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Updated: Mar 17, 2026
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple
Dajun Liu1, Huiping Shang2, Ying Liu3
1Department of Nephrology, Shengjing Affiliated Hospital of China Medical University, Shenyang 110036, China. liudajun_sy2015@sina.com.
Abstract:
Stanniocalcin-1 (STC-1) protects against renal ischemia-reperfusion injury (RIRI). However, the molecular mechanisms remain widely unknown. STC-1 inhibits reactive oxygen species (ROS), whereas most ROS-mediated pathways are associated with ischemic injury. Therefore, to explore the mechanism, the effects of STC-1 on ROS-medicated pathways were studied. Non-traumatic vascular clamps were used to establish RIRI mouse models. The serum levels of STC-1, interleukin-6 (IL-6), interferon (IFN) γ, P53, and capase-3 were measured by ELISA kits. Superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by fluorescence spectrofluorometer. All these molecules changed significantly in a RIRI model mouse when compared with those in a sham control. Kidney cells were isolated from sham and model mice. STC-1 was overexpressed or knockout in these kidney cells. The molecules in ROS-medicated pathways were measured by real-time quantitative PCR and Western blot. The results showed that STC-1 is an effective ROS scavenger. The serum levels of STC-1, MDA and SOD activity were increased while the serum levels of IL-6, iIFN-γ, P53, and capase-3 were decreased in a model group when compared with a sham control (p < 0.05). Furthermore, the levels of STC-1,p53, phosphorylated mitogen-activated protein kinase kinase (p-MEKK-1), c-Jun N-terminal kinase (p-JNK), extracellular signal-regulated kinase (p-ERK), IkB kinase (p-IKK), nuclear factor (NF) κB, apoptosis signal-regulating kinase 1 (ASK-1) and caspase-3 changed significantly in kidney cells isolated from a RIRI model when compared to those isolated from a sham control (p < 0.05). Meanwhile, STC-1 overexpression or silence caused significant changes of the levels of these ROS-mediated molecules. Therefore, STC-1 maybe improve anti-inflammation, anti-oxidant and anti-apoptosis activities by affecting ROS-mediated pathways, especially the phospho-modifications of the respective proteins, resulting in the increase of SOD and reduce of capase-3, p53, IL-6 and IFN-γ.
Insights
Stanniocalcin-1 (STC-1) effectively scavenges reactive oxygen species (ROS), mitigating renal ischemia-reperfusion injury (RIRI). This study reveals STC-1 influences key ROS-mediated pathways, offering a novel therapeutic target for RIRI.
Area of Science:
- Nephrology and Urology
- Molecular Biology
- Biochemistry
Background:
- Renal ischemia-reperfusion injury (RIRI) is a significant clinical challenge with poorly understood molecular mechanisms.
- Stanniocalcin-1 (STC-1) has shown protective effects against RIRI, but its precise role in mitigating oxidative stress remains unclear.
- Reactive oxygen species (ROS) play a critical role in the pathogenesis of ischemic kidney injury.
Purpose of the Study:
- To elucidate the molecular mechanisms by which STC-1 protects against RIRI, focusing on its interaction with ROS-mediated pathways.
- To investigate the impact of STC-1 on key signaling molecules involved in inflammation, oxidative stress, and apoptosis in RIRI models.
Main Methods:
- Established RIRI mouse models using non-traumatic vascular clamps.
- Measured serum levels of STC-1, inflammatory markers (IL-6, IFN-γ), apoptosis markers (P53, caspase-3), and oxidative stress markers (SOD, MDA) using ELISA and fluorescence spectrofluorometry.
- Utilized real-time quantitative PCR and Western blot to analyze ROS-mediated pathway molecules in isolated kidney cells with STC-1 overexpression or knockout.
Main Results:
- RIRI mice exhibited significantly altered serum levels of STC-1, IL-6, IFN-γ, P53, caspase-3, SOD, and MDA compared to sham controls.
- STC-1 overexpression or silence in kidney cells significantly modulated the levels of ROS-mediated pathway proteins, including p-MEKK-1, p-JNK, p-ERK, p-IKK, NF-κB, ASK-1, and caspase-3.
- STC-1 demonstrated effective ROS scavenging activity, increasing SOD and decreasing MDA, caspase-3, P53, IL-6, and IFN-γ levels.
Conclusions:
- STC-1 enhances anti-inflammatory, anti-oxidant, and anti-apoptotic activities in RIRI by modulating ROS-mediated signaling pathways, particularly protein phospho-modifications.
- The findings suggest STC-1's protective role in RIRI is mediated through its influence on the ASK-1/JNK/NF-κB and MAPK pathways.
- STC-1 represents a promising therapeutic agent for RIRI, targeting key oxidative stress and inflammatory cascades.
