Anti-neuroinflammatory and antioxidant effects of N-acetyl cysteine in long-term consumption of artificial sweetener aspartame in the rat cerebral cortex
Afaf Abbass Sayed Saleh;
Abstract
This study specifically focuses to investigate whether N-acetyl cysteine (NAC) has poten-tial ameliorative effects against aspartame-induced brain pathophysiology in rats. Thirty adult male
Wistar rats weighing 200–220 g were randomly divided into three groups as follows: the first group
was administered with distilled water and served as the control group; the second group was given
aspartame at a dose of 75 mg/kg b.wt. and the third group was given both aspartame and N-acetyl
cysteine at dose of 75 mg/kg b.wt. and 600 mg/kg b.wt. respectively. Oral administration was done
in the morning daily for 90 days.
Long term consumption of the artificial sweetener aspartame (ASP) induced large increments in
cortical inflammation and oxidative stress. Daily oral NAC administration can significantly reverse
brain-derived neurotrophic factor (BDNF) levels, blocked the cyclooxygenase-2 (COX-2) and
prostaglandin E2(PGE2) production with selective attenuation in expression of proinflammatory
cytokines of interleukin-6 (IL-6) and tumor necrosis factor-a(TNF-a) in the rat cerebral cortex.
Also, NAC can significantly replenish and correct intracellular glutathione (GSH) levels, modulate
the elevated levels of total nitric oxide (TNO) and lipid peroxidation (LPO). Conclusions: The
present results amply support the concept that the brain oxidative stress and inflammation coexist
in experimental animals chronically treated with aspartame and they represent two distinct thera-peutic targets in ASP toxicity. The present data propose that NAC attenuated ASP neurotoxicity
and improved neurological functions, suppressed brain inflammation, and oxidative stress
responses and may be a useful strategy for treating ASP-induced neurotoxicity.
Wistar rats weighing 200–220 g were randomly divided into three groups as follows: the first group
was administered with distilled water and served as the control group; the second group was given
aspartame at a dose of 75 mg/kg b.wt. and the third group was given both aspartame and N-acetyl
cysteine at dose of 75 mg/kg b.wt. and 600 mg/kg b.wt. respectively. Oral administration was done
in the morning daily for 90 days.
Long term consumption of the artificial sweetener aspartame (ASP) induced large increments in
cortical inflammation and oxidative stress. Daily oral NAC administration can significantly reverse
brain-derived neurotrophic factor (BDNF) levels, blocked the cyclooxygenase-2 (COX-2) and
prostaglandin E2(PGE2) production with selective attenuation in expression of proinflammatory
cytokines of interleukin-6 (IL-6) and tumor necrosis factor-a(TNF-a) in the rat cerebral cortex.
Also, NAC can significantly replenish and correct intracellular glutathione (GSH) levels, modulate
the elevated levels of total nitric oxide (TNO) and lipid peroxidation (LPO). Conclusions: The
present results amply support the concept that the brain oxidative stress and inflammation coexist
in experimental animals chronically treated with aspartame and they represent two distinct thera-peutic targets in ASP toxicity. The present data propose that NAC attenuated ASP neurotoxicity
and improved neurological functions, suppressed brain inflammation, and oxidative stress
responses and may be a useful strategy for treating ASP-induced neurotoxicity.
Other data
Title | Anti-neuroinflammatory and antioxidant effects of N-acetyl cysteine in long-term consumption of artificial sweetener aspartame in the rat cerebral cortex | Authors | Afaf Abbass Sayed Saleh | Keywords | N-acetyl cysteine; Aspartame; Cytokine; Free-radical; Inflammation | Issue Date | 3-May-2015 | Publisher | ELSEVIER B. V | Journal | The Journal of Basic & Applied Zoology | DOI | 10.1016/j.jobaz.2015.05.001 |
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