Title:Ziziphus spina-christi Leaf Extract Mitigates Mercuric Chloride-induced Cortical Damage in Rats
Volume: 25
Issue: 1
Author(s): Rafa S. Almeer*, Saad Alkahtani, Saud Alarifi, Ahmed E. Abdel Moneim, Saba Abdi and Gadah Albasher
Affiliation:
- Department of Zoology, College of Science, King Saud University, Riyadh,Saudi Arabia
Keywords:
Mercury, Ziziphus spina-christi, brain, Nrf2, inflammation, apoptosis.
Abstract:
Background: Mercuric chloride (HgCl2) severely impairs the central nervous system
when humans are exposed to it.
Aims: We investigated the neuroprotective efficiency of Ziziphus spina-christi leaf extract
(ZSCLE) on HgCl2-mediated cortical deficits.
Methods: Twenty-eight rats were distributed equally into four groups: the control, ZSCLE-treated
(300 mg/kg), HgCl2-treated (0.4 mg/kg), and ZSCLE+HgCl2-treated groups. Animals received
their treatments for 28 days.
Results: Supplementation with ZSCLE after HgCl2 exposure prevented the deposition of mercury
in the cortical slices. It also lowered malondialdehyde levels and nitrite and nitrate formation,
elevated glutathione levels, activated its associated-antioxidant enzymes, glutathione reductase,
and glutathione peroxidase, and upregulated the transcription of catalase and superoxide dismutase
and their activities were accordingly increased. Moreover, ZSCLE activated the expression of
nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 when compared with the HgCl2
group. Notably, post-treatment with ZSCLE increased the activity of acetylcholinesterase and
ameliorated the histopathological changes associated with HgCl2 exposure. Furthermore, ZSCLE
blocked cortical inflammation, as observed by the lowered mRNA expression and protein levels of
interleukin-1 beta and tumor necrosis factor-alpha, as well as decreased mRNA expression of
inducible nitric oxide synthase. In addition, ZSCLE decreased neuron loss by preventing apoptosis
in the cortical tissue upon HgCl2 intoxication.
Conclusion: Based on the obtained findings, we suggest that ZSCLE supplementation could be
applied as a neuroprotective agent to decrease neuron damage following HgCl2 toxicity.