ABSTRACT
@#Introduction: Astrocytes are responsible for many essential functions of neurons in CNS. It has been recognised that chronic stress affects the morphology of astrocyte. Natural antioxidant such as honey has been used as one of the therapeutic strategies to lessen the damaging effect of chronic stress on our body. Therefore, the aim of the study is to explore the effect of natural antioxidant, Tualang honey (TH) on the morphology of astrocytes following chronic stress exposure. Methods: Thirty-two male rats were randomly divided into the 4 groups: (i) control, (ii) stress, (iii) honey, (iv) stress plus honey groups.TH was administered via oral gavage at dose of 1.0 g/kg body weight pre and post experiment. Chronic stress was exposed to animals in group (ii) and (iv) for consecutive 21 days. Anti GFAP immunohistochemistry method was employed to label astrocytes in the medial prefrontal cortex. The number of GFAP+ astrocytes and several parameters related to astrocyte processes were measured. Results: The present study showed that chronic stress reduced the GFAP immunoreactive astrocyte number and percentage of GFAP immunoreactive material. Chronic stress also caused a reduction in astrocyte process ramification as indicated by a reduction in astrocyte total number of processes, average length of processes and maximum number of intersections. However, antioxidant treatment using TH could not reverse these stress-induced changes to the astrocytes. Conclusion: These results demonstrate that chronic stress decreases the number of GFAP immunoreactive astrocyte and cause shrinking of astrocyte processes in stress-sensitive brain region, but these changes cannot be reversed by antioxidant treatment.
ABSTRACT
Objective: To investigate the effect of alpha-lipoic acid (ALA) supplementation on systolic blood pressure (SBP), renal oxidant-antioxidant status and renal damage in spontaneously hypertensive rats (SHR) and SHR administered with Nω-nitro-L-arginine methyl ester (L-NAME). Methods: Male rats were divided into four groups (SHR, SHR+ALA, SHR+L-NAME, SHR+ALA+L-NAME). The respective group of rats was administered with ALA (100 mg/kg/day) from age 4 weeks to 28 weeks and L-NAME (25 mg/kg/day) from age 16 weeks to 28 weeks. SBP was measured every two weeks and twenty four hour urine was collected at 4 weeks, 16 weeks and 28 weeks for estimation of protein, creatinine and N-acetyl-β-D-glucosaminidase. At the end of 28 weeks, rats were sacrificed and blood and kidneys collected for assessment of blood creatinine, kidney thiobarbituric acid reactive substances, protein carbonyls, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, glutathione disulfide, glutathione, total antioxidant status and nitric oxide as well as histopathological examination. Results: ALA supplementation significantly reduced SBP of SHR and SHR+L-NAME rats when compared to their respective non-supplemented groups. Renal oxidant status markers including thiobarbituric acid reactive substances and protein carbonyls were significantly reduced on SHR and SHR+L-NAME rats supplemented with ALA at 28 weeks as well as ALA supplementation significantly increased renal antioxidants including superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, glutathione and glutathione/glutathione disulfide ratio at 28 weeks. No significant change in nitric oxide levels was observed between the ALA supplemented and non-supplemented groups. Renal dysfunction was ameliorated on ALA supplementation as evidenced by significant reduction in urine protein levels, N-acetyl-β-D-glucosaminidase activity and significant increase of creatinine clearance in SHR and SHR+L-NAME at 28 weeks. Renal histopathological examination showed that ALA supplementation prevented vascular damage in SHR and ameliorated glomerular damage in SHR+L-NAME at 28 weeks. Conclusions: ALA has hypotensive and renoprotective effects on both SHR and SHR+L-NAME, which could be due to its ability to ameliorate oxidative stress in the kidneys.