Effect of Cananga odorata modulates cholinergic, purinergic enzymes, and elevates antioxidant markers in diabetes-induced cognitive disorder rat brain

Introduction

In the folklore of Chinese traditional medicine, therapeutic materials like Cananga odorata have several attributes that ameliorate non-communicable diseases. This study sought to examine the anti-cognitive dysfunction potential of Cananga odorata leaf extract (COLE) in the brain of diabetes-induced albino male rats.

Methodology

Forty-two mature male Wistar rats weighing between 200 to 250 g (n = 6) were used. They were split into seven groups: Normal control; DM (STZ 50 mg/kg via I.P) group; DM + Acarbose (25 mg/kg BW); DM + 2 mg, DM + 4 mg COLE, 2 mg COLE, and 4 mg COLE. Fasting blood glucose level was determined after 72 h. Behavioral training was conducted on the 14th day of the treatment and the rats were sacrificed. Biochemical indices acetylcholinesterase (AChE), butyrylcholinesterase (BChE), adenosine deaminase (ADA), reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), glutathione (GSH), and superoxide dismutase (SOD) were carried out on the brain tissue samples collected.

Results

The trial results show a significant decrease in the fasting blood glucose levels (FBGL) in the treatment groups. DM rats treated with COLE demonstrated better cognitive performance in the Y-maze behavior test, with considerable increases in alternation behavior. The DM group exhibited considerably higher levels of neurotransmitter enzyme activities, particularly AChE and BChE. However, the administration of COLE therapy attenuated these activities, indicating a protective impact on cholinergic function. Furthermore, the purinergic signaling-related enzymes ATPase and ADA showed decreased activity upon treatment with COLE. ROS and TBARS were considerably higher in the DM group but were successfully decreased by COLE treatment. The DM group had reduced levels of GSH and SOD activity, which was recovered with COLE. This suggests an improvement in the brain's antioxidant defense mechanism. The typical anti-diabetic medication used as a comparator, ACA, likewise showed efficacy but fell short of the effects of a higher dosage of COLE.

Conclusion

In DM-induced cognitive dysfunction, COLE, especially at a dosage of 4 mg, dramatically reduces hyperglycemia, modifies neurotransmitter enzyme activity, and strengthens antioxidant defenses. These results imply that COLE may be useful as a therapeutic agent to treat diabetes-related cognitive deficits.