From:  Biochanin A and its possible involvement in Parkinson’s disease management

 Numerous in vivo and in vitro studies that delineate the anti-Partkinson’s activity of biochanin A

ModelDose/concentrationObserved molecular modulationsReference
LPS-induced oxidative stress and damage rat model(25, 50 mg/kg; i.p., n = 8)Increased SOD, GPx activities in the midbrain.
Reduced MDA level.
Reduced number of apoptotic cells, Iba-1 level in the SNpc.
Increased TH-positive neurons.
Suppressed the expression of p47phox, p67phox, and gp91phox in the SNpc.
[29]
LPS-induced damage to dopaminergic neurons rat model(25, 50 mg/kg; i.p., n = 16)Decreased microglia activation.
Reduced the Iba-1 expression level.
Increased the TH-positive neurons in the SNpc.
Reduced the IL-1β, IL-6, and TNF-α levels in the serum.
Reduced the IL-1β and TNF-α in the brain.
Inhibited the phosphorylation of ERK, JNK, and p38.
[27]
Iron and rotenone-induced Parkinson’s disease rat model(3 and 30 mg/kg; i.p., n = 9)Increased the dopamine level and substantia nigra TH expression in the brain.
Reduced the MDA level in the SNpc.
Increased the level of GSH in the SNpc.
[30]
LPS-induced inflammatory responses in the primary microglia cell model(1.25, 2.5, 5 µM)Reduced the ROS, NO, IL-1β, and TNF-α levels.[27]
LPS-induced inflammatory responses in the primary microglia cell model(15, 20, 25, 30 µM)Reduced the activity of microglia cells.[27]
LPS-induced pro-inflammatory response in the BV2 microglial cell model(1.25–5 µM)Decreased the cell viability and increased pro-inflammatory cytokines.
Reduced the activation of microglia in BV2 cells.
Reduced the increased TNF-α and IL-1β levels.
Decreased the mRNA expression of NO and iNOS.
Reduced the JNK, ERK, p38, ROS, and MAPK levels.
[34]
LPS-induced damage in the microglial cell model(0.25, 1, 2.5 µM)Inhibited the production of pro-inflammatory cytokines such as TNF-α, NO, and SOD.
Increased dopaminergic neurons.
Reduced the TH-IR neurons.
[14]

LPS: lipopolysaccharide; SOD: superoxide dismutase; GPx: glutathione peroxidase; MDA: malondialdehyde; Iba-1: indole-3-butyric acid; SNpc: substantia nigra pars compacta; TH: tyrosine hydroxylase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; TNF-α: tumor necrosis factor alpha; ERK: extracellular signal-regulated kinase; JNK: c-Jun N-terminal kinase; BV2: mouse microglial cell line; iNOS: inducible nitric oxide synthase; ROS: reactive oxygen species; MAPK: mitogen-activated protein kinase