Wei-Hua Liu, Ling Feng, Xuan Wang, Lixin Wei, He-Qun Zou
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Flow cytometry was used to count the M1/M2 macrophages. IHC, WB, and q-PCR experiments were used to evaluate the expression of GDF11.</p><p><strong>Results: </strong>The changes in serum levels of urea nitrogen and creatinine after I/R suggest that an animal model of AKI induced by I/R was successfully established. AKI caused by I/R significantly changed the M1/M2 macrophage polarization balance, with an increase in M2 being significantly higher than M1 as well as increased oxidative stress. Treatment with GDF11 after I/R significantly increased the differentiation of M2 cells and inhibited the differentiation of M1 macrophages, as well as decreased oxidative stress.</p><p><strong>Conclusion: </strong>GDF11 can promote the repair of AKI caused by I/R by regulating the balance of M1/M2 polarization in macrophages and oxidative stress.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":null,"pages":null},"PeriodicalIF":2.3000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10124752/pdf/","citationCount":"0","resultStr":"{\"title\":\"GDF11 Improves Ischemia-Reperfusion-Induced Acute Kidney Injury via Regulating Macrophage M1/M2 Polarization.\",\"authors\":\"Wei-Hua Liu, Ling Feng, Xuan Wang, Lixin Wei, He-Qun Zou\",\"doi\":\"10.1159/000529444\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Acute kidney injury (AKI) is a clinical emergency caused by the rapid decline of renal function caused by various etiologies. 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引用次数: 0
摘要
导言：急性肾损伤（AKI）是由各种病因引起的肾功能急剧下降的临床急症。生长分化因子 11（GDF11）可促进肾小管再生，改善 AKI 患者的肾功能，但其具体机制尚不清楚。在此，我们研究了 GDF11 在改善缺血再灌注（I/R）诱导的 AKI 中的作用和机制：方法：采用 I/R 法建立 AKI 动物模型，测定血清尿素氮和肌酐的变化以评估 AKI。采用酶联免疫吸附试验（ELISA）检测细胞因子、丙二醛、超氧化物歧化酶、一氧化氮合酶和精氨酸酶 1 的水平。流式细胞术用于计数 M1/M2 巨噬细胞。IHC、WB和q-PCR实验用于评估GDF11的表达：结果：I/R后血清中尿素氮和肌酐水平的变化表明，I/R诱导的AKI动物模型已成功建立。I/R引起的AKI明显改变了M1/M2巨噬细胞的极化平衡，M2的增加明显高于M1，氧化应激也增加了。I/R后用GDF11治疗可明显增加M2细胞的分化，抑制M1巨噬细胞的分化，并降低氧化应激：结论：GDF11可通过调节巨噬细胞M1/M2极化和氧化应激的平衡，促进I/R引起的AKI的修复。
Introduction: Acute kidney injury (AKI) is a clinical emergency caused by the rapid decline of renal function caused by various etiologies. Growth differentiation factor 11 (GDF11) can promote renal tubular regeneration and improve kidney function in AKI, but the specific mechanism remains unclear. Herein, we investigated the effect and mechanisms of GDF11 in ameliorating AKI induced by ischemia-reperfusion (I/R).
Methods: An animal model of AKI was established by I/R method, and the changes of serum urea nitrogen and creatinine were measured to evaluate the AKI. Enzyme-linked immunosorbent assay (ELISA) was used to measure cytokines, malondialdehyde, superoxide dismutase, nitric oxide synthase, and arginase 1 levels. Flow cytometry was used to count the M1/M2 macrophages. IHC, WB, and q-PCR experiments were used to evaluate the expression of GDF11.
Results: The changes in serum levels of urea nitrogen and creatinine after I/R suggest that an animal model of AKI induced by I/R was successfully established. AKI caused by I/R significantly changed the M1/M2 macrophage polarization balance, with an increase in M2 being significantly higher than M1 as well as increased oxidative stress. Treatment with GDF11 after I/R significantly increased the differentiation of M2 cells and inhibited the differentiation of M1 macrophages, as well as decreased oxidative stress.
Conclusion: GDF11 can promote the repair of AKI caused by I/R by regulating the balance of M1/M2 polarization in macrophages and oxidative stress.
期刊介绍：
This journal comprises both clinical and basic studies at the interface of nephrology, hypertension and cardiovascular research. The topics to be covered include the structural organization and biochemistry of the normal and diseased kidney, the molecular biology of transporters, the physiology and pathophysiology of glomerular filtration and tubular transport, endothelial and vascular smooth muscle cell function and blood pressure control, as well as water, electrolyte and mineral metabolism. Also discussed are the (patho)physiology and (patho) biochemistry of renal hormones, the molecular biology, genetics and clinical course of renal disease and hypertension, the renal elimination, action and clinical use of drugs, as well as dialysis and transplantation. Featuring peer-reviewed original papers, editorials translating basic science into patient-oriented research and disease, in depth reviews, and regular special topic sections, ''Kidney & Blood Pressure Research'' is an important source of information for researchers in nephrology and cardiovascular medicine.
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