The neurotoxic effects of lead acetate and the abrogating actions of 6-gingerol-rich extract of ginger via modulation of antioxidant defence system, pro-inflammatory markers, and apoptotic cascade.

Abstract

Lead exposure is a public health concern and it has been linked to cognitive deficit, memory impairment, and neurotoxicity. This study was designed to investigate the effect of 6-gingerol-rich extract of ginger (6-GREG) on oxidative stress, inflammation, and apoptosis in lead acetate (PbAc)-induced neurotoxicity in male Wistar rats. Twenty-five (25) male Wistar rats in total were divided into five groups at random (n = 5). The control group received 0.5 ml of normal saline, the PbAc-treated group received 7.5 mg/kg of PbAc, the vitamin C, 6-GREG (100), and 6-GREG (200) groups received 7.5 mg/kg of PbAc followed by administration of vitamin C (100 mg/kg), 6-GREG (100 mg/kg), and 6-GREG (200 mg/kg) respectively for 2 weeks. Following behavioral tests, the rats were euthanized, and their brain tissues were homogenized for biochemical analysis. When compared to the control group, the administration of PbAc caused behavioral alterations as well as a significant (p < 0.05) decrease in the activities of catalase, glutathione peroxidase, as well as reduced glutathione and Bcl-2 levels in the PbAc-treated group. Furthermore, the PbAc-treated group showed a statistically significant rise (p < 0.05) in brain acetylcholinesterase, malondialdehyde, nitric oxide, interleukin-1-beta, tumor necrosis factor-α, and caspase-9 levels in comparison to the control. Administration of both 100 mg/kg and 200 mg/kg of 6-GREG effectively reversed these behavioral and biochemical changes in 6-GREG (100)- and 6-GREG (200)-treated groups respectively compared to the PbAc-treated group. Consequently, the study reveals the role of 6-GREG in attenuating PbAc-induced neurotoxicity and brain damage via antioxidative, anti-inflammatory, and anti-apoptotic mechanisms.