## 3 Results
Hypoxia is a complicated biological process, and hypoxia-regulated CD105 expression (in peripheral blood) suggests its possible involvement in several neurophysiological pathways. In the main group, the mean serum endoglin level was measured at 2.06 \(\pm\) 0.012 ng/mL, with a maximum value of 2.23 ng/mL, whereas in the control group, the mean level was 2.51 \(\pm\) 0.071 ng/mL, reaching a maximum of 4.02 ng/mL (Figure 2). The analysis revealed that the mean serum endoglin levels were statistically significantly lower in the study group compared to the control group (\(p<\) 0.001). These results indicate that the reduced concentration of serum endoglin CD105 during the acute phase of stroke in children correlated with the degree of hypoxia experienced by these patients. A deficiency of CD105 could impair recovery processes following ischemic brain injury by reducing angiogenesis, a critical component in tissue repair and neurodegeneration. Also, the role of another marker of ischemic stroke, the S100B protein, was investigated. It represents a member of the S100 protein family. S100B is a glial-specific, multifunctional protein selectively synthesized by certain astroglial cells (astrocytes) in the brain. Specifically, it is produced by a subtype of mature astrocytes lining blood vessels, which play a role in nerve cell differentiation, neural growth during development, and nerve repair after injury, serving a protective function at physiological levels. Additionally, S100B is synthesized by cells expressing NG2 (neuroglial antigen 2), a chondro sulfate proteoglycan encoded by the CSPG4 gene in humans. NG2-related actions include the stimulation of Ca\({}^{2+}\) influx, the inhibition of phosphorylation mediated by protein kinase C (PKC), and astrocytosis. PKC, a family of enzymes involved in phosphorylating proteins, plays a role in various cell signaling cascades, including those regulated by increased diacylglycerol or Ca\({}^{2+}\) ions. However, in adults, these processes can lead to nervous system damage, making NG2 and related proteins potential clinical and prognostic markers. S100B is released from injured brain cells into the extracellular space or bloodstream and can be detected in peripheral circulation following brain injury. Elevated extracellular concentrations of S100B have been associated with cell damage, possibly contributing to the pathophysiology of neurodegenerative processes [15; 16]. Consequently, a normal serum concentration of the S100B protein typically excludes the likelihood of severe central nervous system (CNS) pathology. The rapid release of S100B into biological fluids, combined with its short half-life, makes it a crucial marker for acute brain tissue injury, such as traumatic brain injury or ischemic/hemorrhagic stroke. Furthermore, chromosomal rearrangements and an altered expression of the S100B gene have been linked to various neurologic, neoplastic, and other diseases, such as Alzheimer's disease, Down syndrome, epilepsy, amyotrophic lateral sclerosis, schwannoma, melanoma, and type I diabetes mellitus [16]. It has been suggested that the regulation of S100B by melittin has potential for the treatment of epilepsy [17]. In this study, it was determined that the serum levels of the S100B protein were significantly elevated in patients during the acute phase of stroke-induced brain injury. Unlike endoglin, S100B protein levels increased during the acute phase in the main group compared to the control group. Specifically, in children with ischemic stroke, the mean S100B protein level was 0.524 \(\pm\) 0.0850 ng/mL, with a maximum value of 4.390 ng/mL. Conversely, in the control group without IS, the mean S100B level was 0.120 \(\pm\) 0.0038 ng/mL, with a maximum value of 0.149 ng/mL. The difference between these groups was statistically significant (_p_ < 0.01) (Figure 3). There was no statistically significant correlation observed between endoglin and S100B protein levels in either the main group or the control group (_p_ < 0.1).