Neuroprotective Potential of Chrysin: Mechanistic Insights and Therapeutic Potential for Neurological Disorders

Abstract

Chrysin, a herbal bioactive molecule, exerts a plethora of pharmacological effects, including anti-oxidant, anti-inflammatory, neuroprotective, and anti-cancer. A growing body of evidence has highlighted the emerging role of chrysin in a variety of neurological disorders, including Alzheimer's and Parkinson's disease, epilepsy, multiple sclerosis, ischemic stroke, traumatic brain injury, and brain tumors. Based on the results of recent pre-clinical studies and evidence from studies in humans, this review is focused on the molecular mechanisms underlying the neuroprotective effects of chrysin in different neurological diseases. In addition, the potential challenges, and opportunities of chrysin's inclusion in the neurotherapeutics repertoire are critically discussed.

Keywords: antioxidant; chrysin; epilepsy; neurodegenerative diseases; neurological disorders; neuroprotective agents.

Figure 1

Chemical structure of chrysin and important pharmacophores for anti-inflammatory and anti-oxidant activity.

Figure 2

Effects of chrysin in the signaling networks associated with multiple neuropathological conditions.

Figure 3

Modulation of the NRF-2 and NF-κB pathway by chrysin. ROS/RNS mediate the alteration of NRF-2 signaling and interconnect with the NF-κB signaling pathway. NRF-2 signaling activates the expression of antoxidant proteins viz, heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase 1 (NQO-1) and Glutamate-cysteine ligase catalytic subunit (GCLC, a rate-limiting enzyme for glutathione synthesis). The degradation of heme produces carbon monoxide (CO), which suppresses redox-sensitive NF-κB activation. The plausible sites of action of chrysin are illustrated.