Animal experiment:

Mice[3]The experiments are carried out on naive male Swiss mice weighing 20-25 g. Drugs are administered intraperitoneally (i.p.) at the volume of 10 mL/kg. Fresh drug solutions are prepared on each day of experimentation. Control groups receive saline injections of the same volume and via the same route of administration. During the acute treatment, the animals are allocated to the following drug groups: saline, rivastigmine (0.5 mg/kg, i.p.), scopolamine (1 mg/kg, i.p.), Imperatorin (1, 5, 10 mg/kg, i.p.), or Imperatorin coadministered with scopolamine. To measure the memory acquisition processes, scopolamine is administered 20 min before the pretest, whereas Imperatorin and rivastigmine are administered 30 min before the pretest. To measure the memory consolidation processes, rivastigmine or scopolamine (1 mg/kg) is administered immediately after the pretest, whereas Imperatorin is administered 15 min after pretest or after scopolamine injection. On the second day, the mice are retested. In the second set of the experiments, animals are randomly allocated to receive 6 days of i.p. injections of Imperatorin (1, 5, and 10 mg/kg, i.p.) or saline, twice daily (8:00 a.m. and 8:00 p.m.). On the seventh day, these animals are subjected to saline, scopolamine (1 mg/kg, i.p.), Imperatorin (1, 5, and 10 mg/kg, i.p.), or Imperatorin coadministered with scopolamine. To measure the memory acquisition processes, scopolamine is administered 20 min before the pretest and Imperatorin 30 min before the pretest. To measure the memory consolidation processes, scopolamine (1 mg/kg) is administered immediately after the pretest, whereas Imperatorin is administered 15 min after the pretest or after scopolamine injection. On the eighth day, the mice are retested.

Imperatorin is reported as an anti-cancer medicine with many targets to induce cell apoptosis, such as enhancing p53 expression [1], inducing Mcl-1 degradation [2], activating activation of caspase-3, caspase-8, caspase-9 [3].

When tested with human cancer cell lines (SNU 449-liver cancer and HCT-15-colon cancer), imperatorin treatment promoted cell apoptosi in a dose-dependent manner via modulating expression of apotosis-related proteins [4]. In human embryonic kidney cells, imperatorin treatment significantly attenuated H2O2-induced ROS production [5]. When tested with human hepatoma HepG2 cells, administration of imperatorin inhibited cell proliferation in a time- and dose- dependent manner [3]. In human lung cancer H23 cells, imperatorin was shown to enhance the expression of p53 and induced cells apoptosis at sub-toxic concentrations [1].

In nude mouse model bearing HepG2 cells, treatment with imperatorin significantly suppressed tumor growth in a dose-dependent manner [3].

It is also reported that imperatorin inhibits voltage-gated K+ channels and ATP-sensitive K+ channels when tested with neuronal NG-108-15 cells [6].

References:
[1].  Choochuay, K., et al., Imperatorin sensitizes anoikis and inhibits anchorage-independent growth of lung cancer cells. J Nat Med, 2013. 67(3): p. 599-606.
[2].  Li, X., et al., Imperatorin induces Mcl-1 degradation to cooperatively trigger Bax translocation and Bak activation to suppress drug-resistant human hepatoma. Cancer Lett, 2014. 348(1-2): p. 146-55.
[3].  Luo, K.W., et al., Anticancer effects of imperatorin isolated from Angelica dahurica: induction of apoptosis in HepG2 cells through both death-receptor- and mitochondria-mediated pathways. Chemotherapy, 2011. 57(6): p. 449-59.
[4].  Rahman, A., et al., Growth inhibition of various human cancer cell lines by imperatorin and limonin from poncirus trifoliata rafin. Seeds. Anticancer Agents Med Chem, 2015. 15(2): p. 236-41.
[5].  Cao, Y., et al., Antioxidant effect of imperatorin from Angelica dahurica in hypertension via inhibiting NADPH oxidase activation and MAPK pathway. J Am Soc Hypertens, 2014. 8(8): p. 527-36.
[6].  Wang, Y.W., et al., Inhibitory effects of imperatorin on voltage-gated K(+) channels and ATP-sensitive K(+) channels. Pharmacol Rep, 2015. 67(1): p. 134-9.