Table 3. Pharmacological findings of biochanin-A established via in vitro experiments.
(↑increase, ↓decrease, × inhibit, + activation).
| Pharmacological application | Study model | Dose and route used | Findings | Reference |
|---|---|---|---|---|
| Diabetes | Cervical carcinoma (HeLa) cells | EC 50 = 1–4 mmol/L | PPAR receptor activator | ( Shen et al., 2006). |
| Obesity | C3H10T1/2 cells | _ | Mitochondrial respiration ↑ AMPK signalling + | ( Rahman et al., 2021) |
| Neuronal cells | _ | ER stress ↓ leptin signalling × | ( Horiuchi et al., 2021). | |
| Airway hyper responsiveness | OVA-Induced Tracheal Contractions In Vitro. | 10–30 μm | anti-spasmodic agent | ( Ko et al., 2011) |
| Osteoarthritis | IL-1β induced rabbit chondrocytes | 5, 25, 50 μM | Cartilage damage ↓ MMP, NF-κB × TIMP-1 + | ( D. Q. Wu et al., 2014) |
| Primary Rat Adipose-Derived Stem Cells (ADSCs). | 0.3 μM | Adipocyte differentiation × PPARγ, LPL, OPN and leptin ↓ OPG ↑ osteoblast differentiation ↑ adipogenesis × | Su et al., 2013) | |
| Inflammation | ADSCs | 0.1–1 μM | cytoplasmic lipid droplet accumulation × PPAR-γ × Runx2, OPG, RhoA protein, OCN ↑ | ( Su et al., 2013) |
| RAW 264.7 and HT-29 cell lines | 100 μM and 50 μM | NO production, LPS, IKK activity × NF-κB + IL-6, IL-1β, and TNF-α production in RAW264.7 cells ↓ cell proliferation in HT-29 cell line × | ( Kole et al., 2011) | |
| Anti-microbial activity | Potential bacterial pathogens of the human digestive system | 0.13mM 0.26–0.51 mM | Clostridium tertium, clostridium clostridioforme × | ( Flesar et al., 2009; Sklenickova et al., 2010 |
| in vitro antibacterial activity | 16 to 128 μg/mL | Growth inhibitory effect to gram-positive and gram-negative bacteria | ( Hummelova et al., 2015) | |
| C. pneumoniae, C. trachomatis | 12 μM & 6.5 μM buccal formulation | Chlamydia growth × Antichlamydial action + | ( Hanski et al., 2014). | |
| HeLa cells/Macrophages | _ | Salmonella infection × AMPK/ULK1/mTOR pathway | Zhao et al., 2018a) | |
| Neurological disorders: | ||||
| Cerebral ischemia: | Mouse hippocampal HT4 neural cells or primary cortical neurons | 25 and 50 μM | GOT mRNA expression ↑ glutamate-induced cell death × | ( Khanna, Stewart, Gnyawali, Harris, Balch, Spieldenner, Chandan K. Sen, et al., 2017) |
| L-glutamate-induced cytotoxic PC12 cell line | 1, 10, 50, and 100 μM | cytotoxicity ↓ glutathione ↑ LDH, caspase-3 | ( Tan et al., 2013) | |
| Parkinson’s disease | Rat mesencephalic neuron-glia cultures | 12.5, 25, 50 mg/kg i.p. | NADPH-oxidase, MDA formation, SOD, and GPx × dopamine neuronal loss ↓ | ( Wang et al., 2015a) |
| BV2 microglial cells | 1.25, 2.5, 5 μM | LPS related microglia activation × TNFα, IL-1β, nitric-oxide, and ROS ↓ | Chen et al., 2007) | |
| LPS treated mice BV 2 microglial cells | 1.25, 2.5, 5 μM | TNFα, IL-1β, nitric oxide, and ROS ↓ MAPK signalling × | ( WU et al., 2015) | |
| BV2 Microglia | 5, 10, 20 μM | PPAR-γ levels ↑ NF-κB release × | ( Zhang and Chen 2015) | |
| Alzheimer's disease | HCN 1-A cell line with H2O2 model | 0.5, 1 and 2 μg/mL | H2O2 induced neurotoxicity ↓ | ( Occhiuto et al., 2009) |
| PC12 cells with β-Amyloid-Induced Neurotoxicity | 100 μM | Amyloid beta induced cell toxicity ↓ cytochrome-c and Puma Bcl-2/Bax ↓ | ( Tan and Kim 2016) | |
| Microglial cells | 1.25, 2.5, 5, 10, 15, 20, 25, 30 μM | microglial activation × nitric oxide, IL-1b, and TNF-α ↓ ROS × MAPK signaling pathway × | ( Wang et al., 2016) | |
| In-vitro BACE-1 activity assay | 28 μM | BACE1 × strong binding between the chemical and the allosteric site of BACE1 |