# Nephroprotective effect of remote ischemic conditioning on type 2 diabetic rats

**Authors:** Seyyed Majid Bagheri, Elham Hakimizadeh, Mohammad Allahtavakoli

PMC · DOI: 10.22038/ijbms.2024.77896.16855 · Iranian Journal of Basic Medical Sciences · 2024-01-01

## TL;DR

This study shows that remote ischemic conditioning may help protect the kidneys in diabetic rats by reducing inflammation and oxidative stress, even without lowering blood sugar levels.

## Contribution

The novel finding is that RIC can delay diabetic nephropathy progression through anti-inflammatory and antioxidant effects, independent of glucose or lipid reduction.

## Key findings

- RIC improved antioxidant enzyme levels and reduced pro-inflammatory gene expression in diabetic rats.
- Histopathological improvements were observed in RIC-treated diabetic rats.
- RIC did not significantly reduce blood glucose or lipid levels but showed nephroprotective effects.

## Abstract

Diabetic nephropathy is one of the main causes of kidney failure in the end stage of diabetes worldwide. The present study was conducted with the aim of using the remote ischemic conditioning (RIC) method to prevent diabetic nephropathy.

Diabetes was induced by high-fat diet (60%) and streptozotocin injection (35 mg/kg) in rats. RIC was performed by tightening a tourniquet around the upper thigh and releasing it for three cycles of 5 min of ischemia and 5 min of reperfusion daily for an 8-week duration. At the end of the experiment, serum and urine parameters were examined. Anti-oxidant enzymes and lipid peroxidation levels in the kidney were also determined along with histological examination. The expression levels of tumor necrosis factor-alpha and transforming growth factor beta genes were also evaluated.

Glucose, cholesterol, triglyceride, and HbA1c concentrations were not significantly reduced in the RIC group. On the other hand, serum creatinine, urea, and albumin levels decreased and increased in urine. Anti-oxidant enzymes did improve in the kidney significantly and the expression of tumor necrosis factor-alpha and transforming growth factor beta genes decreased significantly. Histopathological examination also showed that necrosis, epithelial damage, and leukocyte infiltration increased in the diabetic group and improved in the treatment group.

The results of biochemical analysis, and enzymatic and histological examinations showed that although RIC could not reduce blood glucose and lipids, nevertheless it may delay the progression of diabetic nephropathy due to the presence of anti-inflammatory and anti-oxidant activities.

## Linked entities

- **Chemicals:** streptozotocin (PubChem CID 29327)
- **Diseases:** diabetic nephropathy (MONDO:0005016), type 2 diabetes (MONDO:0005148)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** necrosis (MESH:D009336), Diabetes (MESH:D003920), type 2 diabetic (MESH:D003924), kidney failure (MESH:D051437), inflammatory (MESH:D007249), ischemia (MESH:D007511), end (MESH:D003643), Diabetic nephropathy (MESH:D003928)
- **Chemicals:** urea (MESH:D014508), triglyceride (MESH:D014280), Glucose (MESH:D005947), streptozotocin (MESH:D013311), cholesterol (MESH:D002784), creatinine (MESH:D003404), lipid (MESH:D008055)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11366939/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC11366939/full.md

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Source: https://tomesphere.com/paper/PMC11366939