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.

小儿脓毒症已成为小儿重症监护病房 (PICU) 中死亡的主要原因。靶基因的调控可能是小儿脓毒症治疗的关键。RT-qPCR检测大鼠血清中miR-210的表达。采用全自动生化分析仪检测血清 BUN、Scr、CysC。ELISA检测炎症因子的表达。TUNEL染色检测细胞凋亡水平。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。脓毒症幼崽中 miR-210 的表达异常升高。干预大鼠体内 miR-210 的表达可减轻脓毒症幼崽的肾损伤程度并抑制炎症反应。此外，干扰miR-210可以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、炎症反应和细胞凋亡的抑制作用。干扰 miR-210 通过抑制 JAK-STAT 通路减轻脓毒症大鼠的肾损伤。通路激动剂 SC-39100 可以逆转干扰 miR-210 对肾组织损伤、炎症反应和细胞凋亡的抑制作用。干扰 miR-210 通过抑制 JAK-STAT 通路减轻脓毒症大鼠的肾损伤。通路激动剂 SC-39100 可以逆转干扰 miR-210 对肾组织损伤、炎症反应和细胞凋亡的抑制作用。干扰 miR-210 通过抑制 JAK-STAT 通路减轻脓毒症大鼠的肾损伤。