Amygdalin (Laetrile) has antifibrotic, antitumor, anti-inflammatory and analgesic effects, amygdalin joint HSYA could inhibit the degeneration of the endplate chondrocytes derived from intervertebral discs of rats induced by IL-1beta and better than the single use of Amygdalin or HSYA. Amygdalin induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells by caspase-3 activation through down-regulation of Bcl-2 and up-regulation of Bax.

Amygdalin exhibits antitumor properties, with studies showing progress in elucidating its mechanism of action[1]. Specifically, amygdalin downregulates genes related to the cell cycle, including exonuclease 1, ATP-binding cassette sub-family F, member 2, MRE11 meiotic recombination 11 homolog A, topoisomerase (DNA) I, and FK506 binding protein 12-rapamycin-associated protein 1. RT-PCR analysis has demonstrated that amygdalin treatment leads to reduced mRNA levels of these genes in SNU-C4 human colon cancer cells[2].

Amygdalin demonstrates efficacy in mitigating inflammatory pain, serving as an analgesic endowed with anti-nociceptive and anti-inflammatory properties. Administered intramuscularly, it notably diminishes formalin-induced tonic pain in the initial acute phase (the initial 10 min after formalin injection) as well as the persistent, late phase (10-30 min post-formalin injection). Moreover, amygdalin's pain-reduction effect escalates with increasing doses, up to a threshold of less than 1 mg/kg during the latter period[3].

Cell viability is determined by MTT assay. Cells are seeded in triplicate at a concentration of 1×105 cells/well on a 96-well plate. SNU-C4 cells are treated with amygdalin at concentrations of 0.25, 0.5, 2.5, and 5 mg/mL for 24 h. After MTT is added to each group, the cells are incubated for 4 h. Then, they are further incubated for 1 h, including the solution in which MTT is dissolved[2].