目的 探讨中脑星形胶质细胞源性神经营养因子（MANF）对调节脓毒症相关急性肾损伤（S-AKI）的保护作用。将96只小鼠随机分为对照组、对照MANF组、S-AKI组，和S-AKI MANF组。采用腹腔注射脂多糖（LPS）10 mg/kg建立S-AKI模型。将MANF (200 μg/kg)给予对照MANF和S-AKI MANF组。对照组和S-AKI组每天腹腔注射等剂量的生理盐水。获得血清和肾组织样本用于生化分析。采用Western blotting检测肾脏中MANF蛋白表达量，酶联免疫吸附试验（ELISA）测定血清中MANF、促炎细胞因子（肿瘤坏死因子-α[TNF-α]）的表达量。和白细胞介素 6 [IL-6]）。使用自动生化分析仪检测血清肌酐（SCr）和血尿素氮（BUN）。另外，通过苏木精-伊红染色观察肾组织的病理变化。两组间的比较采用非配对Student's t检验进行，多组间的统计采用单向方差分析(ANOVA)后的Tukey事后检验进行。 P值<0.05为有统计学意义。 S-AKI早期肾组织中MANF表达上调，但随着病情发展，MANF表达下调。 S-AKI组肾功能恶化，TNF-α和IL-6升高。 MANF的施用显着缓解了SCr和BUN的升高水平，并抑制了肾脏中TNF-α和IL-6的表达。 S-AKI组病理改变较S-AKI MANF组更广泛。MANF治疗可显着减轻肾损伤，减轻炎症反应，减轻或逆转肾组织损伤。 MANF 可能对 S-AKI 具有保护作用，这表明了 S-AKI 的潜在治疗方法。版权所有：© 世界急诊医学杂志。

To determine the protective role of mesencephalic astrocyte-derived neurotrophic factor (MANF) in regulating sepsis-associated acute kidney injury (S-AKI).A total of 96 mice were randomly divided into the control group, control+MANF group, S-AKI group, and S-AKI+MANF group. The S-AKI model was established by injecting lipopolysaccharide (LPS) at 10 mg/kg intraperitoneally. MANF (200 μg/kg) was administered to the control+MANF and S-AKI+MANF groups. An equal dose of normal saline was administered daily intraperitoneally in the control and S-AKI groups. Serum and kidney tissue samples were obtained for biochemical analysis. Western blotting was used to detect the protein expression of MANF in the kidney, and enzyme-linked immunosorbent assay (ELISA) was used to determine expression of MANF in the serum, pro-inflammatory cytokines (tumor necrosis factor-α [TNF-α] and interleukin-6 [IL-6]). Serum creatinine (SCr), and blood urea nitrogen (BUN) were examined using an automatic biochemical analyzer. In addition, the kidney tissue was observed for pathological changes by hematoxylin-eosin staining. The comparison between two groups was performed by unpaired Student's t-test, and statistics among multiple groups were carried out using Tukey's post hoc test following one-way analysis of variance (ANOVA). A P-value <0.05 was considered statistically significant.At the early stage of S-AKI, MANF in the kidney tissue was up-regulated, but with the development of the disease, it was down-regulated. Renal function was worsened in the S-AKI group, and TNF-α and IL-6 were elevated. The administration of MANF significantly alleviated the elevated levels of SCr and BUN and inhibited the expression of TNF-α and IL-6 in the kidney. The pathological changes were more extensive in the S-AKI group than in the S-AKI+MANF group.MANF treatment may significantly alleviate renal injury, reduce the inflammatory response, and alleviate or reverse kidney tissue damage. MANF may have a protective effect on S-AKI, suggesting a potential treatment for S-AKI.Copyright: © World Journal of Emergency Medicine.