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Activation of Nrf2 Signaling by Apelin Attenuates Renal Ischemia Reperfusion Injury in Diabetic Rats
Xiaobo Zhang1, Ying Zhu1, Ying Zhou1
1Nephrology Department, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu Province 223300, People's Republic of China.
Objective:
Renal ischemia/reperfusion (I/R) injury is commonly seen in diabetic patients. Apelin has been demonstrated to protect against renal I/R injury, whereas detailed modulatory mechanisms by which Apelin exerts its role in renal I/R injury in diabetic patients remain unclarified. This research aimed to probe the functional molecules under the regulation of Apelin in renal I/R injury in diabetic rats.
Materials And Methods:
First, animal models were established for subsequent assays. Biochemical kits measured the serum levels of blood urea nitrogen (BUN) and serum creatinine (SCR), and hematoxylin and eosin (H&E) staining examined the histopathological changes of kidney tissues. Inflammatory factors containing tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were tested through enzyme-linked immunosorbent assay (ELISA) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), respectively. Reactive oxygen species (ROS) levels in the serum and kidney tissues were separately assessed by specific ROS kits. Cell apoptosis was further estimated through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and Western blot analysis. Eventually, the influences of Apelin on nuclear factor erythroid 2-related factor (Nrf2) and its downstream genes were explored via Western blot analysis and immunohistochemistry (IHC).
Results:
In the present study, Apelin ameliorated the damage to renal function and histological structure, decreased levels of inflammatory factors and ROS, and hampered cell apoptosis in renal I/R injury of diabetic rats. Moreover, Apelin could elevate the levels of Nrf2 and downstream genes which were decreased under renal I/R injury.
Conclusion:
These data indicated that Apelin inhibited renal I/R injury through regulating Nrf2 signaling in diabetic rats, which might shed new light on the treatment of renal I/R injury in diabetic patients.
Insights
Apelin protects diabetic rats from kidney injury caused by ischemia/reperfusion (I/R). It works by activating the Nrf2 signaling pathway, reducing inflammation and cell damage.
Area of Science:
- Nephrology
- Diabetology
- Molecular Biology
Background:
- Diabetic patients are prone to renal ischemia/reperfusion (I/R) injury.
- Apelin shows protective effects against renal I/R injury, but its mechanisms in diabetic contexts are unclear.
Purpose of the Study:
- To investigate the functional molecules regulated by Apelin in diabetic renal I/R injury.
- To elucidate the protective mechanisms of Apelin in this condition.
Main Methods:
- Established diabetic rat models of renal I/R injury.
- Assessed renal function (BUN, SCR) and kidney histology (H&E).
- Measured inflammatory factors (TNF-α, IL-1β, IL-6, MCP-1), reactive oxygen species (ROS), and apoptosis (TUNEL, Western blot).
- Explored the role of Apelin in the Nrf2 signaling pathway (Western blot, IHC).
Main Results:
- Apelin treatment improved renal function and histological structure.
- Apelin reduced inflammatory factors, ROS levels, and cell apoptosis.
- Apelin upregulated decreased levels of Nrf2 and its downstream genes.
Conclusions:
- Apelin mitigates renal I/R injury in diabetic rats by modulating the Nrf2 signaling pathway.
- This finding offers potential therapeutic strategies for diabetic kidney injury.
