MFGE8 通过抑制 HMGB1 减少蛛网膜下腔出血引起的神经元凋亡和神经炎症，从而改善早期脑损伤。
MFGE8 decreased neuronal apoptosis and neuroinflammation to ameliorate early brain injury induced by subarachnoid hemorrhage through the inhibition of HMGB1.
机构信息
Department of Neurology, 519688Yantaishan Hospital, Yantai, China.
Department of Interventional Medicine, 519688Yantaishan Hospital, Yantai, China.
出版信息
Hum Exp Toxicol. 2022 Jan-Dec;41:9603271221093635. doi: 10.1177/09603271221093635.
AIM
Both MFGE8 and HMGB1 were vital players for aneurysmal subarachnoid hemorrhage. However, whether HMGB1 was served as the downstream target of MFGE8 was unknown. To test this new mechanism, we performed the SAH model in rats.
METHOD
All treatments were injected intraventricularly into the right lateral ventricles. SAH grade, brain water content, and neurological function scores were evaluated. HMGB1 expression was studied by double immunofluorescence staining. HE and Nissl's staining were performed to observe the pathological change. Inflammatory factors were measured by ELISA method.
RESULTS
High expression of MFGE8 could improve neurological function and reduce the brain edema and pro-inflammatory factors. Injection of rhMFGE8 inhibited HMGB1. To further verify the regulation of MFGE8 in HMGB1, we used rhHMGB1 and glycyrrhizin, and the results indicated MFGE8 produced excellent effect on SAH rats via inhibiting HMGB1.
CONCLUSION
In a word, MFGE8 improved EBI caused by SAH, depending on HMGB1 that was the potential mechanism.
目的
MFGE8 和 HMGB1 均是蛛网膜下腔出血的关键因子。然而，HMGB1 是否是 MFGE8 的下游靶点尚不清楚。为了验证这一新机制，我们在大鼠中建立了蛛网膜下腔出血模型。
方法
所有处理均通过侧脑室注射入右侧侧脑室。评估蛛网膜下腔出血分级、脑含水量和神经功能评分。通过双重免疫荧光染色研究 HMGB1 的表达。通过 HE 和尼氏染色观察病理变化。通过 ELISA 法测量炎性因子。
结果
高表达 MFGE8 可改善神经功能，减轻脑水肿和促炎因子。rhMFGE8 的注射抑制了 HMGB1。为了进一步验证 MFGE8 对 HMGB1 的调节作用，我们使用 rhHMGB1 和甘草酸，结果表明 MFGE8 通过抑制 HMGB1 对蛛网膜下腔出血大鼠发挥了良好的作用。
结论
总之，MFGE8 改善了 SAH 引起的 EBI，其潜在机制可能依赖于 HMGB1。
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