No. 2 Department of Neurology, Cangzhou Central Hospital, Cangzhou, Hebei, China.
Mediators Inflamm. 2022 Aug 4;2022:1376959. doi: 10.1155/2022/1376959. eCollection 2022.
Cerebral infarction is a common disease with a higher disability and fatality rates. The incidence rates of cerebral infarction or cerebral ischemic stroke gradually increase with aging and cerebrovascular disease progression. This study is aimed at evaluating the effects of HMGA2 on cerebral infarction-induced brain tissue damage and its underlying mechanisms. Adult Sprague Dawley rats were pretreated with sh-HMGA2 before cerebral infarction operation. The effect of HMGA2 on the arrangement, distribution, and morphological structure of neurons and the cell apoptosis ratio in brain tissue were detected via hematoxylin and eosin staining, brain-water content, TTC staining, and TUNEL staining. The results from ELISA assay, qPCR, and western blot indicated that downregulation of HMGA2 mitigated inflammatory stress via regulating the expression of TLR4/NF-B. In addition, results showed that suppressed HMGA2 attenuated the neurological dysfunction of brain injury rats and markedly reduced infarct volume. HMGA2 might be able to alleviate the damage associated with cerebral infarction-induced inflammatory response and cell apoptosis. Moreover, downregulation of HMGA2 had a protective effect on the brain damage derived from cerebral infarction by mediating the TLR4/NF-B pathway. In conclusion, the current study demonstrated that downregulation of HMGB2 decreased the infarct size, inflammatory responses, and apoptosis in cerebral injury and further had neuroprotective effects against cerebral infarction-induced brain damage. Finally, these results indicated that the downregulation of the TLR4/NF-B pathway after ischemia by HMGB2 inhibition is a potential mechanism of the neuroprotective effect of cerebral injury.
脑梗死是一种常见疾病，具有较高的残疾率和死亡率。脑梗死或脑缺血性卒中的发病率随着年龄的增长和脑血管病的进展逐渐增加。本研究旨在评估 HMGA2 对脑梗死引起的脑组织损伤的影响及其潜在机制。成年 Sprague Dawley 大鼠在脑梗死手术前用 sh-HMGA2 预处理。通过苏木精-伊红染色、脑水含量、TTC 染色和 TUNEL 染色检测 HMGA2 对神经元排列、分布和形态结构以及脑组织细胞凋亡率的影响。ELISA 检测、qPCR 和 Western blot 结果表明，下调 HMGA2 通过调节 TLR4/NF-B 的表达减轻炎症应激。此外，结果表明，抑制 HMGA2 可减轻脑损伤大鼠的神经功能障碍，显著减少梗死体积。HMGA2 可能通过调节 TLR4/NF-B 通路减轻与脑梗死相关的炎症反应和细胞凋亡引起的损伤。综上所述，本研究表明下调 HMGA2 可减少脑损伤的梗死面积、炎症反应和细胞凋亡，并对脑梗死引起的脑损伤具有神经保护作用。最后，这些结果表明，HMGA2 抑制缺血后 TLR4/NF-B 通路的下调是脑损伤神经保护作用的潜在机制。
