Dynamic Changes in Toll-Like Receptor 4 in Human Perihematoma Tissue after Intracerebral Hemorrhage

With the increase in the aging population and unhealthy lifestyles, the prevalence of intracerebral hemorrhage (ICH) continues to increase. The secondary injury to brain tissue after ICH might play a significant role in the prognosis of the patient; however, the underlying mechanisms of this process are unclear. This study aimed to explore the function of the toll-like receptor 4 (TLR4)-mediated myeloid differentiation primary response 88 (MyD88)-dependent pathway in inflammatory injury and apoptosis in the perihematoma tissues of patients with ICH.

We included 24 patients who were diagnosed with hypertensive supratentorial ICH and collected perihematoma tissue samples from them. We explored the pathologic changes and the expression of TLR4, MYD88, nuclear factor κB, and CASPASE-3 in these tissues.

In patients with ICH, the pathologic changes appeared within 6 hours of the onset of disease, peaked (maximum damage) at 24-72 hours, and the damage subsided after 72 hours. The expression of TLR4, MYD88, nuclear factor κB, and CASPASE-3 began to increase within 6 hours after ICH, peaked during 24-72 hours after ICH, and decreased after 72 hours.

The TLR4-mediated MyD88-dependent pathway plays a significant role in the mechanism of tissue injury after ICH in human tissues. Our study sheds light on the regulation of inflammation and apoptosis as potential novel targets to prevent secondary injury after ICH. Moreover, our results indicate that the optimal window for antiinflammation and antiapoptosis treatment is within 6 hours after ICH.