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Objective: This study aimed to analyze the role of mitochondrial Omi/HtrA2 signaling pathway in neuronal apoptosis in patients with cerebral hemorrhage (CH)., Methods: In this retrospective analysis, the clinical data of 60 patients with CH who received craniotomy or minimally invasive intracranial hematoma (MIIH) were included in the case group, which was sub-divided into a craniotomy group (n=22) and a minimally invasive group (n=38) depending on the type of surgery. The brain tissue specimens of the above patients were retained in the surgical specimen repository of Yuhuan Second People's Hospital. Another 15 normal brain tissue samples retained in the surgical specimen repository were included in the normal group. The expression levels of Omi/HtrA2, X-linked inhibitor of apoptosis protein (XIAP), poly-adenosine diphosphate-ribose polymerase (PARP), pro-caspase 3, and pro-caspase 9 were determined using Western blotting., Results: The case group exhibited a higher proportion of neuronal apoptosis, higher expression levels of Omi/HtrA2, PARP, and pro-caspase 3 and 9, higher activities of caspase 3 and caspase 9 ( P < 0.05), and lower XIAP expression ( P < 0.05) in brain tissue than the normal group. The proportion of neuronal cell apoptosis in brain tissues was positively correlated with the expression of Omi/HtrA2, PARP, and pro-caspase 3 and pro-caspase 9 ( r > 0, P < 0.05), and the activity of caspase 3 and caspase 9 was negatively correlated with XIAP expression ( r < 0, P < 0.05). Compared with the craniotomy group, the minimally invasive group demonstrated higher efficacy and hematoma removal rate, shorter hematoma removal time, hematoma drainage time, operation time, and hospital stay, less intraoperative bleeding, and lower postoperative complication rates ( P < 0.05). The minimally invasive group showed higher expression level of serum XIAP and lower levels of serum caspase 3 and caspase 9 than the craniotomy group ( P < 0.05)., Conclusions: Mitochondrial Omi/HtrA2 signaling pathway may be involved in neuronal apoptosis. MIIH has the advantages of high efficacy, high hematoma clearance rate, and few complications for the treatment of CH., Competing Interests: None., (AJTR Copyright © 2023.)

Traumatic brain injury (TBI) is a major cause of injury-related deaths, and the mechanism of TBI has become a research focus, but little is known about the mechanism of microRNAs in TBI. The aim of this study is the role of microRNA-22 (miR-22) in TBI-induced neuronal cell apoptosis. Rat cortical neurons were cultured and the TBI model was induced by scratch injury in vitro, before which miR-22 level was altered by transfection of agomir or antagomir. Lactate dehydrogenase (LDH) release and TUNEL assays were performed to examine neuronal cell injury and apoptosis. The activity of caspase 3 (CASP3) and level changes of several apoptosis factors including B-cell lymphoma 2 (BCL2), BCL2-associated X protein (BAX), phosphatase and tensin homolog (PTEN) and v-AKT murine thymoma viral oncogene homolog 1 (AKT1) were detected. Results showed that TBI model cells possessed a downregulated miR-22 level (P < 0.001) and more LDH release and apoptotic cells indicating the aggravated neuronal cell injury and apoptosis induced by TBI. miR-22 agomir attenuated neuronal cell injury and apoptosis of the TBI model. It also caused the corresponding changes in CASP3 activity and other apoptosis factors, with cleaved CASP3, BAX and PTEN inhibited and BCL2 and phosphorylated AKT1 promoted, while miR-22 antagomir had the opposite effects. So miR-22 has neuroprotective roles of attenuating neuronal cell injury and apoptosis induced by TBI, which may be associated with its regulation on apoptosis factors. This study reveals miR-22 as a potential approach to TBI treatment and detailed mechanism remains to be uncovered.