Context: Naturally occurring polyphenols including olive oil (OO) and its constituents hydroxytyrosol (HT) and tyrosol (TY), consumed in the Mediterranean diet, have shown to treat various ailments due to their remarkable antioxidant properties. Objective: The present study investigates the hepatoprotective effects of OO and its phenolic compounds HT and TY against TCDD-induced hepatotoxicity in male Wistar rats. Materials and methods: TCDD was administered at a dose of 100 ng/kg p.o. for 20 d. Administration of OO (10 ml/kg; oral), HT (0.5 mg/kg; oral), and TY (30 mg/kg; i.p) was started 5 d prior to TCDD administration, and continued for 25 d with or without TCDD administration. At the end of the experiment (25 d), blood was taken for biochemical analyses and liver for the measurement of macromolecular damages, antioxidant status, expressions of CYP1A1, and apoptotic factors. Results: TCDD administration resulted in significant (p50.05) increase in the level of hepatic stress markers ALT (101.6 ± 3.07 IU/l), AST (295.0 ± 3.0 IU/l), and ALP (266.66 ± 3.7 IU/l). Also, biochemical analyses of liver reported elevation in nitrite and protein carbonyl content and depletion of NQO1 and HO. However, OO, HT, and TY restored the antioxidant status. Protein expressions by Western Blot technique showed an increase in the level of CYP1A1 and Bax and a decreased level of Bcl-2 on TCDD treatment, and vice versa on OO, HT, and TY treatment. Discussion and conclusion: Our work concludes that dietary supplementation of OO, HT, and TY could serve as a potential preventive drug for TCDD-induced hepatotoxicity.
Neurodegenerative disease is a collective term given for the clinical condition, which results in progressive degeneration of neurons and the loss of functions associated with the affected brain region. Apart from the increase in age, neurodegenerative diseases are also partly affected by diet and lifestyle practices. Parkinson’s disease (PD) is a slow onset neurodegenerative disorder and the second most common neurodegenerative disease, which affects the motor system. Although there is no prescribed treatment method to prevent and cure PD, clinical procedures help manage the disease symptoms. Green tea polyphenols are known for several health benefits, including antioxidant, anti-inflammatory, and neuroprotective activity. The current manuscript summarizes the possible mechanisms of neuroprotective potential of green tea with a special focus on PD. Studies have suggested that the consumption of green tea protects against free-radicals, inflammation, and neuro-damages. Several in vivo studies aid in understanding the overall mechanism of green tea. However, the same dose may not be sufficient in humans to elicit similar effects due to complex physiological, social, and cultural development. Future research focused on more clinical trials could identify an optimum dose that could impart maximum health benefits to impart neuroprotection in PD.
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