# Effects of Carvacrol on Aortic Damage in a Streptozotocin-Induced Type 1 Diabetic Rat Model

**Authors:** Seda Cetinkaya Karabekir, Burcu Gultekin, Hasan Basri Savas, Gokhan Cuce, Serpil Kalkan

PMC · DOI: 10.3390/biom16030431 · Biomolecules · 2026-03-13

## TL;DR

This study shows that carvacrol, a natural compound, can protect the aorta from damage in diabetic rats by reducing oxidative stress and tissue injury.

## Contribution

The study demonstrates carvacrol's protective effects against diabetic vascular complications in a rat model through experimental validation.

## Key findings

- Carvacrol reduced ischemia-modified albumin levels and caspase-3 expression in diabetic rats.
- Carvacrol improved aortic and cardiac tissue damage in diabetic rats.
- Carvacrol modulates oxidative stress and apoptosis in diabetes-induced vascular injury.

## Abstract

Diabetes mellitus (DM) is associated with vascular complications that increase morbidity and mortality. Natural antioxidants play a vital role in reducing diabetes-related damage. This study investigated the protective effects of the phenolic monoterpene carvacrol (CAR) against diabetic complications. Thirty-two male Wistar Albino rats (4 months, 250–300 g) were divided into four groups: control, DM, DM + DMSO, and DM + CAR. Type 1 diabetes was induced via intraperitoneal injection of 50 mg/kg streptozotocin (STZ). The DM + CAR group received 20 mg/kg CAR daily for four weeks. Body weight and blood glucose levels were regularly monitored. At the end of the study, aortic tissues were examined using hematoxylin–eosin (H&E), Verhoeff–Van Gieson, and immunohistochemical staining, while cardiac tissues were analyzed with H&E and Masson’s trichrome. Serum levels of ischemia-modified albumin (IMA), cholesterol (CHOL), triglycerides (TG), and high-density lipoprotein (HDL) were measured. In the DM group, IMA and CHOL levels were increased (p = 0.0208 and p = 0.0207, respectively), apoptosis was elevated (caspase-3 expression, p = 0.0001), and marked tissue damage was observed. In contrast, in the DM + CAR group, IMA levels (p = 0.0228) and caspase-3 expression (p = 0.0457) were reduced, and notable improvements were detected in vascular and cardiac tissues. These results suggest that CAR protects against diabetic complications by modulating oxidative stress, inhibiting apoptosis, and preventing tissue injury.

## Linked entities

- **Proteins:** Casp3 (caspase 3)
- **Chemicals:** carvacrol (PubChem CID 10364), streptozotocin (PubChem CID 29327), cholesterol (PubChem CID 5997)
- **Diseases:** Diabetes mellitus (MONDO:0005015), Type 1 diabetes (MONDO:0005147)

## Full-text entities

- **Genes:** Casp3 (caspase 3) [NCBI Gene 25402] {aka CPP32-beta, Lice, Yama}, Alb (albumin) [NCBI Gene 24186] {aka Alb1, Albza}
- **Diseases:** diabetic complications (MESH:D048909), vascular complications (MESH:D003925), DM (MESH:D003920), Aortic Damage (MESH:D001018), Type 1 Diabetic (MESH:D003922), tissue damage (MESH:D017695)
- **Chemicals:** STZ (MESH:D013311), CHOL (MESH:D002784), phenolic monoterpene (-), TG (MESH:D014280), DMSO (MESH:D004121), blood glucose (MESH:D001786), CAR (MESH:C073316), hematoxylin (MESH:D006416)
- **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/PMC13023609/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023609/full.md

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Source: https://tomesphere.com/paper/PMC13023609