Dataset Information

Neuroprotective potential of Indigofera oblongifolia leaf methanolic extract against lead acetate-induced neurotoxicity.

ABSTRACT: 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 of Indigofera 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 antioxidant and anti-apoptotic activities.

SUBMITTER: Al-Quraishy S

PROVIDER: S-EPMC5204236 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Neuroprotective potential of <i>Indigofera oblongifolia</i> leaf methanolic extract against lead acetate-induced neurotoxicity.

Al-Quraishy Saleh S Dkhil Mohamed A MA Ibrahim Shaimaa R SR Abdel Moneim Ahmed E AE

Neural regeneration research 20161101 11

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 of <i>Indigofera oblongifolia</i> 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 meas ...[more]

PMID: 28123424

Similar Datasets

Project description:Heavy metal exposure, in lead (Pb) particularly, is associated with severe neuronal impairment though oxidative stress mediated by reactive oxygen species, and antioxidants may be used to abolish these adverse effects. This study investigated the potential neuroprotective role of coenzyme Q10 (CoQ10) against lead acetate (PbAc)-induced neurotoxicity. Twenty-eight male Wistar albino rats were divided into four equal groups (n = 7) and treated as follows: the control group was injected with physiological saline (0.9% NaCl); the CoQ10 group was injected with CoQ10 (10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQ10 group was injected first with PbAc, and after 1 h with CoQ10. All groups were injected intraperitoneally for seven days. PbAc significantly increased cortical lipid peroxidation, nitrate/nitrite levels, and inducible nitric oxide synthase expression, and decreased glutathione content, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activity and mRNA expression, as well as nuclear factor erythroid 2-related factor 2 (Nrf2) and homoxygenase-1 (HO-1) expression. PbAc also promoted the secretion of interleukin-1ß and tumor necrosis factor-?, inhibited interleukin-10 production, triggered the activation of pro-apoptotic proteins, and suppressed anti-apoptotic proteins. Additionally, PbAc increased the cortical levels of serotonin, dopamine, norepinephrine, GABA, and glutamate, and decreased the level of ATP. However, treatment with CoQ10 rescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism. Altogether, our findings indicate that CoQ10 has beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities.

Dataset Information

Neuroprotective potential of Indigofera oblongifolia leaf methanolic extract against lead acetate-induced neurotoxicity.

Publications

Neuroprotective potential of <i>Indigofera oblongifolia</i> leaf methanolic extract against lead acetate-induced neurotoxicity.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets