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A double-hit biological alteration involving exposure to oxygen deprivation in hypothyroid condition may exacerbate cellular oxidative and inflammatory disturbances comparative to a one-hit biological exposure. This study investigated the therapeutic effect of Ginkgo biloba as cardioprotective against aortic oxido-inflammatory disturbances following oxygen deprivation in hypothyroid mice. Male Swiss mice were partitioned into 5 groups (n = 6) for hypothyroidism (Carbimazole 1.2 mg/kg) and hypoxia induction. Group 1 (normal control), group 2 (hypoxic stress control), group 3 (hypoxic and hypothyroid stress), group 4 (hypoxic and hypothyroid stress and Ginkgo biloba 20 mg/kg; p.o) and group 5 (hypoxic and hypothyroid stress and Levothyroxine 10 μg/kg; p.o) for 14 days. Thereafter, serum and aorta was collected for biochemical evaluation. GBS did not up-regulate the serum thyroid hormone imbalances (tri-iodothyronine (T3), thyroxin (T4)) but maintains the TSH levels. The blood glucose level was reduced with decrease oxidative stress and inflammatory mediators in the serum/aorta indicated by inhibited redox status following treatment with GBS. Moreover, endothelin-1/nitric oxide signaling pathways were markedly regulated in the aorta. Conclusively, GBS acts as a therapeutic agent and may be consider as a potential vasodilator candidate in the management and control of hypoxic stress in hypothyroid condition. PRACTICAL APPLICATIONS: Treatment with Gingko biloba supplement abated endothelial abnormalities via elevation of nitric oxide release and suppression of endothelin activity in hypothyroid mice exposed to hypoxic hypoxia. The activity of myeloperoxidase enzyme and redo-inflammatory status was downregulated following treatment with Gingko biloba supplement in hypothyroid mice exposed to hypoxic hypoxia. Treatment with Gingko biloba supplement modulates hypothalamic-pituitary-adrenal (HPA) axis by inhibiting corticosterone release in hypothyroid mice exposed to hypoxic hypoxia., (© 2022 Wiley Periodicals LLC.)

Asymptomatic and early clinical stages of Parkinson's disease (PD) have been linked with comorbid non-motor symptoms including dysfunction of the gastrointestinal (GI) tract. Notwithstanding, neuroprotective and gastroprotective effects of Ginkgo biloba supplements (GBS) have been investigated independently. Hence, whether GBS-mediated GIT-protective capacity could be helpful in PD via gut-brain anti-inflammatory signaling still remains unknown. Treatment with GBS significantly repressed the motor behavioral and neuromuscular deficits and prevented loss of striatal dopaminergic loss by improving the level of tyrosine hydroxylase enzyme and suppressing synucleinopathy development. Striatal neurons and ileal epithelial injury following intraperitoneal rotenone administration were accompanied with oxidoinflammatory/nitroinflammatory stress and marked inhibition of cholinergic transmission. Moreover, there was increased striatal executioner caspase-3 and decreased nuclear factor erythroid-2-related factor 2 (Nrf2) immunoexpression, loss of striatal pyramidal neuron with a marked decrease in length and width of the dendritic spines as well as significant hyperplasia of cryptal cells in the ileal epithelial tissues, all which were reversed by the pretreatment + concurrent (Pre-CONC) and concurrent (CONC) GBS treatment pattern. In sum, we proved the potential dual effects of GBS in preventing both dopaminergic neural-related impairments and gut wall abnormalities linked with PD., (© 2022 Wiley Periodicals LLC.)

Purpose: It has been hypothesized that compounds with strong anti-oxidant activity might mitigate lead-induced neurotoxicity that resulted to neuronal degeneration.Ginkgo biloba supplement (GB-S) is a neuroactive supplement which has been reported to demonstrate neuroprotective effects. In this study, we investigated the reversal effect and the underlying mechanism of GB-S following lead-induced neurotoxicity in mice., Methods: Male Swiss mice (n = 8) were pre-treated with lead acetate (100 mg/kg) for 30 min before GB-S (10 mg/kg and 20 mg/kg) or Ethylenediaminetetraacetic acid (EDTA) (50 mg/kg) intraperitoneally for 14 consecutive days. Memory impairment symptoms were evaluated on day 13 and 14 using Y-maze and Novel object recognition test (NORT) respectively. Thereafter, spectrophotometry, ELISA, immunohistochemistry and histomorphormetry were used to estimate the degree and expression of biomarkers of neuronal inflammation: oxido-inflammatory stress, apoptosis and degeneration in the hippocampus (HC)., Results: Lead acetate treatment significantly (p < 0.05) induced neurobehavioral impairment which was reversed by GB-S as evident in increased percentage alternation and discrimination index. GB-S significantly (p < 0.05) reduced lipid peroxidation and nitrite level, inhibited TNF-α and acetylcholinesterase activity and improved glutathione, catalase and superoxide dismutase activity in the HC. Moreover, GB-S inhibited hippocampal apoptosis via elevated expression of caspase-3 with marked increase level of brain derived neurotrophic factor (BDNF). Also, the histomorphormetric study showed that GB-S rescued death of pyramidal neurons (CA3) in the HC., Conclusion: Our findings however suggest that GB-S decreased memory impairment progression induced by lead acetate via mechanisms connected to inhibition of oxido-inflammatory stress mediators, restrained acetylcholinesterase activity, up-regulated BDNF/Caspase-3 expression and suppression of hippocampal pyramidal neuron degeneration in mice., (Copyright © 2022 Elsevier GmbH. All rights reserved.)

Neuroimmune alterations have important implication in the neuropsychiatric symptoms and biochemical changes associated with lead-induced neurotoxicity. It has been suggested that inhibition of neuroinflammatory-mediated lead-induced neurotoxicity by phytochemicals enriched with antioxidant activities would attenuate the deleterious effects caused by lead. Hence, this study investigated the neuroinflammatory mechanism behind the effect of Ginkgo biloba supplement (GB-S) in lead-induced neurotoxicity in mice brains. Mice were intraperitoneally pretreated with lead acetate (100 mg/kg) for 30 min prior the administration of GB-S (10 and 20 mg/kg, i.p.) and ethylenediaminetetraacetic acid (EDTA) (50 mg/kg, i.p.) for 14 consecutive days. Symptoms of neurobehavioral impairment were evaluated using open field test (OFT), elevated plus maze (EPM), and tail suspension test (TST) respectively. Thereafter, mice brain hippocampi were sectioned for myeloperoxidase activity (MPO), pro-inflammatory cytokine (TNF-α and IL-6) estimation and inflammatory protein (NF-κB) expression. Furthermore, histomorphormetric studies (Golgi impregnation and Cresyl violet stainings) were carried out. GB-S (10 and 20 mg/kg) significantly restores neurobehavioral impairments based on improved locomotion, reduced anxiety- and depressive-like behavior. Moreover, GB-S reduced the MPO activity, inhibits TNF-α, IL-6 release, and downregulates NF-κB immunopositive cell expression in mice hippocampus. Histomorphometrically, GB-S also prevents the loss of pyramidal neuron in the hippocampus. The endpoint of this findings suggest that GB-S decreases neuropsychiatric symptoms induced by lead acetate through mechanisms related to inhibition of release of pro-inflammatory mediators and suppression of hippocampal pyramidal neuron degeneration in mice., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)