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. 2025 Feb;15(2):923-930.
doi: 10.5455/OVJ.2025.v15.i2.41. Epub 2025 Feb 28.

Effect of cinnamon oil (Cinnamomum burmannii) on the histological kidney of male diabetic rats (Rattus norvegicus)

Affiliations

Effect of cinnamon oil (Cinnamomum burmannii) on the histological kidney of male diabetic rats (Rattus norvegicus)

Budiastuti Budiastuti et al. Open Vet J. 2025 Feb.

Abstract

Background: Chronic systemic disease known as diabetes mellitus is defined by elevated blood glucose levels and problems with fat, carbohydrate, and protein metabolism. In Indonesia, the cinnamon species found include Cinnamomum burmannii, which also has hypoglycemic activity. The primary antioxidant chemicals found in C. burmannii bark extract are polyphenols, which include tannins and flavonoids.

Aim: The antidiabetic activity of cinnamon essential oil (C. burmannii) against streptozotocin (STZ) was examined in this study.

Methods: STZ (45 mg/kg BW) was administered intraperitoneally as a single dose. Twenty male rats were employed in this investigation. The rats were divided into five groups: treatment 1 (P1) was administered with STZ and provided with 100 mg/kg BW; treatment 2 (P2) was administered with STZ and provided with 200 mg/kg BW; and treatment 3 (P3) was administered with STZ and provided with 400 mg/kg BW. The negative control group (K-) was not treated with STZ and was treated with 1% Tween 80. For 14 days, the medication was administered daily.

Results: The essential oil of cinnamon may lessen glomerulosclerosis, tubular necrosis, tubular degeneration, and glomerular necrosis. The kidney P3 treatment (400 mg/kg BW) produced negligible effects.

Conclusion: It is possible to create cinnamon essential oil as an herbal antidiabetic medication by lowering the degree of kidney cell damage.

Keywords: Antidiabetic; Cinnamomum burmannii; Essential oil; Kidney; Streptozotocin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.. Microscopic image of degeneration of white rat kidney cells (H&E staining with 200x magnification) groups: K, K+, P1, P2, and P3. (a) normal cells (b) hydropic degeneration.
Fig. 2.
Fig. 2.. Microscopic image of tubular cell necrosis. Renal cortex (H&E staining with 200x differed significantly frommagnification) K–, K+, P1, P2, and P3 groups. (a) normal peritubular cells (b) tubular cell necrosis.
Fig. 3.
Fig. 3.. Microscopic image of glomerular necrosis. Kidney cortex of white rats (H&E staining with 200x magnification) groups: K, K+, P1, P2, and P3 (a) Normal Glomerulus(b) Glomerular necrosis.
Fig. 4.
Fig. 4.. Microscopic image of glomerulosclerosis. Renal cortex of white rats (H&E staining with 200x magnification) groups: K, K+, P1, P2, and P3 (a) fibrosis in the parietal layer(b) focal glomerulosclerosis (c) (synechiae) adhesions between the glomerulus and the parietal layer.

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