miR-10a Ameliorates Renal and Myocardial Injury in Sepsis Through Regulation of PI3K/AKT Signaling

PI3K/AKT/mTOR通路 蛋白激酶B 败血症 医学 兴奋剂 急性肾损伤 内科学 炎症 内分泌学 信号转导 受体 生物 生物化学
作者
Chenglian Hu,Ying Yang,Lun Ye
出处
期刊:Journal of Biomaterials and Tissue Engineering [American Scientific Publishers]
卷期号:13 (2): 301-308
标识
DOI:10.1166/jbt.2023.3255
摘要

miR-10a participates in the prognosis of patients with sepsis, which also influence multiple organs and cause damages to the kidney and myocardial tissues. This study intends to assess miR-10a’s role in sepsis-induced renal and myocardial injury. 50 Wistar rats were randomized into sham-operation group, model group, MiR-10a group, positive control group and PI3K/AKT-agonist group ( n = 10) followed by analysis of the histopathological changes of myocardial and renal tissues, kidney injury, expression of renal GR- α and CK-MB/CK, levels of inflammatory factors (IL-10, IL-6, IL-1 β and TNF- α ) and the level of miR-10a, PI3K and AKT. Rats in model group and PI3K/AKT-agonist group exhibited highest pathological score of kidney injury, expression of CK-MB, CK and renal GR- α , followed by rats in positive control group and miR-10a group. Furthermore, model group and PI3K/AKT-agonist group showed the highest level of inflammatory factors (TNF- α , IL-1 β , IL-6, and IL-10), followed by positive control group and miR-10a group. Lowest miR-10a expression and highest mRNA levels of PI3K and AKT was detected in model group, PI3K/AKT-agonist group and positive control group, followed by miR-10a group. PI3K is a target of miR-10a. In conclusion, miR-10a alleviates the sepsis-induced renal and myocardial injury mainly by mediating the PI3K/AKT transduction pathway, indicating that miR-10a can be utilized as a target gene for sepsis treatment.

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