Coompo Research Chemicals

Baicalein has been shown to inhibit certain types of lipoxygenases and act as an anti-inflammatory agent. It has antiproliferative effects on ET-1-induced proliferation of pulmonary artery smooth muscle cell proliferation via inhibition of TRPC1 channel expression. Possible antidepressant effects have also been attributed to baicalein in animal research.

Baicalein and baicalin demonstrated a strong activity on eliminating the superoxide radical (O2-) (baicalein: 7.31 x 10(4) u/g; baicalin: 1.19 x 10(5) u/g). The IC50 of baicalein was 2.8 fold higher than that of baicalin. However they had no significant effect on scavenging hydroxyl radical (OH). The present results demonstrated that baicalein and baicalin posed a different pathological pathway. The antioxidant function of baicalin was mainly based on scavenging superoxide radical whilst baicalein was a good xanthine oxidase inhibitor.
Baicalein is an inhibitor of CYP2C9, an enzyme of the cytochrome P450 system that metabolizes drugs in the body.

In vitro the radical scavenging effect of baicalein in detail using electron spin resonance spectrometry. Furthermore, we examined in vivo its effect on the thiobarbituric acid-reactive substances (TBARS) levels and superoxide dismutase in the brain of rats with FeCl3-induced epilepsy and on hippocampal delayed neuronal death in gerbils with transient ischemia. In in vitro experiments, baicalein quenched in a dose-dependent manner 1,1-diphenyl-2-picrylhydrazyl, superoxide, and hydroxyl radicals. In the FeCl3-induced epileptic model, baicalein suppressed the increase in the TBARS level at the FeCl3-injected site. Baicalein also inhibited hippocampal neuronal death induced by 5 min of cerebral ischemia in gerbils. Hence the present study suggested that baicalein is one of the active components in TJ-960, which partially contributes to the antiepileptic and neuronal protective effects of TJ-960, and that the mechanism of its pharmacological action is based upon radical quenching and antioxidative effects.

Low micromolar concentrations of baicalein, and especially its oxidized forms, inhibit the formation of α-synuclein fibrils. In addition, existing fibrils of α-synuclein are disaggregated by baicalein. The product of the inhibition reaction is predominantly a soluble oligomer of α-synuclein, in which the protein molecules have been covalently modified by baicalein quinone to form a Schiff base with a lysine side chain in α-synuclein. The binding of baicalein was abolished by conversion of the Tyr residues into Phe, demonstrating that Tyr is involved in the interaction of α-synuclein with baicalein. In disaggregation baicalein causes fragmentation throughout the length of the fibril. These observations suggest that baicalein and similar compounds may have potential as therapeutic leads in combating Parkinson's disease and that diets rich in flavonoids may be effective in preventing the disorder.