Effects of rosmarinic acid on cognitive and biochemical alterations in ovariectomized rats treated with D-galactose

Introduction. Animal models designed to mimic certain features of Alzheimer’s disease (AD) can help us to in­crease our understanding of the underlying mechanisms of disease. Previous studies have revealed that long-term D-galactose injection combined with ovariectomy results in pathophysiologic alterations associated with AD. Thus, the aim of the present study was to investigate the effects of rosmarinic acid (RA) administration on pathological changes associated with ovariectomy and D-galactose injection, which serve as a two-insult model for AD. Material and methods. One hundred female Wistar rats were divided into five equal groups: control (C), Sham (Sh), rosmarinic acid treated (R), ovariectomized rats treated with D-galactose (OD), ovariectomized rats treated with D-galactose and rosmarinic acid (ODR) groups. D-galactose (80 mg/kg/day) was administered by i.p. injection and RA (50 mg/kg/day) was given via gavage for 60 days. Open field and Y-maze tests were used to assess locomotor activity and short-term spatial memory, respectively. Biochemical and histopathological analyses of the brain tissue were performed. Results. Open field testing showed that the locomotor activity and exploratory behavior of rats were prominent­ly impaired in the OD group as compared to the other studied groups. Similarly, Y-maze test results revealed a decrease of short-term spatial memory in the OD rats. A concomitant treatment with RA significantly restored altered locomotor activity and cognitive functions in the ODR group. Lipid peroxidation levels, cyclooxygen­ase-2 expression and prostaglandin E2 levels in the brain tissue were higher in the OD group and RA treatment inhibited these changes. AD-like histopathological alterations and amyloid b peptide (Ab) depositions were observed in the OD group. Normal cell structure and lower Ab depositions were observed in the ODR group compared with the OD group. Conclusions. RA could have the potential to prevent some psychological and biochemical alterations of brain tissue found in a rat model of AD probably by attenuating lipid peroxidation and inflammatory response

The effect of increase in blood glucose level on hearing loss

Objective: Previous studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. Methods: 25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. Results: At 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. Conclusion: These results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. Level of evidence: Level 3

Effect of sodium tungstate on visual evoked potentials in diabetic rats

AIM: To evaluate the effect of sodium tungstate on visual evoked potentials (VEPs) in diabetic rats. METHODS: Wistar rats were randomly divided into three groups as normal control, diabetic control and diabetic rats treated with sodium tungstate. Diabetes was induced by single intraperitoneal injection of streptozotocin (50 mg/kg). Sodium tungstate [40 mg/(kg·d)] was administered for 12wk and then VEPs were recorded. Additionally, thiobarbituric acid reactive substance (TBARS) levels were measured in brain tissues. RESULTS: The latencies of P1, N1, P2, N2 and P3 waves were significantly prolonged in diabetic rats compared with control group. Diabetes mellitus caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. However, prolonged latencies of VEPs for all components returned to control levels in sodium tungstate-treated group. The treatment of sodium tungstate significantly decreased brain TBARS levels and depleted the prolonged latencies of VEP components compared with diabetic control group. CONCLUSION: Sodium tungstate shows protective effects on visual pathway in diabetic rats, and it can be worthy of further study for potential use