As an essential constituent of the mitochondrial contact site and cristae organization system (MICOS), MIC19 plays a crucial role in maintaining the stability of mitochondrial function and microstructure. However, the mechanisms and functions of MIC19 in intracerebral hemorrhage (ICH) remain unknown and need to be investigated. Sprague Dawley (SD) rats injected with autologous blood obtained from the caudal artery, and cultured neurons exposed to oxygen hemoglobin (OxyHb) were used to establish and emulate the ICH model in vivo and in vitro. Lentiviral vector encoding MIC19 or MIC19 short hairpin ribonucleic acid (shRNA) was constructed and administered to rats by intracerebroventricular injection to overexpress or knock down MIC19, respectively. First, MIC19 protein levels were increased after ICH modeling. After virus transfection and subsequent ICH modeling, we observed that overexpression of MIC19 could mitigate cell apoptosis and neuronal death, as well as abnormalities in mitochondrial structure and function, oxidative stress within mitochondria, and neurobehavioral deficits in rats following ICH. Conversely, knockdown of MIC19 had the opposite effect. Moreover, we found that the connection between MIC19 and SAM50 was disrupted after ICH, which may be a reason for the impairment of the mitochondrial structure after ICH. In conclusion, MIC19 exerts a protective role in the subsequent injury induced by ICH. The investigation of MIC19 may offer clinicians novel therapeutic insights for patients afflicted with ICH.

Noble gases were chemically inert elements that have attracted increasing interest because of their potential neuroprotective properties. Among them, xenon had long been used as an inhalational anesthetic, while xenon, argon, and helium had also been investigated for possible neuroprotective effects. This narrative review focused on acquired brain injury, particularly ischemic stroke, post-cardiac arrest hypoxic-ischemic brain injury, and traumatic brain injury. Preclinical studies had suggested that several noble gases might reduce secondary neuronal injury, although the strength and consistency of evidence varied across gases and experimental models. Proposed mechanisms included attenuation of excitotoxicity, apoptosis, oxidative stress, and neuroinflammation, although these pathways had not been fully clarified for all gases. This review summarizes and compares the available preclinical and early clinical evidence on xenon, argon, and helium in acquired brain injury. Among these gases, xenon currently had the strongest and most consistent evidence base, whereas evidence for argon remained heterogeneous and evidence for helium was limited. Although the preclinical findings were promising, clinical translation remains limited, and further standardized studies were needed to define efficacy, safety, timing of administration, and feasible delivery strategies.