Renal failure · 2020
Atorvastatin protects against contrast-induced acute kidney injury via upregulation of endogenous hydrogen sulfide.
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Yan Lin, Jiaqiong Lin, Yue Guo, Xiaoyong Li, Xuexian Tan, Ming Long, Yinglan Li, Xinxue Liao, Zena Huang
Аннотация
BACKGROUND: Contrast-induced acute kidney injury (CIAKI) is the third leading cause of acute renal failure in hospitalized patients. This study was aimed to investigate whether atorvastatin could upregulate the expression of hydrogen sulfide (H2S) and hence protect against CIAKI.
METHODS: We treated male rats and NRK-52E cells by iopromide to establish in vivo and in vitro models of CIAKI. Pretreatment with atorvastatin was given in CIAKI rats to investigate its effect on CIAKI. We collected serum and urine samples to detect renal function. We obtained kidney tissue for histological analysis and detection of protein concentration. We tested the serum concentration of H2S and renal expression of two H2S synthetases [cystathionine γ-lyase (CSE) and cystathionine-β synthase (CBS)]. NaHS was pretreated in NRK-52E cells to testify its underlying effect on contrast-induced injury.
RESULTS: Atorvastatin significantly ameliorated renal dysfunction and morphological changes in CIAKI rats, as well as inflammation, apoptosis, and excessive oxidative stress. Atorvastatin also markedly increased the serum concentration of H2S and renal expression of CSE and CBS. Moreover, pretreatment with NaHS in NRK-52E cells considerably attenuated contrast-induced cell death and inflammation.
CONCLUSION: Atorvastatin protects against CIAKI via upregulation of endogenous hydrogen sulfide.
METHODS: We treated male rats and NRK-52E cells by iopromide to establish in vivo and in vitro models of CIAKI. Pretreatment with atorvastatin was given in CIAKI rats to investigate its effect on CIAKI. We collected serum and urine samples to detect renal function. We obtained kidney tissue for histological analysis and detection of protein concentration. We tested the serum concentration of H2S and renal expression of two H2S synthetases [cystathionine γ-lyase (CSE) and cystathionine-β synthase (CBS)]. NaHS was pretreated in NRK-52E cells to testify its underlying effect on contrast-induced injury.
RESULTS: Atorvastatin significantly ameliorated renal dysfunction and morphological changes in CIAKI rats, as well as inflammation, apoptosis, and excessive oxidative stress. Atorvastatin also markedly increased the serum concentration of H2S and renal expression of CSE and CBS. Moreover, pretreatment with NaHS in NRK-52E cells considerably attenuated contrast-induced cell death and inflammation.
CONCLUSION: Atorvastatin protects against CIAKI via upregulation of endogenous hydrogen sulfide.