Neuroprotective effect of quercetin and Zingiber officinale on sodium arsenate-induced neurotoxicity in rats

Abstract

The study was aimed at determining the ameliorative potential of quercetin and Zingiber officinale (ZO) against sodium arsenate-induced neurotoxicity in male Wistar rats. Thirty adult animals were randomly allocated to five groups (n = 6). Group I served as control, groups II and IV were treated with ZO [300 mg/kg, PO (per os)/day], and group V animals were administered quercetin (50 mg/kg, PO/day) for 18 days. Groups III, IV, and V were injected with sodium arsenate (20 mg/kg, intraperitoneally/day) for 4 days starting from day 15. The administration of sodium arsenate resulted in a significant decrease in total antioxidant status, total thiols, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and aryl esterase in brain tissue of the animals compared with the control group. In addition, a significant increase was observed in malondialdehyde, advanced oxidation protein product and plasma nitric oxide levels, indicating oxidative stress-mediated neuronal damage. However, these arsenic-induced alterations were significantly reversed by quercetin or ZO in the treatment groups, indicating their ameliorative potential. These positive effects were further confirmed by histopathological examination of brain tissue revealing the suppression of severe neuronal injury, spongiosis and gliosis in the samples pretreated with quercetin and ZO. Our results suggest that inclusion of ZO and quercetin-rich foods in the diet can help in preventing the neurotoxic effects in areas with elevated levels of arsenic in food chain and ground water.

Keywords: Wistar rats; Zingiber officinale; antioxidant status; arsenic; neurotoxicity; quercetin.

FIGURE 1

Changes in the body weight of animals on day 1 and day 18 of different treated groups (a) and plasma level of nitric oxide (NO) in Wistar rats following treatment of Z. officinale and sodium arsenate alone and along with Z. officinale and quercetin (b).

FIGURE 2

Histopathology of normal cerebral parenchyma was seen in control animals (a) and no pathological changes seen in cerebrum of the group II (b). Group III showed perineuronal edema (arrowhead), neuronal degeneration and necrosis (arrow) (c) and perivascular edema, endothelial hypertrophy and spongiosis (arrow) (d). Group IV rat cerebrum revealed mild spongiotic vacuolation (arrow) and neuronal degeneration (e), whereas in group V moderate spongiosis and neuronal degeneration (arrow) were observed (f).

FIGURE 3

Histology of normal cerebellum with Purkinje cells and granule cell neurons were observed in group I (a) and no pathological alterations were noted in group II (b). Group III indicated severe spongiosis and degeneration of Purkinje cells (c) and meningeal edema (arrow) and degeneration of Purkinje cells (arrowhead) (d). Group IV showed mild spongiosis (arrow) and Purkinje cell degeneration (e) and group V showed spongiosis and degeneration of Purkinje cells (arrow) (f).