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Chinese Journal of Critical Care Medicine(Electronic Edition) ›› 2021, Vol. 14 ›› Issue (03): 187-191. doi: 10.3877/cma.j.issn.1674-6880.2021.03.003

• Original Article • Previous Articles     Next Articles

Protective effect of sulforaphane on oxidative response in rats with sepsis-associated acute kidney injury

Luming Tang1, Junnan Xu1, Hainiao Lin1, Ting Yang1, Xiaodong Pan1, Laifang Sun1,()   

  1. 1. Department of Emergency Medicine, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China
  • Received:2021-01-15 Online:2021-06-30 Published:2021-08-13
  • Contact: Laifang Sun

Abstract:

Objective

To explore the protective effect of sulforaphane on the oxidative response in rats with sepsis-associated acute kidney injury (SA-AKI).

Methods

Fifteen Sprague-Dawley rats were randomly allocated into a control group, a sepsis group and a treatment group, 5 rats in each group. Rats in the sepsis group and treatment group accepted cecal ligation and puncture (CLP) operation, while rats in the control group received celiotomy without ligation and puncture. Then rats in the treatment group received 5 mg / kg of sulforaphane for 15 min at 6 h after CLP, and rats in the other two groups received an equal amount of isotonic NaCl solution by intraperitoneal injection at the same time. At 24 h after CLP, blood samples from each group were collected to detect the levels of blood urea nitrogen and creatinine. Then, the rats were sacrificed and their renal tissue was collected to determine the levels of catalase (CAT), malondialdehyde and superoxide dismutase (SOD) by enzyme-linked immunosorbent assay. Meanwhile, the neutrophil gelatinase associated lipocalin (NGAL) messenger RNA (mRNA) expression in the renal tissue was detected by fluorescence real-time quantitative PCR.

Results

The levels of blood urea nitrogen (F = 922.714, P < 0.001), creatinine (F = 4 790.001, P < 0.001), CAT (F = 237.331, P < 0.001), malondialdehyde (F = 913.260, P < 0.001), SOD (F = 752.292, P < 0.001) and NGAL mRNA (F = 319.468, P < 0.001) all showed significant differences among the three groups. Further pairwise comparison revealed that compared with the control group, the levels of blood urea nitrogen [(5.98 ± 0.12), (14.93 ± 0.43), (11.99 ± 0.26) mmol / L], creatinine [(27.4 ± 0.9), (97.9 ± 1.0), (75.0 ± 1.2) μmol / L], malondialdehyde [(11.9 ± 0.4), (27.5 ± 0.7), (21.8 ± 0.4) nmol / mg] and NGAL mRNA in the sepsis group and treatment group increased obviously, which increased most in the sepsis group, and the levels of CAT [(21.64 ± 0.32), (17.06 ± 0.29), (19.96 ± 0.29) U / mg] and SOD [(71.6 ± 0.3), (54.2 ± 1.0), (59.7 ± 0.4) U / mg] decreased markedly, which decreased most in the sepsis group (all P < 0.05).

Conclusion

Sulforaphane can attenuate oxidative stress injury in rats with SA-AKI, and the mechanism is probably related to the inhibition of NGAL mRNA expression in kidney tissue.

Key words: Sepsis, Sulforphane, Acute kidney injury, Oxidative response, Rats

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