Treatment with Ginkgo biloba supplement modulates oxidative disturbances, inflammation and vascular functions in oxygen deprived hypothyroid mice: Involvement of endothelin-1/NO signaling pathways.

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.

Involvement of striatal oxido-inflammatory, nitrosative and decreased cholinergic activity in neurobehavioral alteration in adult rat model with oral co-exposure to erythrosine and tartrazine.

Overuse or overconsumption of food additive or colorant cannot be ignored in our society and there are several reports of it harmful effect on the body system. This study investigated the toxicity effect of tartrazine and erythrosine (ET, 50:50) on neurobehavioral alteration, striatal oxido-nitrosative and pro-inflammatory stress and striatal acetylcholinesterase activity in experimental rat model. Rats were co-exposed to ET (2 mg/kg, 6 mg/kg and 10 mg/kg) and distilled water (control), p.o for 6 weeks. The change in neurobehavioral function (Open field test, Forced swimming test and Tail suspension test), Lipid peroxidation (Malonaldehyde, MDA), Antioxidants (Glutathione, GSH; Catalase, CAT) Nitrite, Pro-inflammatory cytokine (Tumor necrosis factor-alpha, TNF-α) and Acetylcholinesterase (AChE) activity were evaluated. Results showed significant decrease in neurobehavioral functions after co-exposure to ET. Moreover, there were significant increase in MDA and Nitrite level, significant decrease in the concentration of GSH and CAT and a significant increase TNF-α concentration and AChE activity after co-exposure to ET. Oral co-exposure to tartrazine and erythrosine induced decrease in locomotion and exploration, increase anxiety and depression-like behavior and altered the cholinergic system through upregulation of oxido-nitrosative stress, pro-inflammatory cytokine and acetylcholinesterase activity.