Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity[1]. Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation[2]. Caspase-3

Lycopodine (5.22-78.3 μg/mL; 12 hours) has 50% viability at 57.62±0.086 μg/mL and 51.46±1.43 μg/mL for PC3 and LnCaP, respectively[1].Treated with Lycopodine (74-222 mM; 12 hours), the apoptotic index is with respect to the gradual increase in doses for the PC3 and LnCaP cells[1].Lycopodine (74-222 mM; 12 hours) induces cell cycle arrest at G0/G1 phase in PC3 and LnCaP cells[1].Lycopodine (0-200 μg/mL; 48 hours) shows cytotoxicity to HeLa cells in a dose and time dependent manner. However, Lycopodine shows minimal cytotoxic effects in normal peripheral blood mononuclear cells (PBMC) even at the highest dose (200 μg/mL)[2].Lycopodine (100, 200 μg/mL; 24 hours) increases level of Bax and decreases the mitochondrial cytochrome c. This is followed by an increase in expression of cytochrome c in cytosolic fraction. Lycopodine also cleaves the caspase-3 in the total cell lysate, while the expression of Bcl-2 is down regulated[2]. Cell Viability Assay[1] Cell Line: PC3 and LnCaP cells

[1]. Bishayee K, et al. Lycopodine triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in androgen sensitive and refractory prostate cancer cells without modulating p53 activity: signaling cascade and drug-DNA interaction. Eur J Pharmacol. 2013 Jan 5;698(1-3):110-21. [2]. Mandal SK, et al. Lycopodine from Lycopodium clavatum extract inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation. Eur J Pharmacol. 2010 Jan 25;626(2-3):115-22.

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