Abstract
Intracerebral hemorrhage (ICH) is a devastating disease that is characterized by high morbidity and high mortality. ICH has an annual incidence of 10–30/100,000 people and accounts for approximately 10%–30% of all types of stroke. ICH mostly occurs at the basal ganglia, which is rich in nerve fibers; thus, hemiplegia is quite common in ICH patients with partial sensory disturbance and ectopic blindness. In the clinic, those symptoms are considered to originate from the white matter injury in the area, but the exact mechanisms are unknown, and currently, no effective drug treatments are available to improve the prognosis. Clarifying the mechanisms will contribute to the development of new treatment methods for patients. The transient receptor potential ankyrin 1 (TRPA1) channel is a non-selective cation channel that plays a role in inflammatory pain sensation and nociception and may be a potential regulator in emotion, cognition and social behavior. Here, we report that TRPA1 is involved in myelin damage and oxidative stress injury in a mouse ICH model. Intervention with the TRPA1 channel may be a new method to improve the motor function of patients in the early stage of ICH.
Highlights
Intracerebral hemorrhage (ICH) comprises 10%–30% of all stroke cases (Balami and Buchan, 2012)
Compared with those of the sham group mice, the ICH mice showed a lower score in the basso mouse scale (BMS) and beam balance tests on D0-D3 (Figures 1A,B)
White matter injury has long been considered the major cause of hemiplegia, partial sensory disturbance and ectopic blindness in ICH patients, our understanding of the mechanisms of white matter injury is still quite limited
Summary
Intracerebral hemorrhage (ICH) comprises 10%–30% of all stroke cases (Balami and Buchan, 2012). White matter injury is considered the major cause of hemiplegia with partial sensory disturbance and ectopic blindness, which are quite common symptoms in ICH patients. Significant myelin and axonal injury were shown to occur in both an animal model and ICH patients. Severe myelin destruction and swelling axons are typical in the ICH animal model, but the exact mechanisms contributing to the loss of motor function are uncertain. This lack of understanding has hampered efforts to develop a therapeutic strategy aimed at protecting and repairing the damaged white matter of the ICH patients (Cheng et al, 2015; Tao et al, 2017)
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