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Effects of 1,8-Cineole on Diabetic Muscular Atrophy
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Introduction:
This study aimed to address the effects of 1,8-cineole on
diabetic muscular atrophy in streptozotocin (STZ)-induced diabetic rats.
Materials and Methods:
Adult male rats were divided into three groups (n = 15): nondiabetic
control (ND), diabetic (D), and diabetic rats treated with 1,8-cineole
intraperitoneally for 21 days. A single low-dose intraperitoneal injection of STZ (50
mg/kg) was used to induce diabetes. At the end of the experiment, blood and muscle
tissue samples were collected for analysis.
Results:
There was a significant increase in blood glucose levels in diabetic rats,
which coincided with significant increases in the skeletal muscles' mRNA expression
levels of two inflammatory markers, transforming growth factor-β1 (TGF-β1) and tumor
necrosis factor-α (TNF‑α), and in two biomarkers of skeletal muscle atrophy, F-boxonly
protein 32 (FBXO32) and muscle RING-finger protein-1 (MuRF1). Additionally,
diabetic rats showed a significant decrease in the expression of skeletal muscle
glucose transporter 4 (GLUT4) levels. The malondialdehyde (MDA) level was
increased, while the activity of superoxide dismutase (SOD) was not changed in the
skeletal muscle of the D group compared to the ND group. Cineol treatment reversed
the diabetes-induced changes in the relative mRNA expression levels of TGF-β1, TNF-
α, FBXO32, MuRF1, and GLUT4 in the skeletal muscle and significantly decreased
MDA levels with a non-significant increase in skeletal muscle SOD activity.
Discussion:
These results suggest that 1,8-cineole protects diabetic skeletal muscles
in multiple ways, including reducing oxidative stress, inhibiting the generation of
inflammatory cytokines, and preventing the expression of proteolytic genes. Its
capacity to increase GLUT4 levels enhances glucose absorption and insulin sensitivity.
Therefore, in diabetic situations, 1,8-cineole may help maintain muscle structure and
function. These findings add to the increasing amount of data indicating that 1,8-
cineole is a viable option for treating diabetes-induced muscle problems brought on by
diabetes. To fully understand its therapeutic potential, further research is necessary,
including studies on muscle mass, myostatin levels, and protein expression.
Conclusion:
1,8-cineole tr1eatment decreased blood glucose levels and attenuated
oxidative stress and inflammation in the skeletal muscles of diabetic rats, thereby
protecting rats against diabetic muscle atrophy.
Bentham Science Publishers Ltd.
Title: Effects of 1,8-Cineole on Diabetic Muscular Atrophy
Description:
Introduction:
This study aimed to address the effects of 1,8-cineole on
diabetic muscular atrophy in streptozotocin (STZ)-induced diabetic rats.
Materials and Methods:
Adult male rats were divided into three groups (n = 15): nondiabetic
control (ND), diabetic (D), and diabetic rats treated with 1,8-cineole
intraperitoneally for 21 days.
A single low-dose intraperitoneal injection of STZ (50
mg/kg) was used to induce diabetes.
At the end of the experiment, blood and muscle
tissue samples were collected for analysis.
Results:
There was a significant increase in blood glucose levels in diabetic rats,
which coincided with significant increases in the skeletal muscles' mRNA expression
levels of two inflammatory markers, transforming growth factor-β1 (TGF-β1) and tumor
necrosis factor-α (TNF‑α), and in two biomarkers of skeletal muscle atrophy, F-boxonly
protein 32 (FBXO32) and muscle RING-finger protein-1 (MuRF1).
Additionally,
diabetic rats showed a significant decrease in the expression of skeletal muscle
glucose transporter 4 (GLUT4) levels.
The malondialdehyde (MDA) level was
increased, while the activity of superoxide dismutase (SOD) was not changed in the
skeletal muscle of the D group compared to the ND group.
Cineol treatment reversed
the diabetes-induced changes in the relative mRNA expression levels of TGF-β1, TNF-
α, FBXO32, MuRF1, and GLUT4 in the skeletal muscle and significantly decreased
MDA levels with a non-significant increase in skeletal muscle SOD activity.
Discussion:
These results suggest that 1,8-cineole protects diabetic skeletal muscles
in multiple ways, including reducing oxidative stress, inhibiting the generation of
inflammatory cytokines, and preventing the expression of proteolytic genes.
Its
capacity to increase GLUT4 levels enhances glucose absorption and insulin sensitivity.
Therefore, in diabetic situations, 1,8-cineole may help maintain muscle structure and
function.
These findings add to the increasing amount of data indicating that 1,8-
cineole is a viable option for treating diabetes-induced muscle problems brought on by
diabetes.
To fully understand its therapeutic potential, further research is necessary,
including studies on muscle mass, myostatin levels, and protein expression.
Conclusion:
1,8-cineole tr1eatment decreased blood glucose levels and attenuated
oxidative stress and inflammation in the skeletal muscles of diabetic rats, thereby
protecting rats against diabetic muscle atrophy.
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