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Fig. 5 | Future Journal of Pharmaceutical Sciences

Fig. 5

From: The neuroprotective attribution of Ocimum basilicum: a review on the prevention and management of neurodegenerative disorders

Fig. 5

A Main resources and pathways for oxidant generation in NDs. NO and O2·- are produced in the brain during NDs. NO induces protein nitrosylation as well as ONOO_ generation by reacting with O2·-. SOD detoxifies O2·- to H2O2, which is converted to H2O by catalase or GSHPx. ·OH, which is produced from H2O2 through the Fenton or Haber-Weiss reactions, causes cell injury through oxidized lipid, protein, DNA, and RNA. GSHPx glutathione peroxidase, H2O2 hydrogen peroxide, NO nitric oxide, O2·- superoxide anion, ·OH hydroxyl radical, ONOO_ peroxynitrite, SOD superoxide dismutase. Mechanism of action of O. basilicum antioxidant and its bioactive compounds. The inhibition of reactive oxygen species (ROS) by the direct scavenging activities prevents lipid peroxidation as well as cell death. O. basilicum and its bioactive compounds elevate endogenous antioxidant (glutathione, GSH, superoxide dismutase, SOD, and Catalase and others) and subsequently ameliorate lipid/protein peroxidation-induced cell death. B Neuroprotective effects of O. basilicum and its bioactive compounds also showed restoration of neuronal marker genes (brain-derived neurotrophic factor, BDNF and tyrosine hydroxylase, TH), reduction of acetylcholinesterase (AChE) and inhibition of Keap1-Nrf2 binding

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