mesenchymal Stem Cells to Neurons

“…N eurological injuries, the functional loss of neurons due to the death of nerve cells over time, and cognitive deficit are all symptoms of neurodegenerative diseases like Alzheimer's disease (AD), 1 Parkinson's disease (PD), 2 Huntington's disease (HD), 3 spinal cord injury (SCI), 4,5 stroke, 6 and amyotrophic lateral sclerosis (ALS). 7 Neurodegenerative processes start years before any clinical symptoms appear and progress slowly and irreversibly over time.…”

“…Neurological injuries, the functional loss of neurons due to the death of nerve cells over time, and cognitive deficit are all symptoms of neurodegenerative diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), spinal cord injury (SCI), , stroke, and amyotrophic lateral sclerosis (ALS) . Neurodegenerative processes start years before any clinical symptoms appear and progress slowly and irreversibly over time. , Only a limited amount of progress has been made in this area, despite significant research and ongoing clinical efforts, such as diagnosable treatments and precautions to enhance patients’ quality of life.…”