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Updated: Jun 6, 2025
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Diosgenin Mediated JAK/STAT Signal Channel Improving SD Rat Renal Ischemia-Reperfusion
Jinran Yang1, Xinchang Li1, Chengmei Long1
1Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Organ Transplantation Department, Nanchang, China.
Objective:
To explore the mechanism of action of diosgenin and JAK/STAT in SD rat renal ischemia-reperfusion (I/R) injury.
Method:
A renal I/R injury model was established, rat was divided into four groups: control group, sham surgery group, I/R model group, and diosgenin pretreatment group. 48 hours after the completion of modeling, blood was collected for testing of SCr, BUN, and Kim-1. After blood collection, bilateral kidneys were cut and stored in liquid nitrogen for HE staining. Western blot was used to detect the protein expression levels of JAK and STAT in each group. Compare and analyze the differences in JAK/STAT expression levels among different groups.
Result:
Compared with the I/R model group, the Scr, Bun, and Kim-1 concentrations of the three treatment groups were significantly lower, the other three treatment groups showed significant improvement in symptoms of renal vacuolar degeneration and interstitial edema in rats, the expression levels of JAK and STAT in the three groups were significantly lower, while the difference between the three groups was not significant.
Insights
Diosgenin effectively mitigates renal ischemia-reperfusion (I/R) injury in rats by reducing kidney damage markers and downregulating Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway proteins.
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Background:
- Renal ischemia-reperfusion (I/R) injury is a significant clinical challenge.
- The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway plays a crucial role in inflammatory responses and cellular damage.
- Diosgenin, a natural compound, has shown potential therapeutic properties.
Purpose of the Study:
- To investigate the protective mechanism of diosgenin against renal I/R injury in Sprague-Dawley (SD) rats.
- To elucidate the role of the JAK/STAT signaling pathway in diosgenin's therapeutic effects.
Main Methods:
- Establishment of a rat model for renal I/R injury.
- Administration of diosgenin as a pretreatment in one group.
- Assessment of renal function through serum creatinine (SCr), blood urea nitrogen (BUN), and kidney injury molecule-1 (Kim-1) levels.
- Histopathological examination using Hematoxylin and Eosin (HE) staining.
- Evaluation of JAK and STAT protein expression via Western blot.
Main Results:
- Diosgenin pretreatment significantly reduced SCr, BUN, and Kim-1 levels compared to the I/R model group.
- Histological analysis revealed reduced renal vacuolar degeneration and interstitial edema in diosgenin-treated rats.
- Western blot analysis showed significantly lower expression of JAK and STAT proteins in the diosgenin-treated groups compared to the I/R group.
Conclusions:
- Diosgenin demonstrates a protective effect against renal I/R injury in SD rats.
- The mechanism of action involves the downregulation of the JAK/STAT signaling pathway.
- Diosgenin holds promise as a therapeutic agent for renal I/R injury.
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