Hippocampal CA1 neuronal programmed necrosis induced by global cerebral I/R injury is prevented by CA074-me (1 μg, 10 μg) both pre-treatment and post-treatment. The rupture of lysosomal membrane and the leakage of cathepsin-B, and this is strongly inhibited by CA074-me pre-treatment. The overexpression and nuclear translocation of RIP3 and the reduction of NAD+ level after I/R injury are also inhibited, while the upregulation of Hsp70 is strengthened by CA074-me pre-treatment[1]. CA-074Me (30 mg/kg) is capable of inhibiting osteoclastogenesis and bone degradation in vivo[2]. In the CVB+CA-074Me (4 mg/kg/day i.m.) guinea pigs group, the scores of inflammation significantly decrease in comparison with the CVB+None group. In CVB+CA-074Me group, the number of CD8+T cells decrease in comparison with the sham group[3].
In Vitro
CA-074Me (5 μM and 50 μM) inhibits RANKL-induced osteoclastogenesis in BMM cells derived from C57BL/6J and NOD/ShiLtJ mice. CA-074Me exerts its anti-osteoclastogenic effect within 24 hours post-RANKL stimulation in vitro. CA-074Me does not exert its anti-osteoclastogenic effect via the MAPK-ERK signaling cascade. CA-074Me inhibits c-FOS upregulation and subsequent NFATc1 autoamplification following RANKL stimulation.[2]. CA-074Me reduces apoptosis induced by CVB1[3].
Kinase Assay
Cell Assay
Animal Administration
References
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