Lead （Pb） is one of the most common environmental toxicants, exposure to which can cause significant neurotoxicity and an associated decline in brain function. This study investigated the possible neuroprotective ro...Lead （Pb） is one of the most common environmental toxicants, exposure to which can cause significant neurotoxicity and an associated decline in brain function. This study investigated the possible neuroprotective role oflndigofera oblongifolia leaf methanolic extract （IOLME） against lead-induced neurotoxicity. Rats were intraperitoneally injected with lead acetate, with or without IOLME （intragastric administration for 5 days）, and the neuroprotective effect of IOLME was assessed by measuring the lead concentration, redox status （lipid peroxidation, nitric oxide and glutathione）, enzymatic antioxidant activities （superoxide dismutase, catalase, glutathione peroxidase and reductase）, PCR assays of apoptosis markers （Bax and Bcl-2） and histopathology of the brain. The increases in the lipid peroxidation, nitric oxide, and apoptosis, the decreases in the glutathione level and the activity of antioxidant enzymes, and the altered histology of the brain induced by lead acetate were mitigated in the brain of rats pre-treated with IOLME. These findings indicate that IOLME has beneficial effects and it mitigates lead acetate-induced neurotoxicity via its antiox-idant and anti-apoptotic activities.展开更多
基金the Deanship of Scientific Research at King Saud University for funding the work through the research group project,No.PRG-1436-02
文摘Lead （Pb） is one of the most common environmental toxicants, exposure to which can cause significant neurotoxicity and an associated decline in brain function. This study investigated the possible neuroprotective role oflndigofera oblongifolia leaf methanolic extract （IOLME） against lead-induced neurotoxicity. Rats were intraperitoneally injected with lead acetate, with or without IOLME （intragastric administration for 5 days）, and the neuroprotective effect of IOLME was assessed by measuring the lead concentration, redox status （lipid peroxidation, nitric oxide and glutathione）, enzymatic antioxidant activities （superoxide dismutase, catalase, glutathione peroxidase and reductase）, PCR assays of apoptosis markers （Bax and Bcl-2） and histopathology of the brain. The increases in the lipid peroxidation, nitric oxide, and apoptosis, the decreases in the glutathione level and the activity of antioxidant enzymes, and the altered histology of the brain induced by lead acetate were mitigated in the brain of rats pre-treated with IOLME. These findings indicate that IOLME has beneficial effects and it mitigates lead acetate-induced neurotoxicity via its antiox-idant and anti-apoptotic activities.
