Department of Critical Care Medicine, The People's Hospital of Longhua, Shenzhen, Shenzhen, 518109, Guangdong Province, China.
Department of Infection Disease, Children's Hospital of Nanjing Medical University, No.72, Guangzhou road, Gulou District, Nanjing, Jiangsu Province, 210000, China.
Inflammation. 2020 Dec;43(6):2156-2165. doi: 10.1007/s10753-020-01283-0.
Pediatric sepsis has become the leading cause of death in pediatric intensive care units (PICU). The regulation of target genes may be the key to the treatment of pediatric sepsis. The expression of miR-210 in rat serum was detected by RT-qPCR. The serum BUN, Scr, and CysC were detected by an automatic biochemical analyzer. The expression of inflammatory factors was detected by ELISA. The apoptosis level of the cells was detected by TUNEL staining. The expression of apoptotic proteins Bcl2, Bax, Cleaved caspase3, caspase3, and JAK/STAT3 pathway-related proteins were detected by western blot. The expression of miR-210 was abnormally elevated in sepsis pups. Interfering with the expression of miR-210 in rats could reduce the degree of renal injury and inhibit the inflammatory response in sepsis pups. In addition, interference with miR-210 could inhibit the apoptosis level of renal tissue cells, and the expression of apoptosis-related proteins was also significantly decreased. During this process, we found that after interfering with the expression of miR-210, the expression of the JAK/STAT pathway was inhibited. Then, pathway agonist SC-39100 can reverse the inhibitory effects of interfering with miR-210 on renal tissue damage, inflammatory response, and apoptosis. Interference with miR-210 alleviated renal injury in septic rats by inhibiting JAK-STAT pathway.
儿科脓毒症已成为儿科重症监护病房（PICU）死亡的主要原因。靶基因的调控可能是治疗儿科脓毒症的关键。通过 RT-qPCR 检测大鼠血清中 miR-210 的表达。用自动生化分析仪检测血清 BUN、Scr 和 CysC。通过 ELISA 检测炎症因子的表达。TUNEL 染色检测细胞凋亡水平。通过 Western blot 检测凋亡蛋白 Bcl2、Bax、Cleaved caspase3、caspase3 和 JAK/STAT3 通路相关蛋白的表达。脓毒症幼鼠血清中 miR-210 表达异常升高。干扰大鼠 miR-210 的表达可减轻脓毒症幼鼠的肾损伤程度并抑制其炎症反应。此外，干扰 miR-210 可抑制肾组织细胞的凋亡水平，凋亡相关蛋白的表达也明显降低。在此过程中，我们发现干扰 miR-210 的表达后，JAK/STAT 通路的表达受到抑制。然后，通路激动剂 SC-39100 可以逆转干扰 miR-210 对肾组织损伤、炎症反应和凋亡的抑制作用。干扰 miR-210 通过抑制 JAK-STAT 通路减轻脓毒症大鼠的肾损伤。
